Uroradiology

Text and Atlas

 Uroradiology
Text and Atlas

Suresh M Bakle DMRD MD (Radiology)

Professor in Radiology
Nijlingappa Medical College, Bagalkot
Karnataka, India
Bipin V Daga MD DNB (Radiology)
Lecturer in Radiology
VM Govt Medical College, Solapur
Maharashtra, India

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Uroradiology: Text and Atlas

© 2010, Jaypee Brothers Medical Publishers
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First Edition: 2010
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 Preface

This book intends to present complex information on Uroradiology in easily accessible formats. The notes and
images contained within this book have been structured to conform to the format needed for undergraduate and
postgraduate examinations.
In addition, the authors have, where relevant, not only tried to give complete material but also management
aspect in an attempt to provide a useful acid memory for the students.
The main use of this book as opposed to others is for pictorial review of all important cases of urology. Despite
the concise nature of the material and the inevitable omission of some of more complicated issues, we believe
that this book fulfills its purpose and will support the education of postgraduates apart from supporting the practitioners
in the glorious art and science of uroradiology.
The images in the book are unique and the most interesting part of this book mainly includes the common
and classical uroradiology cases.

Suresh M Bakle
Bipin V Daga
 Contents

1. Embryology ............................................................................................................................ 1
2. Anatomy and Normal Variants .............................................................................................. 3
3. Various Imaging Modalities and Techniques in Uroradiology ............................................... 7
4. Congenital Anomalies of Urorenal Tract ............................................................................. 27
5. Cystic Disease of Kidney .................................................................................................... 71
6. Calculus Diseases of Kidney ............................................................................................... 78
7. Obstructive Diseases of Kidney .......................................................................................... 92
8. Renal Infections ................................................................................................................ 103
9. Urorenal Trauma ................................................................................................................ 120
10. Urorenal Neoplasms .......................................................................................................... 140
11. Medical Renal Disease ...................................................................................................... 161
12. Renal Vascular Diseases ................................................................................................... 168
13. Radiology of Renal Transplant .......................................................................................... 182
14. Urethral Diseases .............................................................................................................. 192
15. Urinary Bladder Diseases .................................................................................................. 199
16. Diseases of Prostate .......................................................................................................... 212
17. Urorenal Interventions ....................................................................................................... 223
18. Miscellaneous Genitourinary Conditions ........................................................................... 225
19. Recent Advances in Uroradiology ..................................................................................... 231
20. Radiological Contrast Media ............................................................................................. 234

Bibliography ................................................................................................................................... 239

Index ............................................................................................................................................... 241
 Introduction and Historical Aspect

“Urology can be said to owe its existence as a specialty to inventing genius of Sir Thomas Edison and
Sir Wilhem Conrad Roentgen. The roentgen rays provided a means whereby diagnostic studies of the
entire genitourinary tract could be carried out.”
— RM NESBITT (1956)

MILESTONES IN URORADIOLOGY
• In 1896, first preoperative radiograph of a calculus was reported by John McIntyre.
• In 1897, French physician Theodore Tuffier introduced a metal stylet into a ureteral catheter to make the catheter
radiopaque and outlined the ureter.
• In 1903, Wittek first used air as a contrast agent.
• In 1905, Voelcker and von Lichtenberg devised first liquid contrast using colloidal A. They also emphasized
the value of lateral and oblique views.
• In 1923, first clinical trial of 10% sodium iodide was done by Earl Osborn, which later became the basis of
present-day IVU study.
• In 1929, Swick first described IVU.
• Smith (1994) first described the role of non-contrast spiral/helical CT in calculus disease.

Uroradiology is a discipline involving imaging techniques like plain radiography, contrast radiography, ultrasound,
computed tomography, radionuclide imaging and magnetic resonance imaging and in any given clinical situation,
the relevant information can be obtained most rapidly and efficiently by using a specific order of radiological modalities
for investigation and evaluation.
 Abbreviations

ADPKD Autosomal dominant polycystic kidney disease

ARPKD Autosomal recessive polycystic kidney disease
ATN Acute tubular necrosis
CT Computed tomography
CTA CT angiography
DRC (DIC) Direct radionuclide (isotope) cystogram
DSA Digital subtraction arteriography
IRC Indirect radionuclide cystogram
IVC Inferior vena cava
IVU Intravenous urogram
MCU Micturating cystourethrogram
MRI Magnetic resonance imaging
PUJ Pelviureteric junction
PUV Posterior urethral valve
UTI Urinary tract infection
VUR Vesicoureteral reflux
MIBG Meta-iodobenzyl guanidine
RVT Renal vein thrombosis
RLQ Right lower quadrant
 Embryology 1

KIDNEY
The development of the embryonic urinary system
involves three separate stages (Figure 1.1):
1. Pronephros
2. Mesonephros and
3. Metanephros.

1. The earliest structure, the pronephros, forms at about

3 weeks in utero, never functions and is reabsorbed
by the fourth week. Its caudal portion, however, plays
a role in the development of the mesonephros. The
longitudinal pronephric duct becomes the meso-
nephric or Wolffian duct, which is initially connected
to the primitive cloaca.
2. Primitive excretory tubules and glomeruli develop
symmetrically from this duct to comprise the meso-
nephros which regresses in the latter part of the
second month.
3. The metanephros or permanent kidney. It then
undergoes division into several small tubules, each
of which becomes associated with a thin part contri-
buted by the metanephric blastema. These caps
differentiate into the mature excretory tubules or
nephrons. The presence of the ureteric bud is believed
necessary for the differentiation of tissues into mature
renal parenchyma. The metanephros is initially located
in the lower lumbar or sacral region and its shift to
FIGURE 1.1: Developmental sequence of urinary tract
(For color version see Plate 1)
the more cranial position of the mature kidney is
achieved through differential growth of the urinary
tract relative to the trunk (Figure 1.2).
BLADDER AND URETHRA
The urogenital sinus is formed from the anterior part of
the cloaca at the time of the descent of the urogenital
septum. That portion of the urogenital sinus above the
entrance of the mesonephric ducts is called the
vesicourethral canal and this becomes the bladder.
The portion which is inferior is termed the definitive uro-
genital sinus.
2 Uroradiology: Text and Atlas

FIGURE 1.2: Development of collecting system of kidneys

(For color version see Plate 1)
With further development, the distal mesonephric duct
is absorbed into the urogenital sinus until the metanephric
duct (now the ureteric bud) enters separately from, and
superior to, the mesonephric duct. The latter will become FIGURE 1.3: Ascent of kidneys (For color version see Plate 1)
the Wolffian duct, precursor to the ductus deferens in
the male. At maturation it enters into that portion of the responsible for the development of the penile urethra of
definitive urogenital sinus which will become the prostatic the male does not occur and, instead, a connection with
urethra. the developing müllerian ducts gives rise to the lower
The development of the definitive urogenital sinus urethra, a small portion of the vagina and the vestibule
proceeds differently in the female. The elongation (Figure 1.3).

NORMAL ANATOMY
• Anatomy of retroperitoneum
• Anatomy of kidney, ureter and bladder
• Anatomy of prostate.
ANATOMY OF RETROPERITONEUM
The transversalis fascia lines the inside of the abdo-
minopelvic cavity, including the inferior aspect of the
diaphragm, the posterior and medial surfaces of the
anterior and lateral abdominal wall muscles respectively,
FIGURE 2.1: Schematic representation of retroperitoneal anatomy (For color version see Plate 2)
Anatomy and Normal Variants 3
the anterior aspect of the spinal column, psoas and
paraspinal muscles and the superior aspect of the pelvic
diaphragm. The major organs and their associated fascia
develop within the space defined by the transversalis
fascia (Figure 2.1).
During embryological development, as the kidneys
ascend from the pelvis the surrounding (perinephric)
fascia forms a cone, with its apex superiorly. The
perinephric fascia anterior to the kidney is often referred
to as Gerota’s fascia, the posterior fascia as Zuckerkandl’s
4 Uroradiology: Text and Atlas
fascia and the enclosed space as the perinephric space.
It contains the kidney, the suprarenal gland anteromedial
to the kidney on the left, It superomedial to the kidney
on the right the upper ureter and the perinephric fat. There
is a small space between the posterior perinephric fascia
and the adjacent transversalis fascia which contains only
fat (the posterior pararenal space). This space is of interest
to the interventional radiologist as a potential area in
which to kink a guide-wire and mistakenly position a drain
intended for the renal collecting system. There is a more
substantial space anterior to the perinephric spaces
between the anterior perinephric fascia and the posterior
layer of the peritoneum, the anterior pararenal space.
This contains the pancreas and duodenum centrally, with
the ascending colon on the right and the descending on
the left. These organs are therefore in direct contact with
the anterior perinephric fascia.
Laterally the anterior and posterior perirenal fasciae
fuse with the lateroconal fascia at the fascial trifurcation.
The lateroconal fascia continues laterally and anteriorly
to fuse with the parietal perietal peritoneum.
The retroperitoneum is a large space bounded
anteriorly by the posterior parietal peritoneum, posteriorly
by the transversalis fascia, and superiorly by the diaphragm.
Inferiorly, it extends to the level of the pelvic brim.
On either side, the retroperitoneum is divided into
three compartments by coronally oriented anterior and
posterior renal fasciae, which lie anterior and posterior
to the kidneys, respectively.
The anterior renal fascia is a thin layer of connective
tissue, which is difficult to identify on images.
The anterior and posterior renal fasciae fuse laterally
to form the lateroconal fascia. The lateroconal fascia
extends posterolaterally to the ascending and descending
colon and fuses with the parietal peritoneum. Superiorly,
both layers of renal fasciae blend with the diaphragmatic
fascia, and inferiorly, this fuses with the iliac fascia and
periureteric connective tissue at the level of the iliac crest.
Medially, the anterior renal fascia blends with the
connective tissue and fat that surround the great vessels,
and the posterior renal fascia blends with the fascia of
the psoas and quadratus lumborum muscles.
Each perirenal space, which is situated between the
anterior and posterior renal fasciae, contains a kidney,
adrenal gland, pelvocalyceal system, proximal ureter, and
neurovascular and lymphatic structures. No potential
communication exists between the 2 perirenal spaces.
The anterior pararenal space is limited anteriorly by
the posterior parietal peritoneum and posteriorly by the
anterior renal fascia.
The contents are the first, second, and third parts of
the duodenum; the pancreas; the ascending colon; the
descending colon; and the splenic, hepatic, and proximal
superior mesenteric arteries. The anterior pararenal space
communicates across the midline.
The posterior pararenal space is bounded anteriorly
by the posterior renal fascia and posteriorly by the
transversalis fascia. The medial extent of this space is
limited by the fusion of posterior renal fascia with the
fasciae of the psoas and quadratus lumborum muscles;
however, communication with the retrocrural space, and
therefore the mediastinum, is possible. Laterally, the fat
of the posterior pararenal space continues as the
properitoneal fat stripe. The posterior pararenal space
contains no organs. The anterior and posterior pararenal
spaces communicate along their inferior margin.
STRUCTURE OF THE KIDNEY, URETER AND BLADDER
(FIGURE 2.2)
1. Cortex
2. Compound calyx
3. Minor calyx
4. Medullary pyramid
5. Papilla
6. Renal sinus
7. Renal pelvis
8. Infundibulum of major calyx
9. Ureter.
Ureter to the level of the ischial spine, from where
it runs anteromedially until it enters the superolateral angle
of the bladder base. The vas deferens crosses over the
ureter, separating it from the bladder just before the ureters
enter the bladder wall. The ureters run obliquely through
the bladder wall for around 2 cm.
A fibrous capsule is closely applied to the renal cortex
over the entire kidney apart from the hilum. The kidney
is surrounded by perinephric fat and lies within a space
partly enclosed by layers of fascia, traditionally referred

FIGURE 2.2: The vasculature of kidney: note the main renal artery,
the hilar branches, the lobar branches, the segmental branches and
finally the arcuate arteries (For color version see Plate 2)
to as the perinephric space (perirenal space). The
perinephric space is one of a number of spaces within
the abdomen and pelvis that are important determinants
of the direction of disease spread.
MR ANATOMY OF PROSTATE
The prostate and periprostatic tissue are visualized well
using CT. On older generation CT scanners, neither the
zonal anatomy nor the differentiation between the
prostatic parenchyma and the prostatic capsule were
visualized. With dynamic fast-scanning CT, the contrast
resolution of CT has markedly improved and intrapro-
static anatomy can be demonstrated. On sequential CT
scans, prostatic volume can be measured by using the
single parameters of length, width and AP diameter, or
by summation of the prostatic volumes on each slice.
On MRI, the ability to demonstrate the zonal anatomy
of the prostate gland and the distinction between the gland
and periprostatic tissue varies with the imaging planes
and sequences used. On spin-echo (SE) T1-weighted
images, regardless offield strength, the prostate shows an
homogeneous intermediate signal intensity, and the zones
cannot be differentiated. On T2-weighted images, the
Anatomy and Normal Variants 5
zonal anatomy is well delineated, with the prostatic urethra
serving as the key reference point. On T2-weighted
images, the peripheral zone demonstrates a higher signal
intensity than either the central or the transition zones.
The peripheral and central zones are consistently
distinguishable in men under 35 years old and in 35%
of older patients. The central and transition zones have
similar lower signal intensity and can be differentiated
from each other only by knowledge of their anatomical
location. In young subjects, the transition zone has a
uniformly low signal intensity, but it becomes
heterogeneous with the development of BPH. The
surgical pseudocapsule can be seen in older subjects at
the interface between the transition and peripheral zones.
The anterior fibromuscular band covering the antero-
lateral surface of the prostate gland demonstrates a low
signal intensity, allowing distinction between the prostate
and the anterior periprostatic space composed of vascular
areolar tissue. On axial T2-weighted images, the shape
of the peripheral zone changes from the base to the apex.
At the base, the peripheral zone surrounds the
posterolateral aspect of the central zone. The ejaculatory
ducts can be visualized coursing through the central zone
towards the verumontanum. At the apex, the peripheral
zone is nearly concentric around the urethra (with the
exception of the thin anterior fibromuscular band). The
apical urethra is surrounded by muscular fibers giving
low-intensity signals. The prostatic capsule is visualized
as a thin rim giving a low-intensity signal, surrounding
the peripheral zone. The NVB are seen as punctate signal
voids posterolateral to the capsule at the 5 and 7 O’clock
positions. The seminal vesicles look like grapes, and are
well seen in any plane of section.
Periprostatic structures can be differentiated from the
prostatic parenchyma. The periprostatic venous plexus
(PVP) is seen on the anterior and lateral aspects of the
prostate gland. The levator ani muscles give a lower signal
intensity than the peripheral zone, regardless of which
spin-echo TR or TE is used, though the contrast between
the peripheral zone and the levator ani muscle is enhanced
on T2-weighted images. Unlike CT, MRI in all three planes
enables the prostate to be differentiated from the
surrounding levator ani muscle, bladder neck and lower
rectum. In the assessment of prostate size using the formula,
MR is more accurate than either USG or CT.
6 Uroradiology: Text and Atlas

NORMAL VARIANTS (PSEUDOTUMORS)
• Fetal lobulations
• Dromedary or splenic hump
• Column of Bertin (hypertrophied)
Column of Bertin is an extension of normal renal
cortex into the medulla, towards the hilum. It is a normal
variation in renal morphology and should not be confused
with a mass. The column of Bertin anatomically and
functionally resembles the rest of the renal cortex.
The use of different imaging modalities to
differentiate a column of Bertin from a renal tumor is
listed below:

Modality Column of Bertin Renal neoplasm

1. Ultrasound Isoechoic to cortex Hypo- or hyperechoic relative to cortex
2. 99mTc DMSA Normal uptake Photon deficient area
3. 99mTc DTPA Normal uptake Photon deficient area
4. CT Isodense to cortex Hypodense, rarely hyperdense
Homogeneous contrast Decreased contrast enhancement
enhancement Peripheral Increase
Puddling
Nonhomogeneous
5. MRI Isointense to cortex Hypo- or hyperintense
Nonhomogeneous
 Various Imaging Modalities and Techniques in Uroradiology 7

VARIOUS IMAGING MODALITIES AND Satisfactory bowel preparation is important prerequi-

TECHNIQUES site.
• 90% radiopaque calculi (calcium oxalate phosphate,
• Plain radiography (KUB film)
triple, cystine)
• Intravenous urography (IVU)
• ‘Radiologists graveyard’
• Retrograde urography (RGP)
• Antegrade urography (AGP) • Radiolucent calculi missed (uric acid, xanthine matrix,
• Nephrotomography orotic acid stones)
• Cystography and cystourethrography • Other radiopaque densities like pheloboliths, arterial
a. With voiding urethrogram calcifications, lymph nodes, masses may be mis-
b. Retrograde urethrogram leading.
c. Cystogram
d. With DC (air) THINGS TO BE SEEN ON KUBU FILM
e. Triple contrast (angiography plus pneumocysto- 1. Bowel preparation
gram plus interstitial air in wall of UB) 2. Visualized bones
f. Chain urethrogram
3. Properitoneal fat lines
g. Choke urethrogram
4. Renal outlines/shadows
• Ultrasound
5. Psoas shadows
• Color Doppler
6. Calcific density along kidney, ureter, bladder or
• Computed tomography
urethra.
• Non-contrast CT
• Contrast CT
• Magnetic resonance imaging (MRI) FEW ILLUSTRATIONS SHOWING DIAGNOSTIC USE OF
KUB RADIOGRAPHS
• Radionuclide Imaging
• Arteriography See Figures 3.1 to 3.12.

PLAIN KUBU RADIOGRAPH MIMICS OF RENAL COLIC (PLAIN KUBU FILM)

The main use of plain radiography is in calculus diseases. See Figures 3.13 to 3.18
8 Uroradiology: Text and Atlas

FIGURE 3.1: Ectopia vesicae FIGURE 3.2: Prune belly syndrome FIGURE 3.3: Right pyonephrosis with
calculi

FIGURE 3.4: Nephrocalcinosis FIGURE 3.5: Vesical calculus FIGURE 3.6: Multiple calculi in right kidney
with DJ stent

RETROGRADE UROGRAPHY (RGP)
Close attention to detail in performing a tailored IVU will
usually result in a satisfactory demonstration of the
pelvicaliceal systems and ureters and retrograde
pyelography should rarely be necessary. The latter is
indicated mainly in those patients suspected of having
a urothelial tumour of the upper urinary tract and in whom
excretion urography is normal. Bulb ureterography will
give a good demonstration of the ureter, and the
retrograde introduction of a catheter into the upper ureter
or renal pelvis is the best method for demonstrating the
pelvicaliceal system (Figure 3.18). Fluoroscopic guidance
should be used and the study should include some oblique
views of the kidney and ureter. The catheter may be left
in a selective position for some hours to collect urine for
cytological examination.
 Various Imaging Modalities and Techniques in Uroradiology 9

FIGURE 3.7: Left putty kidney FIGURE 3.8: The lower poles of both kidneys—renal FIGURE 3.9: Seminal vesicle calcification
shadows are seen approaching towards spine
instead of divergent or laterally directed lower poles
as should be seen normally—Horse-shoe kidney)

FIGURE 3.10: Bladder-wall calcification— FIGURE 3.11: Postoperative KUB film with
schistosomiasis some prosthesis in urinary bladder

INDICATIONS ANTEGRADE UROGRAPHY (AGP)

• Mainly used for better visualization of lower ureter
and pelvi-caliceal system
• IVU not satisfactory
• Contrast reaction render IVU hazardous
• Renal failure
• To delineate exact site of the Ureteric strictures
• Filling defects like: tumors, sloughed papillae
radiolucent calculus, are better seen on RGP.
Antegrade pyelography is an accurate method of
demonstrating precisely the site of an obstruction to the
upper urinary tract. The IVU with delayed films may
outline the obstruction, but the concentration of contrast
may be poor and the final diagnosis only made on a
24 hour film. Helical CT is a more rapid and accurate
method of demonstrating the site (and possible cause)
of obstruction.
10 Uroradiology: Text and Atlas
FIGURE 3.12: Large calculus in a FIGURE 3.13: Extensive pancreatic calcification
horse-shoe kidney on left side
FIGURE 3.15: Colon studded with fecoliths
Ultrasound will rapidly confirm the presence of
dilatation in the pelvicaliceal system and one can then
proceed directly to antegrade pyelography. With the patient
prone, a fine 20 or 22 gauge Chiba needle is inserted under
ultrasound guidance or fluoroscopic control beneath the
12th rib into a lower pole calyx, under local anesthesia. As
soon as the collecting system is punctured, trapped urine
will escape through the needle. This should be aspirated
and sent for culture and, if a urothelial tumor is suspected,
FIGURE 3.14: Worm infestation, as seen in
right lower quadrant
FIGURE 3.16: Enteroliths
for cytology. Once some reduction of pressure has been
achieved within the system, contrast medium is injected
to outline the pelvis and ureter down to the level of
obstruction and it may be necessary to tilt the patient into
a semierect position to achieve this.
INDICATIONS
It gives an opportunity to perform interventional
procedures like:
 Various Imaging Modalities and Techniques in Uroradiology
FIGURE 3.17: Ovarian dermoid with tooth-
like calcification
• Decompression of PUJ obstruction
• Drainage of pus in pyonephrosis
• PCNL-Stone removal and Stenting
• Biopsy and balloon occlusion.
ADVANTAGES OF AGP
• Direct site of obstruction shown (mid. 1/3 ureter)
• Ureteral stenting can be done
• Brush—Biopsy from suspected lesions can be obtained
• Stone manipulations can be attempted.
DISADVANTAGES OF AGP
• To assess the prognostic value of therapeutic
intervention, urosurgeons demand IVU and the
functional aspect of urinary system is always better
commented and documented on IVU only
• Invasive procedure.
INTRAVENOUS UROGRAPHY (IVU)
INTRODUCTION
• Widely used study
• Require bowel preparation
• IV contrast media required
• Indirect signs-delayed nephrogram urogram,
hydronephrosis, hydroureter can be absent in acute,
partial obstruction.
11
FIGURE 3.18: Normal RGP
• Longer duration required
• Radiation hazard.
An Intravenous Urogram (IVU) is an X-ray examina-
tion of the kidneys, ureters and urinary bladder. Most
people are familiar with X-ray images, which produce
a still picture of the body’s interior by passing small, highly
controlled amounts of radiation through the body and
capturing the resulting shadows and reflections on film.
An IVU study uses a contrast material (iodine) to enhance
the X-ray images. The contrast material is injected into
the patient’s system and its progress through the urinary
tract is then recorded on a series of quickly captured images.
The exam enables the radiologist to review the anatomy
and the function of the kidneys and urinary tract.
EXCRETORY UROGRAPHY (INTRAVENOUS
UROGRAPHY, IVU, IVP)
Since 1929, when the first intravenous contrast agent was
developed by Swick, excretory urography has been the
primary modality for imaging the urinary tract. This
original agent, Uro-selectan, was the precursor of the
numerous excellent contrast agents available at the
present time. As early as 1937, Berger made several
recommendations for improvement in technique that are
still valid today. The elimination of the obscuring effect
of abdominal gas has since been accomplished by
12 Uroradiology: Text and Atlas
routine tomography. A greater renal concentration of
contrast media has been facilitated by use of higher doses
of the safer modern contrast agents, and ureteral
compression, also advocated, is now widely practiced.
State of the art urography is now such that with
“tailoring” and proper attention to detail, the renal
margins and parenchyma, as well as the entire collecting
system including the ureters and bladder, can be visualized
diagnostically. Techniques have also been described for
evaluating the urethra as a final step in urography. This
procedure has now attained a high degree of safety as
well as efficacy. The mortality rate of 1 in 75,000 is similar
to that expected from the parenteral administration of
penicillin.
PHYSIOLOGY OF RADIOGRAPHIC CONTRAST
EXCRETION
Commercially available contrast agents that are approved
for urography consist of ionic salts of benzoic acid
derivatives containing three iodine atoms. The two anions
used most widely in the United States are diatrizoate and
iothalamate. Following injection, their distribution in the
body and routes of excretion are identical, and their
visualization in the kidneys is equal. Assuming normal
renal function, their route of excretion is greater than 99%
by glomerular filtration. Other commercially available
anions are Iodamide and Metrizoate. Cations most
commonly encountered are sodium and methylglucamine
(meglumine) or a mixture of the two.
After intravenous injection, whether by bolus or by
infusion, these preparations leave the vascular system
in two ways. First, rapid permeation of the capillary wall
and equilibration with the extracellular fluid occurs. At
the same time, contrast in the bloodstream undergoes
glomerular filtration and subsequent excretion in the
urine. As plasma contrast concentration falls as a result
of ongoing renal excretion, there is a continual
redistribution of the extracellular contrast into the vascular
system.
Meglumine is not metabolized and is excreted entirely
by glomerular filtration. This results in a higher urinary
solute output and a subsequent increase in urinary flow
rate due to an osmotic diuresis. The final result is a lower
concentration of urinary iodine with the meglumine salts
and yet the potential for greater distention of the collecting
system. Conversely, sodium undergoes extensive
reabsorption by the renal tubule. While the plasma half-
life is relatively low for both meglumine and the contrast
anions, that for sodium is longer because of reabsorption
and subsequent refiltration. The delayed excretion of
sodium due to reabsorption by the tubules leads to a
decreased osmotic diuresis compared with that achieved
with the meglumine salts and thus results in increased
concentrations of iodine in the urine, purportedly
providing higher contrast and hence better visualization.
Facts such as these have led some investigators to
recommend using only the sodium salts for urography
because of the supposed increased contrast attainable.
Others have recommended the meglumine salts because
of the increased distention of the collecting system that
may be encountered. In fact, McClennan and Becker
showed that in a comparison of sodium and meglumine
salts, films showed no reliable difference in a
heterogeneous patient population or even in the same
patient. The advantage of greater collecting system filling
as may be seen with the meglumine salts can be achieved
with any of the commercial preparations by application
of adequate ureteral compression. Attempts to maximize
the benefits of both cations have resulted in the production
of preparations combining the two.
The quality of the urogram depends on good
pelvocaliceal concentration of contrast media as well as
sufficient distention of the collecting system. All attempts
to improve urographic quality are based on manipulation
of these two variables. Elkin has found that as one goes
from small to large doses of contrast media, the urine
concentration of organic iodide increases. He also found,
however, that there was an upper limit of such
concentration, which, when exceeded, led to even greater
diuresis and subsequent dilution of iodine in the urine.
With the high doses of contrast now in common use,
the production of urine with a very high concentration
of iodine is not so much the main objective as is the
duration of the high concentration of the contrast medium
in the urine. Thus exposures have a greater likelihood
of being obtained at a time of peak concentration, and
there is also a prolongation of the interval during which
optimal tomography can be performed. Talner states that
 Various Imaging Modalities and Techniques in Uroradiology
with large doses of contrast (30–42 g of iodine),
urographic quality will be consistently good. With average
doses (17–20 g of iodine), urographic quality can be just
as good if one pays attention to details of technique. In
a busy department in which many urograms are
performed each day, large doses may be justifiable as
routine simply because the radiologist may not have time
to monitor each study carefully. There have been no
reports of any increase in the incidence of side-effects
with the use of larger contrast doses.
INDICATIONS
By current standards of medical practice, almost anyone
suspected of urologic disease will be recommended for
an intravenous urogram, although this may vary from
hospital to hospital because of the availability and
acceptance of the newer imaging techniques. Another
variable is the preference and experience of the referring
clinician. Among the more common indications for
urography, Friedland and co-workers list infections, acute
genitourinary pain, hematuria (microscopic or gross),
trauma, suspected neoplasm, renal transplantation,
neurogenic bladder, congenital anomalies, and
investigation of complications following a surgical
procedure. These investigators further stated that
urography often is not useful in the evaluation of acute
pyelonephritis (unless obstruction is suspected), ureteral
colic in which the calculus is clearly visible on the plain
film, in the staging of lymphoma or testicular neoplasms,
in cases of medical renal disease, in medical hematuria,
in renal failure, and for the investigation of benign
prostatic hypertrophy. However, clinical experience
indicates that many patients with these diagnoses will
eventually undergo urography at some stage of their
diagnosis or treatment.
There are several indications for immediate urography.
These include trauma involving the genitourinary system,
massive gross hematuria of unknown cause, a suspected
vascular accident involving the kidneys, overwhelming
sepsis that may possibly have its source in the urinary
tract, and suspected ureteral calculus.
In the past, indications for urography have included
the evaluation of hypertension. The hypertensive
urogram involves obtaining coned-down films of the
13
kidneys in a rapid sequence following bolus injection of
contrast. The minimum series includes films at 1, 2, and
3 minutes post injection. The radiographic criteria for
renovascular hypertension include delayed visualization
of contrast in the collecting system on the affected side,
decreased renal size, and delayed wash-out of contrast
on the later films in the urogram. A secondary finding
is that of notching of the proximal ureter on the involved
side due to development of collateral flow via the
periureteral plexus reconstituting the renal artery.
Thornbury and co-workers have evaluated the
hypertensive urogram with regard to its efficacy. They
found the true-positive rate in 197 patients with
renovascular hypertension to be only 60%. Furthermore
the predictive value for favorable surgical outcome in
hypertensive patients with positive hypertensive urograms
was only 24%. They concluded that the examination is
a nondiscriminatory test for renovascular hypertension.
Their recommendation was that the suspicion of
renovascular hypertension likely to be surgically
correctable should prompt the clinician to select renal
arteriography and assays of peripheral and renal venous
renin activity. Recently, digital subtraction angiography
has been claimed to provide good visualization of the
renal arteries and may eventually become a satisfactory
screening examination for renovascular hypertension.
The present-day urogram is not a reliable test for either
the presence or severity of functional impairment of the
kidneys. Modern contrast media contain more iodine
atoms per molecule than did the older agents and are
of exceedingly low toxicity. The current use of high doses
results in such high plasma concentration of contrast that
even kidneys with significantly decreased function may
produce diagnostic studies.
Useful information can be gained with regard to the
presence or absence of obstruction in many patients with
renal failure, assuming tomography is used for better
visualization of the poorly opacified collecting systems.
A better modality for evaluating such patients, however,
is renal ultrasound, which is an excellent screening
examination for suspected urinary tract obstruction. Its
usefulness is based on its ability to detect hydronephrosis.
However, it must be realized that there exist a significant
14 Uroradiology: Text and Atlas
number of conditions that can mimic or produce dilatation
of the collecting system in the absence of obstruction.
Renal sonography suggestive of hydronephrosis should
be followed by additional diagnostic studies to confirm
or exclude obstruction.
CONTRAINDICATIONS
There are no absolute contraindications to urography.
There are, however, several situations in which the
potential risks must be weighed against the possible
diagnostic benefits. These conditions; include combined
renal and liver failure, multiple myeloma, pregnancy,
previous reactions to contrast media, history of allergy,
infancy, thyroid disease, renal failure, and diabetes
mellitus.
In patients with multiple myeloma or diabetes, proper
hydration may prevent the possibility of renal damage
from injected contrast. If it is essential to perform
urography during pregnancy, minimal radiation exposure
can be accomplished by obtaining a plain film and a
30 minutes postinjection film. In patients with a history
of previous serious reactions to contrast, pretreatment with
cortico-steroids and the use of a different type of contrast
are recommended, although this is not a proven means
of preventing another reaction. Major life-threatening
reactions do not usually recur, whereas minor reactions
tend to be repeated more often. During infancy, normal
hydration will counteract the marked rise in plasma
osmolarity that may occur following contrast injection.
Urography should be avoided in patients with thyroid
disease who are undergoing either diagnosis or treatment
of their problem, since the iodine-containing contrast may
block the thyroid uptake of radioisotopes of iodine. In
renal failure, it must be accepted that in a very few cases
renal function will decrease following urography.
PATIENT PREPARATION
Dehydration
It has been well established that no significant dehydration
(change in urine osmolality) occurs with the standard
regimen of nothing by mouth (NPO) after midnight.
Further, it has been shown that at least 22 hours of fluid
restriction is required to reliably dehydrate human
subjects. Effective fluid restriction may produce a slightly
detectable increase in urographic density, but the
nephrogram is unaffected. Also to be remembered is that
severe fluid restriction may occasionally result in
inadvertent dehydration, which may be detrimental to
the patient with multiple myeloma, diabetes, or renal
failure who is undergoing urography. The purpose of
maintaining the patient on an NPO basis for several hours
prior to the examination has as its primary purpose the
prevention of emesis with possible aspiration following
injection of the contrast.
BOWEL PREPARATION
In the past, enemas have been advocated before
urography. However, water may be absorbed from the
bowel, and in some cases large amounts of gas are actually
introduced into the colon during the enema. Many bowel
preparation kits are available commercially. Dulcolax
tablets, two to four 5 mg tablets at bedtime prior to study,
usually provide an adequate bowel preparation. They
are useful in eliminating feces and gas.
PSYCHOLOGICAL PREPARATION
Lalli has reported that anxiety appears to be a factor in
the so-called idiosyncratic reactions (nausea and vomiting,
urticaria) following contrast injection, although this is an
unproven hypothesis. Certainly, every effort should be
made to decrease patient anxiety during any procedure.
A gentle, relaxed approach to the patient in an
atmosphere of pleasant ambiance can do much toward
putting the patient at ease. If possible, to minimize pain,
larger rather than the smaller veins should be used for
the injection.
INFORMED CONSENT
The need for informed consent prior to urography is
controversial at the present time. Certainly, the time
required to inform the patient in detail of the possible
complications from urography as well as to obtain his
witnessed signature delays the completion of a heavy
schedule. It is recommended that the patient be
questioned regarding previous reactions to contrast and
informed that he will likely feel a warm flushed feeling,
a metallic taste in the mouth, and perhaps a mild wave
of nausea during and following the injection.
 Various Imaging Modalities and Techniques in Uroradiology
EXPOSURE FACTORS (THE PHYSICS OF UROGRAPHY)
Both the plain film and the urogram should be exposed
at 66 kV(p)–70 kV(p). In general, the mean energy of
polychromatic radiation is between one third and one
half of its peak energy. Thus, the mean energy of the
recommended X-ray beam will be very close to the
K-shell binding energy of iodine (33.2 keV). If the binding
energy of iodine and the mean of the diagnostic X-ray
beam are approximately the same, many interactions will
occur at the K-shell level. This allows maximum
attenuation of the beam, since attenuation is increased
when the photoelectric effect predominates. As the
radiation energy is increased, compton scattering comes
more into play and cannot attenuate a beam as rapidly
as the photoelectric effect.
Another advantage of the diagnostic beam energy of
66 kV(p)–70 kV(p) is the increased ability to image
calcium-containing structures. At lower beam energies,
calcium structures have a higher linear attenuation
coefficient than soft tissue, resulting in greater contrast.
As the energy of the X-ray beam increases, differential
attenuation between calcium structures and soft tissue
is not nearly as large, resulting in reduction of image
contrast. Therefore, small stones that are seen easily at
70 kV(p) are progressively more difficult to see as the
voltage increases. At 100 kV(p) many small stones cannot
be seen.
Generally speaking, a medium-speed calcium
tungstate screen/film combination is most desirable for
urography. If this combination is assigned a speed of 1,
screen/film systems in the speed range of 2 to 5 offer
improvement in overall quality due to diminished
respiratory motion at the cost of some loss of detail and
increase in mottle. However, this trade-off is less significant
if higher-output generators are used to minimize the
exposure time.
In tomography, the motion of the arm should be linear
as the study progresses along the long axis of the kidney.
A medium arc of 30º to 40º is thought to be preferable.
There is an inverse relationship between the magnitude
of the arc and the thickness of the cut obtained. The
greater the arc, the thinner the section, resulting in
sharpening of detail. However, more tomographic cuts
may be needed, and, as section thickness decreases, as
would occur with larger arcs, contrast may also decrease,
15
tending to cancel the sharper detail. Tube sweep times
of less than 1 second require generation of very high
current. A tube sweep time of greater than 2 seconds
invites patient motion and tube sway or unsmoothness.
PLAIN FILM OF THE ABDOMEN (SCOUT FILM;
KIDNEYS, URETERS, BLADDER; PRELIMINARY FILM)
A preliminar y plain film of the abdomen is an
indispensable adjunct to excretory urography (See Table
3.1). No attempt to interpret a urogram should be made
if a scout film is not available. Otherwise, erroneous
interpretations of areas of increased contrast density such
as calculi may be made, and, conversely, when stones
are present, they may be obscured by the contrast and
thus missed entirely.
The most common deficiency of the preliminary film
is failure to demonstrate the upper poles of the kidney
or the region of the prostate. It has been reported that
the entire urinary tract is included on a single 14 × 17
inch film in only 17% of adult patients of average height.
This figure seems somewhat high, but certainly, in a
significant percentage of patients, coned plain views of
the kidneys or pubic area may be necessary to complete
the preliminary evaluation. The importance of visualizing
the upper renal poles and adrenal areas is self-evident
in that calcifications or a mass effect may be detected
on the plain film. Similarly, evaluation of the prostatic
area is necessary prior to administration of contrast to
determine the presence or absence of calcifications that
may suggest the diagnosis of prostatitis. In trauma
patients, it is especially important to visualize the lower
ribs and the entire bony pelvis for the evaluation of
possible fractures that could affect the urinary system.
If calcifications are seen on the plain film overlying
the renal shadows, it becomes necessary to further study
the patient with appropriate oblique views. A right
posterior oblique is necessary for evaluation of
calcifications questionably within the right kidney, and
similarly, a left posterior oblique is obtained to evaluate
left-sided calcifications. If, on the oblique views, the
calcifications remain in constant relationship to the renal
shadow, it can be stated with a reasonable degree of
assurance that they are renal in origin. On the oblique
views, calcifications anterior to the kidney will be projected
lateral to the renal shadow and calcifications posterior
16 Uroradiology: Text and Atlas

Table 3.1: Intravenous urography

Radiography Modification Purpose
Plain films Additional obliques or tomograms To assist the location of potentially intrarenal opacities
Rarely required; ultrasound and other imaging maneuver usually
preferable

Nephrogram Thick slice tomogram To improve definition of the renal outlines

Omit alongwith the 5 min film and To reduce radiation dose
Take a solitary 3 min film

15 min film Second injection of contrast To improve opacification of the pelvicalyceal systems if inadequate

14 min compression Series of 1 cm thick tomograms To differentiate between overlying shadows and filling
film defects within the collecting systems
To delineate the renal outlines when inadequately seen (better done with
ultrasound)

15 min release film Additional bladder views When the bladder is poorly filled on the release film (as is often the
case) delayed films of the fuller bladder may be performed.

When equivocal filling defects are seen in the bladder area oblique films
may be performed

The above additional bladder views are rarely indicated as they increase
the radiation burden to the patient and the relevant clinical problems are
better answered by ultrasound or cystoscopy. However, occasionally a
small suspected calculus in the distal ureter may be confirmed with the
appropriate oblique

Full length post- Bladder area only If the upper tracts have already been adequately imaged then imaging
micturition film the bladder area alone with reduce the patient’s radiation burden

Omit The preceding films may have already provided all the information required
from the investigation

Prone full length film Additional view Where the renal pelvis is dilated, contrast may be slow to pass into the
ureter; this can be accelerated by positioning the patient prone when
the heavier contrast will run anteroinferiorly into the ureter, often to the
level of the obstruction. Simply asking the patient to sit or stand for a
few minutes first may improve the result.

Erect images Additional radiograph or fluoroscopy If it is difficult to determine whether or not there is a small ureteric calculus,
an erect oblique radiograph of the ureter or screening the ureter in this
position may be useful on rare occasions

Frusemide IVU Administration of 20 mg of frusemide If suspected pelviureteric junction obstruction is being

Intravenously after the 15 minute film investigated and there is no evidence of this on the
With a further film 15 minutes later Standard IVU, this maneuver can be performed. It
May provoke hydronephrosis and pain. It is rarely necessary if the patient
is to be investigated with radionuclide renography, as is often the case
in this situation.

to the kidney will be projected medial to the renal shadow.
This allows more cogent comment as to their specific
etiology.
In children, careful coning of the films is necessary
to minimize radiation exposure. The preliminary films
should include the pubic symphysis to exclude exstrophy
and the lumbosacral spine to exclude anomalies that
might suggest neurogenic dysfunction of the lower urinary
tract. If the spine is not seen clearly, lateral views are
recommended for better assessment of its integrity. If
tomograms are planned following injection of contrast,
a scout tomographic section should be obtained to ensure
that the tomographic series will be adequate for evaluation
of the renal outlines. The midpoint for tomographic
 Various Imaging Modalities and Techniques in Uroradiology
sections (distance from table top) is easily determined
by multiplying the thickness of the abdomen in
centimeters at the level of the lower costal margin by 0.4.
The figure obtained is rounded to the nearest whole
number and this becomes the middle of three cuts.
The scout tomographic section should reveal a
reasonably large portion of the renal outline as an
indicator that the planned section levels will encompass
the entire renal outline following injection of contrast.
In accomplishing this, it should be remembered that the
long axis of the kidney is slightly oblique to the long axis
of the body, with the upper pole of the kidney lying more
posterior and the lower pole more anterior.
The limitations of tomography are such that the
normal routine as described above permits visualization
of the renal margins only when they are situated tangential
to the X-ray beam. Distortions of the renal outline in other
areas (anterior or posterior) may thus be missed.
CONTRAST ADMINISTRATION
BOLUS VERSUS INFUSION
The physiology of contrast excretion has been discussed
in an earlier section. There are few if any indications for
choice of a specific contrast agent other than personal
preference and economic factors.
In the past, there has been considerable controversy
regarding the advantages of the bolus injection technique
versus the infusion technique for administration of radio-
graphic contrast agents. There are advantages to both.
In most centers, the bolus technique is currently used.
Its major advantage is that it allows the maximum plasma
concentration of contrast media. An equivalent amount
of iodine given by infusion over a period of 5 to 10
minutes does not allow as high a plasma level as can
be obtained following the bolus injection.
Infusion, on the other hand, is a somewhat more
convenient way of administering the contrast material,
from the point of view of both the physician and the
patient. The unpleasant flushing sensation that often
accompanies bolus injections of a large dose of contrast
is minimized by the longer infusion. Furthermore, infusion
achieves a diagnostically useful nephrogram over a longer
time interval. This allows greater latitude in obtaining
17
tomograms and other special views at a later point in
the study.
DOSAGE
The concept of a routine dose is important, since there
are no useful body nomograms of weight and surface
area for every patient from which to determine an ideal
dose. As discussed above, doses in the range of 17 to
20 g of iodine for the average size adult will result in
diagnostic studies if careful monitoring is performed.
However, larger bolus doses of 28 to 40 g of iodine will
more consistently provide diagnostic urographic studies
in the busy radiology department. Thus, the doses in Table
3.4 reflect the larger dose of radiographic contrast
material. Modification of these doses is recommended
in patients with diabetes, multiple myeloma, renal failure,
and congestive hear t failure. In such patients,
approximately one half the recommended normal adult
dose should be sufficient to gain significant diagnostic
information about the urinary tract.
In children, weight of the patient is a more prominent
factor, and recommended doses are based on this
parameter. Administration of contrast should take place
through a 21 or 23 gauge scalp vein needle, whereas
in the adult, a 19-gauge scalp vein needle is of adequate
caliber for bolus injection or infusion technique. In the
adult, the needle is often left in place for the major portion
of the examination to allow a rapid access to the venous
system should treatment of contrast reaction become
necessary. This is frequently difficult in the younger age-
groups.
FILM SEQUENCING
GENERAL CONSIDERATIONS
The preliminary film of the abdomen and scout
tomographic section have been discussed above. If these
are technically and anatomically adequate, the urogram
can proceed following injection of contrast by whatever
method has been selected. Picture of normal urogram
can be seen in Figures 3.19 to 3.21. Table 3.2 lists a
recommended sequence to be followed for both the
pediatric and adult age-groups. In the infant, bowel gas
may obscure the kidneys to a significant degree. The
adverse effect of this gas can be minimized by allowing
18 Uroradiology: Text and Atlas

the child to drink a commercial soft drink that contains allow adequate visualization of the renal outlines and
carbon dioxide. This causes distention of the stomach parenchyma.
and provides a window for visualization of the kidneys.
Alternatively, prone filming for the early view of the
kidneys will often act as a form of compression and
displace colon and stomach gas away from the renal
areas. In the adult, while abdominal bowel gas is
somewhat bothersome, routine use of tomography should

FIGURE 3.20: Normal IVU

FIGURE 3.19: Schematic diagram showing important renal structures

1. Renal cortex 2. Infundibulum 3. Minor calyx
4. Major calyx 5. Papilla 6. Infudibulopelvic junction
7. Renal pelvis 8. Infundibulum 9. Ureter

Table 3.2: Recommended film sequence

Pediatric urography
1. Plain film of abdomen-appropriate size and collimation
2. Postbolus injection
3. 1 minute full view
4. 10 minute full view
Adult urography
1. Plain film of abdomen
Full view
Coned view as necessary to include kidneys or prostatic area
Oblique views as necessary for calcifications over kidneys
Scout tomogram –0.4 × body thickness at costal margin
2. Postbolus injection FIGURE 3.21: IVU
3. 1-minute tomograms, 3–5 views as necessary
4. 5-minute full view 1. Calyx 2. Infundibulum 3. Pelvis
5. Apply compression
10-minute full view with compression in place As a general rule, all urographic exposures should be
Release compression
Full view immediately after release of compression (“release,”
made with the patient in deep expiration. This allows
“flush,” or “X” film) the kidneys to reach the upward limit of their mobility
6. Full view post voiding
with subsequent straightening of the ureter and minimizes
 Various Imaging Modalities and Techniques in Uroradiology
the possibilities of ureteral tortuosity or kinking.
Furthermore, the patient should be instructed to void prior
to the study to allow better opacification of the bladder
on later films.
It should be remembered that there is no single”best”
method for sequencing of films on the standard urogram.
Indeed, it would be rare to find two institutions performing
exactly the same sequence of films. A ‘‘standard”
urogram, as outlined in Table 3.3, can therefore be
recommended only as a basic guide from which one may
subsequently develop his own criteria and techniques.
TOMOGRAPHY (ADULT)
The astute radiologist should consider using tomography
in virtually every adult patient undergoing an initial
standard intravenous urogram. It should be noted that
tomography of the kidneys during intravenous urography
does not bear the same connotation as the
“nephrotomography” used in the past. This latter
technique involved injection of very high doses of contrast
through a large-bore needle with the timing of the
tomographic sections based on previous determination
of circulation time. With the high doses of contrast
currently used, entirely adequate tomographic sections
are obtained if exposed approximately 1 to 2 minutes
following the bolus injection of contrast or after half of
the contrast (150 ml) has been infused in the drip infusion
technique. If tomography is not to be performed, good
visualization of the renal outlines and full thickness of
parenchyma can be obtained by exposing a coned view
of the kidneys at 1 to 2 minutes following bolus injection
of contrast.
Table 3.3: Contraindications to compression
Suspected or proven aortic aneurysm (check plain film for typical
calcifications)
Evidence of obstruction on early urogram films
Recent abdominal surgery
Urinary diversion
Severe hypertension
Abdominal pain on application of compression device
Recent acute injury (trauma)
Renal transplant
Abdominal distention
Bowel ostomies
19
COMPRESSION
Following the 5 minute full view, many authorities
recommend routine application of ureteral compression
unless contraindicated (Table 3.3). The most significant
of these contraindications is that of known or suspected
aortic aneurysm. This presumes that the preliminary film
of the abdomen will have been scrutinized carefully by
the radiologist for calcifications in the aortic wall of
configuration to suggest aneurysmal dilatation.
While some radiographic tables have a built-in
compression band that can be applied, this does not
appear to be as effective as the Velcro belt device with
inflatable balloons. The position of the balloons is critical
in providing adequate compression of the ureter against
the sacral promontory. The balloons should nearly touch
in the midline when inflated, and their upper edges should
parallel the upper level of the iliac crest. The key to success
is a tight application of the belt while the patient is in
deep expiration prior to inflating the balloons. This allows
as much compression as possible to be obtained with
the belt itself. Pain in the renal areas during or after
application of compression usually indicates that there
has been rupture of the collecting system with pyelosinus
extravasation. Compression should then be released
immediately. This minor complication is usually of no
consequence. However, if the patient is known to have
infected urine, appropriate antibiotic coverage is
indicated.
After the compression cuff has been in place for
approximately 4 or 5 minutes, the 10 minutes full view
is obtained. If compression has been adequately applied,
there will be complete and adequate opacification of the
upper ureters and entire intrarenal collecting system. Not
infrequently there will be mild distention of the collecting
system due to the minimal degree of obstruction caused
by the compression cuff. Following release of
compression, a full view is exposed immediately. This
has been termed the ‘‘flush’’, ‘‘X’’, or ‘‘release” view and
is designed to visualize the distal ureters as a result of
the rapid distal passage of contrast from the distended
upper systems.
20 Uroradiology: Text and Atlas
FIGURE 3.22: IVU: Postvoid film
1. Sacrum 2. Ureter (distal) 3. VUJ 4. Bladder 5. Pubic symphysis
POSTVOID FILM (FIGURE 3.22)
The patient is requested to void in privacy and a full
postvoiding view is obtained. It should be apparent that
the environment in most radiology departments is not
conducive to normal voiding. While comment should be
made on the radiographic report concerning the presence
and amount of postvoid residual urine, the only valid
inference that can usually be drawn from a postvoiding
film will be in those patients who demonstrate an empty
bladder.
TAILORING
If the study is being monitored after each exposure,
significant abnormalities can be noted and appropriate
deviations from the standard sequence requested. These
may include oblique tomographic sections, coned oblique
views of the kidneys, or full oblique or prone views to
hopefully provide better filling of the distal ureters. If it
becomes necessary to better visualize the ureterovesical
junctions, the right posterior oblique coned view of the
bladder will allow visualization of the left ureterovesical
junction and vice versa. Coned oblique views of the
bladder are also useful for imaging filling defects in the
bladder and irregularities of the bladder wall and for
determining the presence of extravasation in the
retrovesical region. A coned postvoid view of the bladder
is a necessity when evaluating questionable filling defects.
This view often enhances a persistent defect.
Delayed films are essential when an obstructive
nephrogram is seen on the routine early views. A
recommended sequence for these delayed views is 30
minutes, 1 hour, 2 hours, 4 hours, 8 hours, and 24 hours.
When obtaining delayed views, the patient should be
instructed to void prior to exposure of the film so that
a calculus at the level of the ureterovesical junction will
not be obscured by the full bladder. Unless the degree
of obstruction is extremely severe, at some point during
this sequence of delayed films contrast can usually be
seen columning in the ureter to the point of obstruction.
If the degree of obstruction is such that there is no
columning by 24 hours, further films are not indicated.
In such patients further imaging modalities will be
necessary to determine the anatomy of the obstructed
system. These may include antegrade or retrograde
pyelography. Routine full views obtained in both
obliquities are a standard part of the urographic sequence
at some institutions. This will depend on the personal
preference of the radiologist.
LIMITED UROGRAM
This study usually consists of a preliminary film of the
abdomen followed by a single full view obtained
10 minutes after injection of a standard dose of contrast.
Indications for such studies would include, for example,
follow-up on a patient who has recently passed a ureteral
calculus that was diagnosed by a standard urogram at
an earlier date. In some institutions, the limited urogram
is used in young female patients with signs and symptoms
of acute pyelonephritis to exclude obstruction as a possible
cause. Certainly, in children, a more limited study is
indicated as is noted. Most reports in the literature and
standard texts recommend a film shortly after injection
followed by another full view at 5 or 10 minutes
postinjection.
 Various Imaging Modalities and Techniques in Uroradiology
FIGURE 3.23: Focal hydrocalicosis at right upper pole with
ureteric strictures–tubercular
FIGURE 3.24: Black or negative pyelogram on right side
An Abnormal Pyelogram
See Figures 3.23 and 3.24
DEMERITS OF IVU
• Contrast materials used in IVU studies can cause
adverse reactions in some people
• Women should always inform their doctor or
X-ray technologist if there is any possibility that they
21
are pregnant. The effective radiation dose from this
procedure is about 1.6 mSv, which is about the same
as the average person receives from background
radiation in six months. Radiation disadvantages are
further minimized by:
• The use of high-speed X-ray film that does not require
much radiation to produce an optimal image
• Technique standards established by national and
international guidelines that have been designed and
are continually reviewed by national and international
radiology protection councils
• Modern, state-of-the-art X-ray systems that have very
tightly controlled X-ray beams with significant filtration
and X-ray dose control methods. Thus, scatter or stray
radiation is minimized and those parts of a patient’s
body not being imaged receive minimal exposure.
LIMITATIONS OF IVU
An IVU shows details of the inside of the urinary tract
including the kidneys, ureters and bladder. CT or MRI
may add valuable information about the functioning
tissue of the kidneys and the surface and surrounding
structures nearby the kidneys, ureters and bladder. IVU
studies are not usually indicated for pregnant women.
MODIFICATIONS OF IVU
Modern non-ionic contrast agents do not provoke an
osmotic diuresis and the degree of opacification is unlikely
to be significantly altered by dehydration. Fluid restriction
should therefore be avoided and if there is a risk that
the patient is dehydrated before the IVU this should be
corrected first.
The classical series of plain films (immediate, 5 and
15 minute, full length release and postmicturition) is
described, with mention of some of many potential
modifications. A preliminary postmicturition plain film
(KUB) is performed. This should be examined to check
exposure factors, centring and obvious pathology, particu-
larly urinary tract calcification. Intravenous contrast is
given relatively rapidly by hand. The standard dose is
50 ml of 350–370 strength water-soluble contrast. Some
understanding of the underlying structure of water-soluble
contrast agents is desirable and a knowledge of potential
adverse reactions and their treatment is imperative. These
22 Uroradiology: Text and Atlas
issues are discussed under water-soluble contrast (p. 926).
At this point it is worth emphasising some safety features.
Although modern contrast medium is exceptionally safe,
there is a small risk of serious reactions. The most
dangerous of these are the anaphylactoid-type
hypersensitivity reactions.
CYSTOGRAPHY AND CYSTOURETHROGRAPHY
a. With voiding urethrogram
b. Retrograde urethrogram
c. Cystogram
d. With DC (air)
e. Triple contrast (angiography plus pneumocystogram
plus interstitial air in wall of UB)
f. Chain urethrogram
g. Choke urethrogram
MCU
The MCU is the most accurate method of demonstrating
posterior urethra and VUR, and it is important in children
with UTI and reflux nephropathy.
It is a relatively uncomfortable investigation.
The catheterization should be carried out gently but
confidently with anesthetic jelly and an appropriately sized
catheter, using a sterile non touch technique. Dilute water-
soluble contrast medium (15–20%) should be used and
the bladder filled to capacity. After removal of the catheter
the patient is tilted with the table to the erect position
and asked to empty the bladder into a plastic jug. Images
during filling and during micturition should be obtained
to document any vesicoureteric reflux. Micturating
radiographs taken with the patient slightly oblique will
demonstrate the posterior urethra. This part of the study
is especially important in children suspected of having
posterior urethral valves, which will only fill out and cause
obstruction during micturition. Contrast medium injected
retrogradely will fail to show valves. When catheterization
is not possible because of a urethral stricture, the bladder
can be filled in the retrograde manner using an ascending
urethrogram.
ASCENDING URETHROGRAM
The ascending urethrogram gives excellent anatomical
information concerning the distal urethra as far as the
distal sphincter mechanism. Water soluble contrast
medium should be introduced by means of either a clamp
and nozzle (Knutsson’s clamp) or a Foley balloon catheter
gently inflated in the fossa naviculare just proximal to
the urethral meatus. For a simple ascending urethrogram
to demonstrate a penile or bulbar urethral stricture the
clamp is easy and quick to use, the whole investigation
taking just a few moments. As soon as the urethra is
filled and contrast medium is seen to be trickling past
the distal sphincter, films are taken in two oblique
projections.
COMBINED ASCENDING URETHROGRAM AND MCU
When both an ascending urethrogram and a descending
(micturating) study are required to show the posterior
urethra, the bladder can be filled slowly using a 50 ml
syringe for repeated injections. After images of the anterior
urethra have been obtained in the usual way, the clamp
or catheter is removed, the patient tilted to the upright
position, and oblique views during micturition obtained
to exclude vesicoureteric reflux and to demonstrate the
posterior urethra. This combined study is of particular
importance in demonstrating the anatomy of strictures
in the proximal and distal urethra after pelvic and perineal
trauma. Films of the urethra obtained during micturition
at the end of an IVU are inadequate, the concentration
of contrast medium being insufficient for this purpose.
ULTRASONOGRAPHY
A normal kidney shows central echogenic sinus fat and
pelvicalyseal system and peripheral sim of cortex (normal
thickness of cortex is 1.8–2.0 cm) with distinct CM-differ
entiation is corticomedullary differentiation as shown in
Figure 3.25.
ADVANTAGES
1. Widely used
2. No hazard of ionizing radiation
3. Easily available
4. Multiplanner capability
DISADVANTAGES
1. Bowel gas obscures especially in mid ureter
2. Obese patients
 Various Imaging Modalities and Techniques in Uroradiology 23

ROLE OF MDCT IN UROLOGIC DISEASES

INCLUDING THE IMAGING PROTOCOLS
INTRODUCTION
CT imaging of the urinary system has essentially replaced
conventional plain film excretory urography. CT scanning
for stones, hematuria, or for evaluating renal masses are
performed worldwide. The appropriate CT protocol will
be selected by the radiologist based on the clinical history
of the patient (see Table 3.4).

INDICATIONS
1. Differentiating cyst from tumor when ultrasound
equivocal
FIGURE 3.25: Ultrasonography: A normal kidney
2. Staging renal tumor
3. Calculus size cannot be evaluated 3. Excluding small tumors in patient with hematuria
and otherwise normal studies
4. Operator dependent
4. Renal tumor
It is a very vital modality especially in pediatric urology
5. Retroperitoneal pathology affecting the upper
practice and in screening for urorenal diseases in all age
urinary tract
groups, e.g. in obstructive diseases: 6. Retroperitoneal fibrosis
Signs of Obstruction 7. Retroperitoneal tumor
Indirect signs: 8. Differentiating uric acid calculi from urothelial tumor
1. Hydronephrosis 9. Filling defects in the pelvicaliceal system
2. Hydroureter 10. Renal trauma
3. Absent ureteric jets 11. If IVU is abnormal will show extent of injury better
4. Renomegaly than ultrasound
5. Renal blood flow changes—can be absent in early 12. Lower tract tumor
obstruction 13. Staging bladder, prostatic and testicular tumors
6. Forniceal rupture, Follow up after surgery, radiotherapy or chemo-
therapy
7. Acute renal failure
14. Calculus disease
8. Extrarenal pelvis.
15. Colic—emergency nonenhanced helical CT precise
Direct Signs localization of stones before treatment.

Calculus itself as a cause may be seen.

Table 3.4: Urinary tract imaging protocols

Stone Protocol
For detection of renal, ureteral, or bladder stones
CT Urography (Hematuria Protocol)
For evaluation for common causes of persistent
hematuria, i.e. stones, urothelial tumors, renal tumors
Non-contrast CT imaging from kidney to bladder.
(May be necessary infrequently to use iodinated contrast
agent to distinguish between ureteral stones and phleboliths)
Follow-up imaging with non-contrast plain film radiography
Non-contrast followed by contrast CT imaging from kidney
to bladder

Renal Mass Protocol

For characterization of renal masses detected by Non-contrast followed by contrast CT imaging of kidneys
other imaging studies, e.g. ultrasound, MRI only
24 Uroradiology: Text and Atlas
STONE PROTOCOL
For detection of renal, ureteral, or bladder stones non-
contrast CT imaging from kidney to bladder (May be
necessary infrequently to use iodinated contrast agent
to distinguish between ureteral stones and phleboliths).
Follow-up imaging with non-contrast plain film
radiography.
Non-contrast followed by contrast CT imaging of
kidneys only axial image from “stone protocol” CT
showing left ureteral stone.
Urolithiasis and Nephrolithiasis
Almost all ureteral and renal stones, including those
containing uric acid, can be detected by non-contrast CT
imaging. The accuracy of the technique in diagnosing
urolithiasis in patients presenting with acute flank pain
has been determined to be as high as 97%, with a
sensitivity of 95% and specificity of 98%. This compares
to sensitivities in the range of 45–58% for non-contrast
plain film radiography and 64–87% for plain film
excretory urography.
However, it is occasionally difficult to distinguish
between non-obstructing distal ureteral calculi and pelvic
phleboliths on non-contrast CT images. In these cases,
it may be necessary to use intravenous contrast agent,
so that the relationship of the calculus to the opacified
ureter can be determined. Another situation in which
intravenous contrast can be helpful is in the detection
of stones in HIV positive patients on protease inhibitors
such as Indinovir. These calculi are typically non-radio
opaque and may go undetected on stone protocol CT
scans. The use of 3-D reconstruction techniques of
contrast-enhanced pyelographic phase images can be
helpful in all of these situations.
The disadvantage of “stone protocol” CT is that the
radiation dose is high (about 500 mrem) compared to
that needed for plain film excretory urography (about
150–350 mrem) and non-contrast plain film radiography
(about 13 mrem). This exposure is a significant concern,
especially as urinary stones frequently affect young
people. For this reason, it is better to avoid CT for follow
up studies wherever possible and to use non-contrast plain
film radiography instead. The initial CT scan and
reconstruction images can be used to aid subsequent
detection of stones on follow-up plain film radiographic
images since the detection rate of stones increases from
45% identified on non-contrast radiographic films alone
to 78% on films viewed together with 3-D reconstructions
of the initial diagnostic CT images.
Pregnant patients should be evaluated initially with
ultrasound imaging, to avoid exposure to any unnecessary
radiation, and MR urography is an alternative imaging
technique for evaluating the renal system in pregnant
women, children, and patients with contraindications to
contrast agents.
CT UROGRAPHY (HEMATURIA PROTOCOL)
For evaluation for common causes of persistent
hematuria, i.e. stones, urothelial tumors, renal tumors.
Non-contrast followed by contrast CT imaging from
kidney to bladder.
RENAL MASS PROTOCOL
For characterization of renal masses detected by other
imaging studies, e.g. ultrasound, MRI.
Many renal lesions are incidentally detected on a
variety of imaging tests, but cannot usually be charac-
terized at the time of detection. Currently, at this institution
“renal-mass protocol” CT is the gold standard for the
characterization of renal masses. This protocol acquires
thin section images of the kidneys before and after
intravenous contrast administration to evaluate the
important characteristic of solid lesions, the unequivocal
demonstration of lesion enhancement post contrast.
Lesions that demonstrate unequivocal enhancement
require histologic diagnosis either by image-guided biopsy
or by surgical resection
ADVANTAGES OF MDCT
1. The advantages of multidetector CT urography over
conventional plain film excretory urography (also
known as IV urography) and ultrasound for the
evaluation of the urinary tract are numerous.
Dedicated CT protocols have been developed for
these new high speed machines for different clinical
indications including “stone protocol” for the
evaluation of urinary tract calculi, CT urography for
the evaluation of patients with hematuria and “renal
 Various Imaging Modalities and Techniques in Uroradiology
mass protocol” for the characterization of known renal
masses. Multidetector CT scanning is fast, taking
around 15 seconds for image acquisition from the
kidneys to the bladder during a single breath-hold.
The images have good spatial resolution, little
misregistration due to respiratory movement, and the
acquisition of multiple thin slices allows excellent two-
and three-dimensional reconstructions of the
abdominal anatomy, making it possible to detect
pathologies outside the urinary tract as well as those
within. Iodinated contrast agents are not usually
required for the detection of renal stones, thus avoiding
the risk of adverse reactions to these agents, but are
routinely used in CT urography and the renal mass
protocol.
2. In comparison to CT, plain film excretory urography
offers excellent delineation of calyceal and papillary
anatomy, the ureters and bladder, but it is inferior
to multi detector CT for imaging of the kidney
parenchyma. Both CT and plain film excretory
urography are associated with a substantial radiation
dose. Ultrasound is good for imaging the kidney
parenchyma and for detecting hydronephrosis, does
not require the administration of iodinated contrast,
and avoids radiation exposure. However, ultrasound
is not good for detecting urinary tract calculi, and does
not adequately image the renal collecting system or
ureters. For these reasons, multidetector CT imaging
has become the gold standard for the diagnosis of
urinary tract calculi, the investigation of hematuria,
and the characterization of renal masses and has
largely replaced both plain film excretory urography
and ultrasound examinations for these purposes.
3. The main causes of hematuria are urinary tract calculi,
renal tumors, urothelial tumors, and infection. CT
urography is the best single diagnostic examination
for diagnosing all of these pathologies, with the
exception of infection, which is effectively diagnosed
in most cases by microbiological analysis of the
urine.
4. CT urography requires the use of contrast agent to
opacify the collecting system, the ureters, and the
bladder. In addition to optimal opacification,
distension appears to be an important requirement
25
for thorough evaluation of the renal collecting system
and ureter. For this reason, intravenous saline is given
at the same time as the contrast material to aid in
the detection of subtle filling defects and the
discrimination between urothelial neoplasms and
other filling defects. Image reconstruction techniques
are used to create images of the entire length of the
urinary system from the kidneys to the bladder. Multi-
planar 3-D reconstruction can provide the anatomic
detail required to correlate the finding with retrograde
ureterography or to perform an endoscopic evalua-
tion. CT has been shown to detect parenchymal
masses in the kidney with a sensitivity of 94%,
compared to 67% for plain film excretory urography
and 79% for ultrasound.
5. Another potential advantage of CT is that reconstruc-
ted images can show tumors in a filled bladder
opacified with contrast agent (“virtual cytoscopy”).
6. In comparison to CT, plain film excretory urography
offers excellent delineation of calyceal and papillary
anatomy, the ureters and bladder, but it is inferior
to multi detector CT for imaging of the kidney
parenchyma. Both CT and plain film excretory.
7. Three dimensional coronal reconstruction of CT
urography image, showing contrast-enhanced renal
collecting system, ureters, and bladder. Note
duplicated system on left side.
8. As Urography is associated with a substantial
radiation dose, ultrasound is not good for detecting
urinary tract calculi, and does not adequately image
the renal collecting system or ureters, multidetector
CT imaging has become the gold standard for the
diagnosis of urinary tract calculi, the investigation of
hematuria, and the characterization of renal masses
and has largely replaced both plain film excretory
urography and ultrasound examinations for these
purposes.
DISADVANTAGES OF MODALITIES IN GENERAL
Conventional cytoscopy remains the “gold standard” for
the detection of tumors of the bladder, as it will detect
early mucosal lesions that do not deform the contour of
the bladder wall. In addition, cytoscopy has the added
capability of biopsy of suspicious lesions.
26 Uroradiology: Text and Atlas
MRI
MRI has as yet less to offer than CT in the imaging of
the upper urinary tract, although the detection of minor
venous involvement by a renal cell carcinoma may
be better shown by MR angiography and MRI plays an
important role in the staging of pelvic malignancy.
The initial results in the staging of prostatic carcinoma
were disappointing but purpose-built, endorectal coils are
producing excellent detail and may well be important
in demonstrating breaks in the prostatic capsule by
prostatic cancer.
MR UROGRAPHY
MR urography is being used in the diagnosis of
obstruction. The coronal images using FlSP, HASTE
sequences rapidly portray a dilated collecting system and
demonstrate the site of obstruction. It avoids irradiation
of the patient; however, CT has the advantage of being
able to show calculi which MR urography cannot
accurately differentiate from other filling defects.
RENAL SCINTIGRAPHY
1. Dynamic renal scan
2. Static renal scan
99M
DYNAMIC SCAN (I-123 HIPPURAN, Tc, DTPA, MAG3)
• Suspected obstruction
• Evaluation of surgical treatment (indirect cystography
and post-renal transplant)
• With captopril for renovascular hypertension—a
sensitive screening test.
STATIC SCAN (DMSA)
• To locate ectopic kidney
• To diagnose intra and extrarenal arterial abnormalities
• In urinary incontinence to detect occult duplication
when IVU and USG are normal
• For renal scarring in Chronic Pyelonephritis or UTI
with VUR
• To estimate differential function.
RENAL CORTICAL SCINTIGRAPHY
It is the most accurate evaluation for renal cortical
scarring. DMSA is bound in the renal tubular cells and
provides excellent visualization of the renal cortex.
Maximal uptake is reached within 3 hours of radiotracer
administration. The typical dose is 5 mCi for adults.
Delayed planar (and pinhole in children) imaging is
acquired 2 hours after injection; in multiple projections.
SPECT is more sensitive and may be helpful, but is usually
not required. Split renal function as a percentage is
typically calculated.
The primary indication for a renal cortical scan is to
assess for renal scarring or acute inflammatory changes.
This technique is superior to both ultrasound and
excretory urography in both instances.
Pyelonephritis is demonstrated as a solitary defect
involving one kidney, multiple focal defects or diffuse
involvement of an entire kidney without volume loss (and
sometimes with evidence of volume expansion).
Decreased uptake of DMSA is associated with ischemia
in the inflamed or scarred zones of renal parenchyma.
An alternative hypothesis proposes failed tubular
transport secondary to paralysis from granulocyte toxic
by-products. Abnormalities resulting from infection are
transient, whereas scars result in a permanent abnor-
mality. Sequential scanning after a newly documented
urinary tract infection in children should be performed
2–3 months after the initial diagnosis to assess for scarring.
The presence of scarring is indicated by photopenia and
cortical contraction (volume loss).
Vesicoureteral reflux (VUR) is present in 25–50% of
kidneys with new renal scarring but the majority of
patients (63–75%) with acute inflammatory changes have
pyelonephritis not associated with VUR. The kidney is
most susceptible to scarring from reflux in the first year
of life and a single instance of pyelonephritis may result
in scarring. Renal scars rarely develop after age 5.
Infection must be present as reflux alone has not been
shown to result in renal scarring.
Renal cortical scanning may also be used as a
secondary means to provide information about renal
tumors or after renal trauma.
ARTERIOGRAPHY (INDICATIONS)
• Renovascular hypertension (gold standard)
• Preceding conservative surgery for Wilms’
• In renal trauma with persistent hematuria, and
hypertension
• In suspected vasculitis (polyarteritis)
• Prior to interventional procedures (like embolization
of AVM, balloon dilatation of RA stenosis).
 Congenital Anomalies of Urorenal Tract 27

INTRODUCTION Agenesis: Bilateral renal agenesis (absence of both

Congenital anomalies of the kidneys are frequently kidneys—Potter’s syndrome) is fatal. It is associated with
encountered and probably related to its complex oligohydramnios, pulmonary hypoplasia, and low-set
ears. Unilateral renal agenesis is not uncommon and
embryogenesis.
usually is accompanied by ureteral agenesis with absence
Congenital anatomic anomalies of the GU tract are
of the ipsilateral trigone and ureteral orifice. Compen-
more common than those of any other organ system.
satory hypertrophy of the solitary kidney maintains
Complications (e.g. urinary obstruction, stasis) may result
normal renal function.
in impaired renal function, infection and calculus
formation, and sexual disability or infertility. Treatment
SUPERNUMERARY KIDNEY
is often surgical.
It is extremely rare. Cleavage of the metanephric blastema
ANOMALIES OF URORENAL TRACT has been suggested as the cause. Most supernumerary
• Kidney kidneys are caudally placed and are hypoplastic. A
• Ureter separate collecting system is generally present.
• Bladder and
• Urethra ANOMALIES OF FUSION
EMBRYOLOGY
KIDNEY
The kidneys begin to form initially in the pelvis and then
• Anomalies of number rise into the upper abdomen later in development. The
• Anomalies of position so called ascent of the kidneys is caused by a
• Anomalies of fusion diminution of the body curvature as well as by the growth
• Anomalies of form of the body in the lumbar and sacral region. During this
ascent they undergo a 90º lateral rotation about a vertical
Anomalies of Number axis with the renal hilus changing from ventral to medial.
1. Agenesis As they ascend the kidneys pass through the arterial
2. Supernumerary kidney fork formed by the umbilical arteries. If one of them fails
28 Uroradiology: Text and Atlas

pass completely, it remains in the pelvis close to the When ureteropelvic junction obstruction is present,
common iliac artery and is a ‘pelvic kidney’. Sometimes pyeloplasty is the treatment of choice (Figures 4.1 to 4.3).
both kidneys are pushed together during their passage
Fused pelvic kidney (pancake kidney) is a much
through the arterial fork and the lower poles become
less common fusion anomaly in which a pelvic renal mass
fused, usually between the 4th and 8th week of fetal
is served by two collecting systems and ureters. If
life. Fusion results in improper rotation and incomplete
obstruction is present, reconstruction is indicated.
ascent.
Anomalies of Position
FUSED KIDNEYS ARE DIVIDED INTO THREE GROUPS
1. Renal ectopia
DEPENDING ON THE RELATIVE HEIGHT AT THE TIME
2. Malrotation.
OF FUSION
1. Kidneys present on either side of the spine with an Renal ectopia: Renal ectopia (abnormal renal location)
isthmus across the midline joining either upper or results from a kidney that fails to ascend from its origin
lower poles are horseshoe kidneys. A central isthmus in the true pelvis or from a superiorly ascended (thoracic)
is a disk kidney and a sigmoid is an upper of one kidney. There is an increased incidence of ureteropelvic
fused to a lower of another. junction obstruction, vesicoureteral reflux, and multicystic
2. Both kidneys fused as irregular masses near the sacral
promontory, a clump kidney.
3. Both fused into one mass which lies on one side of
the spine.
Fusion anomalies (in which the kidneys are joined but
the ureters still enter the bladder on each side) increase
the risk of ureteropelvic junction obstruction, vesicoure-
teral reflux, multicystic renal dysplasia, and injury from
anterior abdominal trauma.
1. Horseshoe kidney
2. Crossed fused renal ectopia
3. Fused pelvic kidney (pancake kidney)
Horseshoe kidney is the most common fusion anomaly.
Renal parenchyma on each side of the vertebral column FIGURE 4.1: Antenatal ultrasound scan crossfused ectopia
is joined at the corresponding (usually the lower) poles,
with an isthmus of renal parenchyma or fibrous tissue
across the midline at the joined areas. The ureters course
medially and anteriorly over this isthmus and generally
drain well. Obstruction, if present, is usually secondary
to high insertion of the ureter in the renal pelvis, not
secondary to the isthmus. Pyeloplasty can be performed
without resection of the isthmus.
Crossed fused renal ectopia is the second most
common fusion anomaly. The renal parenchyma
(representing both kidneys) is on the same side of the
vertebral column. One of the ureters crosses the midline
and enters the bladder on the side opposite the kidneys. FIGURE 4.2: Ultrasound scan (postnatal)—Crossfused ectopia

FIGURE 4.3: Computed tomography: Coronal reconstruction–
Crossfused ectopia on left side
renal dysplasia in incompletely ascended kidneys, but
not in superiorly ascended ones. Surgical correction is
performed when indicated.
Malrotation: This usually minor anomaly of the renal
axis can appear abnormal on radiography of the collecting
system. It should be differentiated from the effects of true
obstruction or renal masses.
Anomalies of Form
1. Duplication anomalies
2. Calyceal diverticulum
3. Renal dysplasias
4. MCDK (Multicystic dysplastic kidney)
5. Medullary sponge kidney
6. Medullary cystic disease of kidney (Juvenile nephro-
nopthesis)
7. Renal hypoplasia and Ask-up mark kidney
8. ARPKD
9. ADPKD.
Duplication anomalies: Supernumerary collecting
systems may be unilateral or bilateral and may involve
the renal pelvis and ureters (accessory renal pelvis, double
or triple pelvis and ureter), calyx, or ureteral orifice.
Congenital Anomalies of Urorenal Tract 29
Duplex kidney (double kidney) consists of a single renal
mass with more than one collecting system. An increased
risk for ureteral ectopy with or without ureterocele exists
in duplex systems; management depends on the anatomy
and function of each separately drained segment. Surgery
may be necessary to correct obstruction or vesicoureteral
reflux.
Renal dysplasias: These parenchymal abnormalities
with consequent renal dysfunction may result from
abnormal development of the renal vasculature, renal
tubules, collecting ducts, or drainage apparatus. Biopsy
may be necessary for diagnosis.
Multicystic dysplastic kidney: This nonfunctioning
renal unit consists of noncommunicating cysts with
intervening solid tissue composed of fibrosis, primitive
tubules, and foci of cartilage. Usually, there is associated
ureteral atresia. A low risk for tumor, infection, and
hypertension exists; some advocate removing these
kidneys, whereas others would observe the patient.
Renal hypoplasia: An underdeveloped kidney is usually
associated with inadequate branching of the ureteral bud.
The kidney is small, with histologically normal nephrons.
Hypertension can occur with segmental hypoplasia, and
ablative surgery may be necessary (Figure 4.4).
FIGURE 4.4: IVU: Small sized right kidney with smooth outline
and small pelvicalyceal system → right renal hypoplasia
30 Uroradiology: Text and Atlas
Autosomal recessive polycystic kidney disease:
Although rare (1/10,000 births), autosomal recessive
polycystic kidney disease is the most common genetically
determined childhood cystic disease of the kidneys
(involving both kidneys and the liver) and frequently
produces renal failure in childhood.
Generally, patients presenting in early childhood show
mainly renal-related symptoms; those presenting in
adolescence show mainly hepatic-related symptoms.
These differences probably reflect phenotypic variation
of the same genetic disorder.
Severely affected newborns commonly have
pulmonary hypoplasia secondary to the in utero effects
of renal dysfunction and associated oligohydramnios. Less
severely affected newborns have a protuberant abdomen
with huge, firm, smooth-surfaced, symmetric kidneys. The
enlarged liver is abnormal with periportal fibrosis, bile
duct proliferation, and rare cysts; the remainder of the
hepatic parenchyma is normal. These pathologic findings
are responsible for perisinusoidal portal hypertension with
minimal or absent hepatic dysfunction. Ultrasonography
is the best diagnostic tool and, in late pregnancy, usually
allows presumptive in utero diagnosis.
In patients aged 5 to 10 years, signs of portal hyper-
tension appear, such as esophageal and gastric varices
and hypersplenism (leukopenia, thrombocytopenia). If
the patient presents in adolescence, nephromegaly is less
marked. Renal insufficiency may be mild to moderate.
The major symptoms are related to progressive hepatic
fibrosis (portal hypertension, gastric and esophageal
varices, hepatic insufficiency, hypersplenism). Diagnosis
is difficult, especially without a positive family history.
Ultrasonography may demonstrate renal or hepatic cysts;
definitive diagnosis may require biopsy.
Many newborns die in the first few days or weeks
of life from pulmonary insufficiency. Most who survive
the first few years have progressive renal failure. Those
with less renal involvement develop progressive portal
hypertension. Portacaval or splenorenal shunts reduce
morbidity but not mortality. Experience with transplan-
tation in these patients is limited. If transplantation is
performed, hypersplenism must be controlled to prevent
immunosuppression; otherwise, hypersplenism may
induce leukopenia, increasing the risk of systemic
infection. Dialysis is used as for other children with chronic
renal insufficiency.
URETER
Ureteral anomalies frequently occur with renal anomalies
but may occur independently. Complications include
obstruction, infection, and sometimes calculus formation
from urinary stasis, as well as urinary incontinence if the
ureter bypasses the bladder and terminates in the urethra,
perineum, or vagina in the female.
1. Peliv-ureteric Junction (PUJ) Obstruction
2. Duplication anomalies
3. Ectopic orifices
4. Ureteral stenosis
5. Ureterocele
6. VUR
7. Megapolycalicosis and megaureter
8. Retrocaval ureter.
CONGENITAL PUJ OBSTRUCTION
INTRODUCTION
It is the most common congenital anomaly of the urinary
tract.
It is also the most common cause of an abdominal
mass in a neonate.
INCIDENCE
Male to female ratio is 2:1. The left side is more commonly
affected. Bilateral PUJ obstruction is present in 10–40%
of cases. A familial tendency has been reported.
PATHOPHYSIOLOGY
The intrinsic form is responsible for 80% of cases and
it thought to be due to a defect in the circular muscle
bundle of the renal pelvis that results in an inability to
transmit normal peristalsis. The extrinsic form accounts
for no more than 15–20% of cases and is usually caused
by aberrant renal vessels that cross anterior to the pelvis
or proximal ureter.
Some authors have postulated less widely held views
regarding the causation of the intrinsic form of PUJ
obstruction, such as the presence of abnormal folds or
a kink of the PUJ, or that the lesion represents an
exaggerated from of extrarenal pelvis.

CLINICAL FEATURES
It may be clinically silent until adulthood, when symptoms
of flank pain, fever or hypertension (rarely) may occur.
However, increasingly, many cases are discovered prior
to birth by obstetric ultrasound. In some cases, a sustained
diuresis may be needed to provoke symptoms (“beer-
drinker’s hydronephrosis”). Such cases may be due
to a mild PUJ obstruction that is compensated in the
absence of diuresis.
ROLE OF RADIOLOGY AND IMAGING
Urography demonstrates a dilated renal pelvis and
calyces. Slow opacification of the affected side is seen.
Delayed radiographs are needed to demonstrate that the
PUJ is the point of obstruction. With high-grade/long-
standing obstruction, the renal pelvis may be markedly
dilated (>10 cm in diameter) with a ballooned appea-
rance. The kidney may be virtually non-functional. If there
is kinking of the PUJ, obstruction secondary to an aberrant
vessel should be considered.
A diuretic renogram or the Whitaker procedure
performed after acute symptoms are brought on may be
helpful to determine whether functionally significant
obstruction is present, in patients with equivocal PUJ
obstruction or if there is a discrepancy between clinical
symptoms and radiologic findings.
Antegrade or retrograde pyelography may help
better define the ureter and thereby establish the
diagnosis. The antegrade procedure may be performed
by percutaneous nephrostomy. The retrograde procedure
may be useful to confirm the diagnosis prior to surgery.
A voiding cystourethrogram is recommended to exclude
vesicoureteral reflux as the cause of the renal pelvic
dilatation.
Ultrasound will demonstrate a very dilated renal
pelvis and caliectasis but will not be able to demonstrate
a dilated ureter.
DIFFERENTIAL DIAGNOSIS
A large extrarenal pelvis may be distinguished by the fact
that the calyces are not dilated.
TREATMENT
It may include pyeloplasty.
Congenital Anomalies of Urorenal Tract 31
Also, percutaneous nephrostomy followed by balloon
pyeloplasty or endoscopic endopyelotomy may be
performed. These may also be performed as secondary
procedures when surgery has failed. Success rates of 85%
have been reported. The procedures should not be utilized
in small infants.
If obstruction secondary to an aberrant vessel is
suspected, the above mentioned procedure should not
be performed until the aberrant vessel has been excluded
by prior angiography.
Duplication Anomalies
Duplication of PC system only with normal ureter is
common and can otherwise be considered as a normal
variant. Partial or complete duplication of one or both
ureters may occur with duplication of the ipsilateral renal
pelvis. The ureter from the upper pole of the kidney opens
at a more caudal location than the orifice of the lower
pole ureter. Ectopia or stenosis of one or both orifices,
vesicoureteral reflux into the lower or both ureters, or
ureterocele may occur. Surgery may be necessary to
correct vesicoureteral reflux, obstruction, or urinary
incontinence (Figures 4.5 and 4.6).
Ectopic Orifices
These malpositioned openings of single or duplicated
ureters may occur on the lateral bladder wall, distally along
the trigone, in the bladder neck, in the female urethra
distal to the sphincter (leading to continuous inconti-
nence), in the genital system (prostate and seminal vesicle
in the male, uterus or vagina in the female), or externally.
Lateral ectopic orifices frequently are associated with
vesicoureteral reflux, whereas distal ectopic orifices more
often are associated with obstruction and incontinence.
Surgery is indicated for obstruction and incontinence and
is sometimes necessary for vesicoureteral reflux.
Stenosis
Narrowing may occur at any location in the ureter, most
commonly at the ureteropelvic junction and less com-
monly at the ureterovesical junction (primary mega-
ureter). Stenoses often improve with time and growth,
but ureteral tapering and reimplantation may be necessary
when there is increasing dilatation and infection. Any
obstruction is also an indication for surgery.
32 Uroradiology: Text and Atlas
FIGURE 4.5: Ultrasound scan: Bifid pelvicalyceal system
Ureterocele
Ballooning of the lower end of the ureter into the bladder
may produce progressive obstructing dilatation, leading
to ureterectasis, hydronephrosis, infection, occasional
calculus formation, and potential loss of renal function.
Treatment includes endoscopic transurethral incision or
open repair. When a ureterocele involves the upper pole
of duplex ureters, treatment may depend on function in
that renal segment because of the significant incidence
of renal dysplasia. Removal of the affected renal segment
and the affected ureter may be preferable to repair of
the obstruction if no segmental renal function is found
or if significant renal dysplasia is suspected.
Vesicoureteral Reflux
Reflux of urine from the bladder into the ureter may result
in damage to the upper urinary tract by bacterial infection
and occasionally by increased hydrostatic pressure. It most
often is due to congenital anomalous development of
the ureterovesical junction. Incomplete development of
the intramural ureteral tunnel causes a failure of the flap
valve action at the ureterovesical junction and permits
backwash of bladder urine into the ureter and renal pelvis.
Reflux can occur even in the presence of an ordinarily
sufficient tunnel when there is bladder outlet obstruction
with increased intravesical pressures or neurogenic vesical
dysfunction.
FIGURE 4.6: CT scan: Coronal reconstruction—Bifid pelvicalyceal
system on left side
Bacteria in the lower urinary tract can be easily
transmitted by reflux to the upper tract, leading to
parenchymal infection with potential scarring and loss
of renal function. Chronically elevated bladder storage
and emptying pressures (> 40 cm H2O) have resulted
in progressive hydrostatic damage to the kidney in most
patients, even without infection or reflux.
Abdominal or flank pain, persistent or recurrent UTI,
dysuria or flank pain with voiding, frequency and urgency,
or signs of renal insufficiency may be secondary to
vesicoureteral reflux. Pyuria, hematuria, proteinuria, and
bacteriuria may be present.
Filling and voiding cystourethrograms demonstrate reflux
and are the preferred means to diagnose bladder outlet
obstruction, which can be surgically repaired. IVU may show
calyceal dilatation, ureteral “ribboning,” and ureterectasis
with dilatation of the upper collecting system. Reflux may
also be demonstrated by direct (catheter) radioisotope
cystogram. Renal cortical involvement with acute infection
or scarring is precisely delineated with succimer
(dimercaptosuccinic acid) nuclear scans, when indicated.
Vesicoureteral reflux is usually mild to moderate (with
little or no calyceal dilatation) and often resolves
spontaneously over months to several years while daily
antibacterial prophylaxis is maintained. Infection despite
 Congenital Anomalies of Urorenal Tract 33

prophylaxis, or significant and progressive renal scarring

is best managed by ureteral reimplantation. When such
reflux is accompanied by high-pressure storage or
emptying of urine in the bladder, the approach is to lower
bladder pressures by pharmacotherapy and/or behavioral
means. Reflux may sometimes resolve with this
management; if not, reimplantation would be appropriate.
This approach almost always eliminates reflux and
minimizes future pyelonephritis, with reduced morbidity
and mortality from renal disease secondary to reflux and
infection.

Retrocaval Ureter
Anomalous development of the vena cava (pre-ureteric
vena cava) allows the infrarenal vena cava to form
anterior to the ureter. A retrocaval ureter on the left is
seen only with persistence of the left cardinal vein
system or with complete situs inversus. It can cause FIGURE 4.7: IVU: Pubic diastasis with small hypoplastic urinary
ureteral obstruction. For significant ureteral obstruction, bladder in a case of bladder exstrophy

surgery consists of division of the ureter with uretero-

ureteral anastomosis anterior to the vena cava or iliac
vessel.
BLADDER
Congenital anomalies of the urinary bladder include
exstrophy; agenesis; duplication; persistent urachus;
megacystis syndrome, which may be a primary
myoneural defect and diverticula.
1. Exstrophy of bladder
2. Congenital bladder diverticuli.
Exstrophy
In this easily detectable and serious major anomaly, the
bladder is open (unroofed) in the suprapubic region with
urine dripping from the ureteral orifices. The bladder
mucosa is continuous with the abdominal skin, and the
pubic bones are separated. The prognosis for main-
tenance of normal renal function is good. The bladder
can almost always be reconstructed and returned to the
pelvis, although vesicoureteral reflux is invariably present.
Ureterosigmoidostomy or other types of continent urinary
diversion may be used to treat a bladder reservoir that
fails to expand sufficiently or has sphincter insufficiency.
Reconstruction of the genitalia is required (Figure 4.7).
Congenital Bladder Diverticula
Bladder diverticula predispose to UTI and may
be associated with reflux. Diagnosis is made by cysto-
graphy and cystoscopy. Surgical removal of diverti-
cula and reconstruction of the bladder wall may be
indicated.
PENIS AND URETHRA
The penis in the male and the urethra in the male or
female may be congenitally absent. Other anomalies
include hypospadias; epispadias; double penis; congenital
penile curvature or malrotation; microphallus; urethral
valves, stricture, stenosis, or duplication; meatal stenosis;
and phimosis and paraphimosis.
1. Hypospadias
2. Epispadias
3. Congenital urethral stricture
4. Urethral meatal stenosis
5. Urethral diverticulum
34 Uroradiology: Text and Atlas
6. Duplication of urethra
7. Phimosis and paraphimosis.
Hypospadias
A displaced urethral opening is caused by failure of
tubularization and fusion of the urethral groove. In female
hypospadias, the urethra opens into the vaginal introitus.
In the male, the foreskin fails to become circumferential
and appears as a dorsal hood. The urethral opening may
be located on the underside of the penile shaft, at the
penoscrotal junction, between the scrotal folds, or in the
perineum. It is often associated with chordee (ventral
curvature of the penis, most apparent on erection), caused
by fibrous tissue along the usual course of the corpus
spongiosum. Prognosis for functional and cosmetic
correction is good. During the first year of life, the chordee
can be repaired and a neourethra constructed using penile
shaft skin or foreskin.
Epispadias
This dorsal fusion defect of the urethra can be partial
(in 15% of cases) or complete, the most severe form being
associated with exstrophy of the urinary bladder. It is more
common in males. In partial epispadias, urinary control
can be satisfactory. Reconstruction of the penis alone may
be associated with persistent incontinence. Bladder outlet
reconstruction is often required to achieve complete
urinary control.
Posterior Urethral Valves
Congenital folds of the urethra act as valves that occur
in the prostatic urethra (posterior urethral valves).
Complications are due to obstruction, which may be
severe and may lead to myogenic bladder malfunction,
massive upper tract damage, and renal insufficiency.
Symptoms and signs include weak and dribbling urinary
stream, overflow incontinence, and UTI. Diagnosis is
established by voiding cystourethrography. Initial treat-
ment is endoscopy. Early surgery may prevent progressive
renal deterioration. A different entity, diverticulum of the
anterior urethra, may act as a valve (anterior urethral
valve) and is also treated endoscopically.
Urethral Stricture
Although urethral stricture in the male is most commonly
acquired, typically from a crush injury after straddle
trauma, it may be congenital. Acquired stricture usually
presents with postvoid bloody urethral discharge and may
heal spontaneously or progress to true stricture. Initial
management is endoscopic urethrotomy.
Urethral Meatal Stenosis
Urethral meatal stenosis associated with hypospadias is
the most common form of congenital urethral stenosis,
although it is more commonly an acquired condition
resulting from healed irritation of the meatus in boys who
are circumcised while still in diapers. Meatotomy is
indicated for a significantly deflected stream or for a
pinpoint stream.
Duplication of Urethra
It may be complete or incomplete. It occurs in sagittal
plane.
Three types known:
1. Epispadic (dorsal) type usually abortive
2. Hypospadic (Ventral) type is more functional
3. Other types: forked
Perneal is a rare variant.
Phimosis and Paraphimosis
Phimosis is congenital or acquired (inflammatory)
constriction of the foreskin, which cannot be retracted.
Paraphimosis is inability of the retracted constricting
foreskin to be reduced distally over the glans. When either
condition is present, surgical circumcision is indicated.
A preliminary dorsal slit may be required. The prognosis
is excellent.
Few important anomalies are discussed in details in
following pages.
RENAL AGENESIS
INTRODUCTION
True renal agenesis is defined as the complete congenital
absence of renal tissue. Acquired forms of agenesis are
characterized by the development of renal tissue which
atrophies either during development or during childhood.
 Congenital Anomalies of Urorenal Tract 35

INCIDENCE

It is between 1:500 and 1:1500 births.

PATHOPHYSIOLOGY

Failure of formation of the ureteral bud or because of

an inherent deficiency of the metanephric blastema.

BILATERAL RENAL AGENESIS

This is extremely rare and is incompatible with life. Males

are affected in three-fourths of cases. Infants demonstrate
characteristic features of Potter’s syndrome including low-
set ears and a prominent palpebral fold.
Bilateral renal agenesis is uncommon and
incompatible life. Newborns that die from chronic renal
failure do so that the end of the first week of life and
those who die in hours or day of life usually do so from FIGURE 4.8: IVU: Left renal agenesis
respiratory. Bilateral renal agenesis is almost always
accompanied by oligohydramnios and there is a high
RENAL ECTOPY
incidence of associate monary hypoplasia. Following
INTRODUCTION
delivery, many affected have a spontaneous pneumo-
thorax or pneumomediastinum they also have a typical It refers to an abnormal position of the kidney.
facies with low-set ears - the so~called ‘Potter facies’. Renal ectopia (abnormal renal location) results from
a kidney that fails to ascend from its origin in the true
ASSOCIATED ANOMALIES pelvis or from a superiorly ascended (thoracic) kidney.
Most commonly, it takes the form of a pelvic kidney,
The ipsilateral adrenal gland is absent in 8–10% of cases.
in which the kidney is located in the true pelvis (pelvic
Some investigators report a two-fold increase in the
kidney) or adjacent to the sacrum (sacral kidney).
incidence of congenital anomalies of the contralateral
Occasionally, the kidney may lie at the level of the iliac
kidney. Associated genital abnormalities in males may
crest (abdominal ectopy). Rarely (1:15,000 births), the
include cysts of the ipsilateral seminal vesicle, absence
kidney ascends to a position higher than the second
of the ipsilateral vas deferens, hypoplasia or agenesis of
lumbar vertebra, and enters the thorax, presumably via
the testicle, and hypospadias. In females, unicornuate
a diaphragmatic aperture (intrathoracic kidney). This
or bicornuate uterus, absence or hypoplasia of the uterus,
anomaly is more common in males and on the left side.
and absence or aplasia of the vagina (Rokitansky-Kuster-
Blood supply to an intrathoracic kidney arises from the
Hauser syndrome) may be present.
abdominal aorta in its normal location.
ROLE OF RADIOLOGY AND IMAGING INCIDENCE
In true agenesis, a hemitrigone is found in the bladder 1:500 to 1:1200.
on cystoscopy. No renal artery is present. The colon
occupies the renal fossa on the affected side, and this PATHOPHYSIOLOGY
may suggest the diagnosis on plain films or barium enema. As the fetal kidneys ascend from their pelvic position to
IVU is helpful (Figure 4.8). meet the adrenal glands, each kidney acquires blood
36 Uroradiology: Text and Atlas

supply from neighboring vessels. The initial supply from If the ectopic kidney is small and no hydronephrosis is
the external and internal iliac vessels is lost and blood present, the kidney may be obscured by the bony pelvis.
supply is acquired directly from the aorta around the 8th In such cases, tomography is useful (Figure 4.9).
week of development. Renal ectopy occurs if there is any
abnormality in acquiring such blood supply or there is Ultrasound
an associated abnormality of the spine which prevents
It is the modality of choice to demonstrate a small ectopic
such cephalic migration from occurring.
kidney not visualized on urography. A reniform mass with
Left-sided ectopia is more common, and men are
affected three times more often than women. It is usually a characteristic pattern of renal sinus echoes will be
unilateral, but may be bilateral Thoracic kidney has been identified in the pelvis (Figure 4.10).
recognized prenatally, and it has also appeared after a
previously normal chest radiograph. High ectopia is
usually not associated with functional abnormality and
is more commonly an incidental finding on chest X-ray,
however, there is an increased incidence of ureteropelvic
junction obstruction, vesicoureteral reflux, and multicystic
renal dysplasia in incompletely ascended kidneys, but
not in superiorly ascended ones. Malrotation may be
present with the renal pelvis anterior to the kidney. The
ureter is elongated. The origin of the renal artery can
be at the level of the opposite renal artery, or it may be
higher. The adrenal gland may accompany the kidney,
and one instance in which ipsilateral superior splenic
ectopia occurred has been reported.

CLINICAL FEATURES
Often asymptomatic.
In nearly 50% of cases, a pelvic kidney is associated with
hydronephrosis or vesicoureteral reflux, leading to
obstruction, infection and related pain. FIGURE 4.9: IVU: Ectopic right kidney with bilateral VUR

ASSOCIATED ANOMALIES
Other GU malformations are commonly present in
patients with pelvic kidneys. These include: Ureteropelvic
junction obstruction; cryptorchidism; hypospadias
(males); and absence of the vagina (females). Also, non-
GU anomalies may be present, such as vertebral and
rib (skeletal) anomalies; septal defects (heart anomalies);
malrotation, imperforate anus (GI anomalies); and, in
nearly 50% of patients with unilateral renal ectopy, an
abnormality of the normally positioned kidney is also
present.
ROLE OF RADIOLOGY AND IMAGING
Urography
Findings depend on the degree of renal function in the
pelvic kidney, and presence of associated anomalies. FIGURE 4.10: Ultrasonography: Ectopic right kidney
 Congenital Anomalies of Urorenal Tract 37

CT
A functional mass of renal parenchyma can usually be
identified.

Angiography
Prior to any surgical procedure contemplated on a pelvic
kidney, angiography is performed to investigate the highly
variable nature of its blood supply.

INTRATHORACIC KIDNEY
Thoracic kidney or superior renal ectopia is the rarest FIGURE 4.11: IVU: Bilateral FIGURE 4.12: IVU: Left intra-
intrathoracic kidneys thoracic kidney-Retrocardiac
of the renal ectopies. The adrenal gland and the spleen opacity
may accompany the kidney. Simple chest film combined
with sonography and confirmed by enhanced CT scan
after or excretory urography readily allows differentiation
from other masses in the chest thus avoiding unnecessary
and even hazardous biopsy or surgery . There is no need
to treat the malformation. If there is an associated
diaphragmatic hernia or eventration containing bowel
or stomach, the diaphragm is repaired.
Intrathoracic kidneys have a reported prevalence of
less than 1 in 10,000 and represent only 5% of ectopic
kidneys. It is a rare form of renal ectopia. Four forms
of intrathoracic ectopy have been reported. Most
commonly, as was found in our patient, a thin membrane
of diaphragm will cover the kidney, thus making it
subdiaphragmatic yet intrathoracic in position. This is also
FIGURE 4.13: CECT (Axial): Left intrathoracic kidney
referred to as a diaphragmatic eventration. The
embryologic origin is debatable; various authors have
CROSSED FUSED RENAL ECTOPIA (CFE)
proposed either an abnormality in pleuroperitoneal
INTRODUCTION
membrane fusion or abnormally high migration of the
kidney due to delayed mesonephric involution. Traumatic It is the fusion of both kidneys, with at least one kidney
rupture of the diaphragm, Bochdalek’s hernia, and on the side opposite its normal location. Originally, this
supradiaphragmatic ectopic kidney without herniation are condition was diagnosed at autopsy; currently, it is
less common causes of an intrathoracic kidney. Anatomi- identified with various imaging studies.
cally, four features are commonly found: Rotational Crossed fused ectopia is seen in 1/1000 to 1/1500
abnormality, in which the hilum is anterior; elongated autopsies. In 85–90% of patients with ectopic kidney will
ureter; high renal vessel origin; and medial deviation of be fused. CFE is believed to occur when either there is
the lower pole. The adrenal gland may or may not be a failure of nephrogenic cells to separate or fusion of 2
ectopic. The possibility of an intrathoracic kidney exists blastemas during abdominal ascent. Typically the lower
with all chest masses, though its likelihood is low (Figures kidney is malrotated and both pelves point toward
4.11 to 4.13). midline. The ureter of the ectopic kidney crosses midline
38 Uroradiology: Text and Atlas

and enters the bladder on the contralateral side. There varies depending on the secondary symptoms and comp-
are no known congenital anomalies associated with lications. In the absence of associated complications and
CFE. symptoms, the condition may be incidentally discovered
Typically CFE is asymptomatic and is an incidental on images obtained for reasons other than the evaluation
finding. There can be an higher risk of injury the ectopic of crossed fused kidneys. Many cases of crossed fused
renal ectopia remain undiagnosed, although the exact
kidney if it overlies the spine.
number is unknown.
PATHOPHYSIOLOGY
Crossed fused renal ectopia often is clinically silent
unless it is detected during imaging for the evaluation
The fusion of the two kidneys is believed to result from of urinary tract infection or abdominal symptoms (e.g.
either of the two events: abdominal pain).
1. Failure of the primitive nephrogenic cell masses to A urinary tract infection may cause dysuria, fever, or
separate or nonspecific symptoms (e.g. failure to thrive), especially
2. Fusion of the two blastemas during their abdominal in the young child. An associated urinary tract calculus
ascent. may present with hematuria or flank pain.
Either component of the fused kidneys can have
Anatomical Basis
associated renal abnormalities such as a Wilms’ tumor,
The ectopic kidney, located entirely or primarily on the
hydronephrosis, multicystic dysplasia, and ectopic
opposite side of the abdomen, typically forms the lower
ureterocele. These abnormalities can occur in unfused
portion of the renal fusion mass. Usually, the lower kidney
nonectopic kidneys or in conjunction with renal ectopia.
is malrotated, and both pelves point toward the midline.
Crossed fused renal ectopia is not known to be associated
The ureter of the upper renal component descends on
with abnormalities of nongenitourinary systems.
the ipsilateral side into the bladder, while the ureter from
Incidence: Crossed fused ectopy occurs in approxi- the crossed ectopic kidney crosses the midline to enter
mately 1:1000 births. The anomaly is more common in the bladder on the contralateral side. Multicystic dysplasia
males (2:1). Left-to-right ectopy is three times more of the crossed renal unit is reported.
common than right-to-left ectopy.
PREFERRED INVESTIGATIONS
Etiology: An abnormally situated umbilical artery
IVU Figure 4.14A.
prevents normal cephalic migration from occurring. As
a consequence, the developing kidney takes the path of
least resistance and crosses to the opposite side, where
cephalic migration resumes. An alternative hypothesis
postulates that the abnormality occurs when the ureteral
bud crosses to the opposite side where it induces nephron
formation in the contralateral metanephric blastema.
Clinical symptoms: rare. These patients generally present
in adulthood with abdominal pain, pyuria, or urinary tract
infection. There is a slightly higher incidence of urinary
tract calculi, probably related to stasis.

CLINICAL FEATURES

Age
Crossed fused renal ectopia is a congenital malformation
that is present at birth. The patient’s age at diagnosis FIGURE 4.14A: IVU: Thyroid kidney

Ultrasonography (USG)
It is the preferred radiologic modality for detecting the
condition because it is noninvasive, involves no ionizing
radiation, usually is readily available, and is less expensive
than either CT or MRI.
Features: Crossed fused renal ectopia is not definable
on plain radiographs. Usually, crossed fused renal ectopia
is apparent on intravenous urograms (IVUs), which
demonstrate an atypical renal mass, 2 collecting systems,
and 2 ureters. Ultrasonograms demonstrate an atypical
or complex appearance of the renal parenchyma, with
no definable contralateral kidney. The overall renal
dimensions should exceed the normal range for the
patient’s age.
Usually, fusion occurs along the longitudinal aspect,
with the kidneys side by side. The result is a dysmorphic
appearance, with a sigmoid or S shape on the ultrasono-
gram. The fused lower pole unit is positioned medially
and extends anterior to the spine (Figure 4.14B).
FIGURE 4.14B: Ultrasonography: crossfused ectopia right kidney
fused to lower pole of left kidney
A multicystic mass of variable size that is contiguous
with the lower pole of the upper renal unit is present in
patients with multicystic dysplasia.
Limitations: On ultrasonograms, overlying abdominal
gas may obscure a portion of the fused kidneys, making
precise diagnosis difficult. This diagnosis should be
considered when 2 separate kidneys cannot be identified.
MRI
MRI findings include fused renal masses with two
collecting systems.
Congenital Anomalies of Urorenal Tract 39
Accuracy is high with MRI, primarily as a result of
its excellent anatomic delineation and the absence of
image degradation due to bowel gas or osseous structures,
unlike with US.
Nuclear Medicine Studies
It demonstrates a single focus of isotope excretion or
localization by a kidney, with no contralateral isotope
excretion or localization.
MORTALITY/MORBIDITY
No mortality or morbidity is observed unless crossed
fused renal ectopia is associated with renal failure that
results from obstruction or chronic pyelonephritis. Patients
with ectopic kidneys have an increased risk for
complications such as hydronephrosis, infection, and
calculus formation.
SUMMARY
Crossed ectopy is defined as a kidney that is located on
the opposite side of the midline from its ureter. The crossed
kidney usually lies below the normally situated kidney.
In 90% of cases, at least partial fusion between the kidneys
is present (called crossed fused ectopy). In the remainder,
two discrete kidneys are present on the same side (crossed
unfused ectopy). Other variations include solitary crossed
ectopy and bilateral crossed ectopy.
HORSESHOE KIDNEY
INTRODUCTION
Horseshoe kidney is probably the most common fusion
anomaly.
The term “horseshoe kidney” refers to the appearance
of the fused kidney, which results from fusion at one pole.
In more than 90% of cases, fusion occurs along the lower
pole. Technically, the term horseshoe kidney is reserved
for cases in which most of each kidney lies on one side
of the spine. It includes:
• Symmetric horseshoe kidney (midline fusion) or
• Asymmetric horseshoe kidney (L-shaped kidney)
when the fused part, or the isthmus, lies slightly lateral
to the midline (lateral fusion).
Horseshoe kidney is generally differentiated from
crossed fused ectopia in which both fused kidneys lie on
40 Uroradiology: Text and Atlas
one side of the spine and the ureter of the crossed kidney
crosses the midline to enter the bladder.
PATHOPHYSIOLOGY
The development of the normal kidney depends on the
union of ureteric buds from the mesonephric ducts with
the nephrogenic cords in the embryo. It is believed to
occur around the fourth gestational week. This union
normally occurs at the level of the first or second sacral
vertebral segment. Subsequent straightening of the hind
end of the embryo, along with differential growth of the
developing pelvic structures, leads to the ascent of both
kidneys to their normal dorsolumbar regions between the
fourth and ninth weeks of gestation.
The abnormal fusion probably occurs at the 5 to 12
mm embryonic stage when the kidneys are in the true
pelvis and the renal capsule has not yet matured. One
embryologic explanation regarding midline fusion is that,
at that stage, abnormal variation in growth, ventral flexion
of the hind end of the embryo, or other variations in the
growth of pelvic structures may bring the metanephric
blastemas (developing kidneys) abnormally close together
for a longer period; this proximity can lead to fusion.
The explanation for lateral fusion is that, during early
embryonic life, lateral flexion of the lumbosacral spine
may push one of the developing kidneys toward the
midline. This positioning can lead to asymmetric fusion.
In later embryonic life, the ascent of the fused kidney
is limited at the level of the inferior mesenteric artery,
when the isthmus of the horseshoe kidney gets trapped
under it. Consequently, the horseshoe kidney always lies
at a position that is lower than normal. However, whether
the cause is abnormal fusion, abnormal migration of the
posterior nephrogenic areas, or another teratogenic factor
is not yet clear.
INCIDENCE
In general population, the incidence of horseshoe kidney
is about 1 case in 400 persons worldwide, and it is the
most common renal fusion anomaly.
CLINICAL FEATURES
Clinically, horseshoe kidney can be divided into two
groups: one with associated anomalies and the isolated
horseshoe kidney without any associated anomaly.
Horseshoe Kidney with Associated Anomalies
About one-third of cases of horseshoe kidney are
associated with other congenital anomalies, which include
anomalies of the urogenital, gastrointestinal, neurologic,
and skeletal systems, as well as some chromosomal
abnormalities. These anomalies include multisystem
abnormalities such as urogenital anomalies (e.g. uretero-
pelvic obstruction, vesicoureteric reflux, ureteral duplica-
tion, hypospadiasis, undescended testis, ectopic ureter,
retrocaval ureter, bicornuate and/or septate uterus).
GI abnormalities include anorectal malformations
such as imperforate anus, malrotation, and Meckel
diverticulum. CNS anomalies such as neural tube defects
may be seen. Skeletal anomalies include rib defects,
clubfoot, or congenital hip dislocation. Cardiovascular
abnormalities, such as a ventricular septal defect (VSD),
may occur in some patients.
Horseshoe kidney has also been found in association
with some chromosomal abnormalities such as Turner’s
syndrome and trisomy 18.
The clinical course largely depends on the nature of
the anomalies, because horseshoe kidney itself is relatively
asymptomatic.
Isolated Horseshoe Kidney
In the pediatric clinical setting, about 90% of patients
are asymptomatic, and the most common presentation
is UTI.
When symptoms are present, they are usually related
to hydronephrosis, infection, stone formation, or hema-
turia. The most common symptom is vague abdominal
pain, which may radiate to the back. Occasionally, nausea
and vomiting may be reported. Also, the so-called Rovsing
sign (nausea, vomiting, and abdominal pain with hyper-
extension of the spine) may be positive in some patients.
A small percentage of patients may have a palpable
lump in the abdomen.
Horseshoe kidney has been reported to be associated
with increased risk for renal neoplasms such as Wilms’
tumors, renal carcinoids, and transitional cell carcinoma.
Sex: Renal fusion anomalies occur predominantly in
males. The male-to-female ratio is approximately 2:1 for
horseshoe kidney and 6:1 for crossed fused ectopia.
 Congenital Anomalies of Urorenal Tract 41

Age: Clinically, this congenital anomaly is diagnosed in 3. Recurrent stone formation related to PUJ obstruction
individuals of all ages, from fetuses to the elderly. or infection may occur.
However, because of its association with other congenital 4. An increased risk of trauma to the isthmus exists
anomalies, horseshoe kidney is more commonly because of its position anterior to the spine.
diagnosed in children. 5. Horseshoe kidney may pose problems for the surgeons
during abdominal surgery for other abdominal
ANATOMICAL BASIS problems.
6. Some evidence suggests an increased incidence of
In horseshoe kidney, fusion occurs at the lower poles in
certain renal tumors in horseshoe kidney.
about 95% cases. This region of fusion, called the isthmus,
7. Horseshoe kidney may occur as an isolated anomaly
is usually composed of renal parenchymal tissue.
or in association with other congenital anomalies. The
However, in many cases, it may consist of fibrous tissue. morbidity and mortality rates largely depend on
The isthmus may be wide or narrow, depending on the whether it is associated with other anomalies.
degree of fusion. The isthmus usually lies anterior to the
aorta and inferior vena cava (IVC) and posterior to the PREFERRED INVESTIGATIONS
inferior mesenteric artery. However, rarely, the isthmus
Plain Radiographs
may pass between the aorta and IVC or even posterior
Plain KUB films may show low-lying renal outlines with
to these vessels. The ureters usually pass anterior to the
an altered renal axis. Usually, the kidneys follow the axis
isthmus, and they may have a high insertion point in
of the psoas muscles, with the lower poles lying at a more
the renal pelvis. The renal pelves are usually malrotated
lateral position than the upper poles. In horseshoe kidney,
and lie anteriorly or laterally. this axis is reversed, and the lower poles lie closer to the
In the midline fusion variety, the kidneys are spine (Figure 4.15).
symmetric, with lower poles converging toward the
midline. In the lateral fusion variety, one kidney is more IVU
vertical, while the other kidney is more horizontal; the For the purpose of diagnosis, IVU is usually the first-
isthmus lies slightly toward one side. In rare cases, the line investigation, followed by CT or scintigraphy in
upper poles may fuse, reversing the appearance of cases with doubtful findings.
horseshoe. Also rarely, both the poles may fuse; the result
is a ringlike mass termed disc kidney, doughnut kidney,
or pancake kidney.
Blood supply of the horseshoe kidney may vary. In
about 30% cases, it consists of one renal artery to each
kidney. Other variants include supply from 2 or 3 renal
arteries to one or both kidneys. The blood supply of the
isthmus also varies. It may come from the renal artery,
or it may directly arise from the aorta above or below
the isthmus. Occasionally, it arises from the common iliac,
external iliac, or inferior mesenteric arteries.

COMPLICATIONS OF HORSESHOE KIDNEY

1. Pelviureteric junction (PUJ) obstruction is a common
complication, possibly because of the high insertion
of the ureter.
2. Recurrent infections occur because of urine stasis and FIGURE 4.15: Plain KUB film showing the altered axes of renal
associated vesicoureteric reflux. shadows with lower poles lying closer to spine→horseshoe kidney
42 Uroradiology: Text and Atlas

Findings:
IVU usually reveals the classical findings associated with
horseshoe kidney. Findings on the initial tomogram may
be deceptive because of the exclusion of the anteriorly
lying isthmus. Renal axis abnormalities are confirmed,
as seen on the plain radiographs. In midline fusion, the
kidneys are symmetric, with the lower pole calyces lying
closer to or actually overlying the spine. The lower calyces
are usually medially rotated, and they may actually lie
medial to the ureters. Some degree of malrotation of the
kidneys is usually present. A renal pelvis is often extrarenal
and large.
The degree of malrotation has been associated with
the degree of fusion. If the isthmus is narrow, the kidneys
are usually less malrotated, with pelvis lying antero-
medially in its near normal position. In cases of a wide
isthmus, the renal pelves lie anteriorly or laterally. FIGURE 4.16: IVU: Altered axes of both kidney, lower poles lying
closer to spine and calyces seen end-on→Horseshoe kidney
Associated UPJ obstruction may be present because of
the higher ureteric insertion point that leads to delayed
pelvic emptying. Ureters may have the so-called flower- in which the continuity of the poles with the isthmus
vase appearance in which the upper ureters diverge cannot be clearly demonstrated.
laterally over the isthmus and then converge inferiorly. Findings: Ultrasonography can be useful for diagnosing
The lateral fusion variety with an L-shaped kidney this anomaly. The most important feature in establishing
can also be readily appreciated on IVUs. In this variety, the diagnosis on the basis of sonographic findings is the
one kidney has a relatively vertical position while the other isthmus and its continuity with the lower poles. Other
is relatively horizontal. features, such as malrotation and an altered renal axis,
Limitations: may be difficult to assess at ultrasonography. In cases
1. Most of the time, IVU cannot be used to differentiate in which the isthmus is composed of only a thin fibrous
between a fibrous isthmus and a parenchymal isthmus. band, this midline soft tissue may not be seen.
Also, in many cases, the diagnosis of a horseshoe Findings such as a curved configuration of the lower
kidney is difficult on the basis of only IVU findings. poles, elongation of the lower poles, and poorly defined
In these cases, CT or scintigraphy may be helpful. lower poles, suggest the presence of this anomaly. Other
2. On IVUs, a malrotated or ectopic kidneys may associated findings, such as stones, hydronephrosis, and
sometimes be confused with a horseshoe kidney. cortical scarring, are reliably depicted on sonograms.
3. Gibbous deformity of the spine may alter the renal Ultrasonography has also been useful in the diagnosis
axis, which may then resemble horseshoe kidney of this anomaly in utero.
(Figure 4.16).

Ultrasonography CECT

Utility of USG depends on the visualization of the isthmus
and the proof of its continuity with both the lower poles.
In many patients, especially patients with a large body
habitus, overlying bowel gas makes the acquisition of
adequate scans difficult, for technical reasons. In cases
Contrast-enhanced CT has a high degree of accuracy
in defining the structural abnormalities such as the
degree and site of fusion, degree of malrotation,
associated renal parenchymal changes (e.g. scarring,
cystic disease), and collecting system abnormalities (e.g.

duplex system, hydronephrosis). It can also be used to
differentiate a fibrous isthmus from a parenchymal
isthmus and show its relation to the surrounding
structures.
Although routine CT may show the variant arterial
supply, this is better defined with CT angiography with
3D reconstruction and volume rendering. The use of 3D
multisection helical CT has also been advocated in cases
of neoplasm associated with horseshoe kidney, because
it further clarifies the structural details.
Limitations: Figure 4.17.
MRI
Although MRI accurately reveals the anatomy, it is not
generally used for diagnosis because of its high cost. MR
angiography provides additional information about the
vascular anatomy. A voiding cystourethrogram is usually
required to evaluate associated vesicoureteric reflux.
Findings: MRI has an advantage in depicting the structural
details because of its ability to permit multiplanar imaging,
but it is more costly than other examinations. However,
an added advantage may be obtained by using MR
angiography to delineate the vascular anatomy. MRI is
probably the best modality to use in evaluating the extent
of renal tumors associated with horseshoe kidney.
With MRI diagnosis, as well as defining other
associated structural findings is better. However, asso-
ciated small stones may be missed on MRIs.
FIGURE 4.17: CECT–Axial section: Enhancing/functioning
parenchyma isthmus seen joining the two kidneys
Congenital Anomalies of Urorenal Tract 43
RNI
A diuretic renal scintigram is helpful in differentiating
obstructed and nonobstructed dilated collecting
systems.
Findings: Scintigraphy demonstrates the fusion best if the
isthmus consists of functioning parenchymal tissue,
because this imaging modality depends not only on the
structure but also on the function of the tissue. 99mTc–
labeled dimercaptosuccinic acid (DMSA) can be used to
define the fused segments, as well as the altered axis of
both kidneys.
This condition is incidentally diagnosed on bone scans,
99m
Tc-labeled RBC studies, or other nuclear medicine
studies obtained for reasons other than the evaluation
of horseshoe kidney. The use of mercaptoacetyltriglycine
(MAG-3) with diuresis is helpful in differentiating
nonobstructed and obstructed parts of the collecting
systems.
Horseshoe kidney can be confidently diagnosed with
scintigraphy, which reveals the functioning parenchymal
isthmus (Figure 4.18).
FIGURE 4.18: Renal scintigraphy: altered axis of both kidneys with
functioning isthmus seen joining lower poles of kidneys
44 Uroradiology: Text and Atlas
Angiography
It is usually reserved for presurgical planning to fully
evaluate the arterial supply pattern.
CTA: CT angiography with 3-dimensional (3D)
reconstruction may also reveal the vascular anatomy and
collecting system for presurgical planning.
Angiography is not normally performed to diagnose
this condition, but it is performed to evaluate the vascular
anatomy and its variations in a presurgical setting.
Angiograms may show 1, 2, or 3 renal arteries on either
side and a large variation in the blood supply of the
isthmus. However, in cases of associated renal tumors,
angiography is used to evaluate tumor vascularity.
Angiography is occasionally performed to check renal
artery stenosis in hypertensive patients who have this
anomaly.
INTERVENTION
Image-guided percutaneous nephrostomy can be
performed to relieve hydronephrosis associated with
horseshoe kidney. Percutaneous stone removal may also
be achieved with image guidance
AUTOSOMAL RECESSIVE POLYCYSTIC
KIDNEY DISEASE (ARPKD)
INTRODUCTION
It is the most common heritable cystic renal disease
occurring in infancy and childhood. It is distinct from
autosomal dominant polycystic kidney disease (ADPKD),
which tends to occur in an older population. The clinical
spectrum shows a wide variability, ranging from perinatal
death to a milder progressive form, which may not be
diagnosed until adolescence.
PATHOPHYSIOLOGY
ARPKD follows an autosomal recessive inheritance
pattern, with siblings of either sex having a 25% chance
of developing disease while the parents are unaffected.
The disease has variable expression, such that siblings
may manifest different degrees of disease. Despite the
clinical variability of ARPKD, it appears that a single
unidentified gene is responsible for all forms of the disease.
Linkage studies have localized an area on chromosome
6 (PKHD1) as the genetic locus. The frequency of the
heterozygous state is estimated to be one in 70. The
PKHD1 gene is expressed at high levels in the fetal and
adult kidney and at lower levels in the liver, which
corresponds to the principle sites of disease.
ARPKD is characterized by pathologic changes in the
kidney and/or liver. In the kidney, epithelial hyperplasia
occurs along the collecting duct of the nephron. The
hyperplastic cells undergo a functional change from being
resorptive to becoming secretory. The fluid secreted from
these abnormal cells is rich in epithelial growth factors,
which further stimulate epithelial proliferation. The
combination of epithelial hyperplasia and fluid secretion
results in significant ductal ectasia. Approximately
10-90% of the ducts may be affected, resulting in a
wide variability of renal dysfunction. Depending on
the number of ducts involved, the kidneys may be
massively enlarged. Examination of the kidney reveals
multiple small subcapsular cystic spaces that correspond
histologically with radially oriented, ectatic collecting
ducts.
Liver disease is present in every patient with ARPKD,
with the manifestations varying according to the patient’s
age at presentation. The chief pathologic hallmarks of
liver disease are periportal fibrosis and biliary duct ectasia.
Significant liver involvement is referred to as congenital
hepatic fibrosis. Although the mechanism is not clearly
defined, the most common clinical manifestation of
congenital hepatic fibrosis is portal hypertension.
CLASSIFICATION OF ARPKD
Blyth and Ockenden initially classified ARPKD into four
groups:
1. Perinatal
2. Neonatal
3. Infantile
4. Juvenile
The four categories are based on the individual’s age
and the onset of clinical manifestations; however, the
disease is expressed as a part of a spectrum of findings
rather than fitting into clearly defined subcategories.
1. Category 1 is perinatal ARPKD. Patients with the
perinatal form are born with a markedly enlarged
abdomen due to nephromegaly, which may interfere
with delivery. Approximately 90% of the collecting

ducts are dilated with minimal liver involvement.
Severe renal impairment in utero leads to oligo-
hydramnios and subsequent pulmonary hypoplasia.
Other clinical findings may include sequelae of
oligohydramnios, such as Potter facies and clubfoot.
Most of these infants do not survive beyond the first
week of life. Unfortunately, approximately 75% of all
cases of ARPKD is this severe.
2. Category 2 is neonatal ARPKD. Patients with the
neonatal form have palpable kidneys at birth.
Approximately 60% of the kidney is affected and there
is mild liver disease. Pulmonary involvement is less
of a factor in this form because renal impairment is
often less severe in utero. Progressive renal failure is
the dominant feature of this form, resulting in death
within a few months.
3. Category 3 is infantile ARPKD. The infantile form
of the disease tends to present after a few months
of life. Approximately 25% of renal collecting ducts
are dilated, with moderate hepatic periportal fibrosis.
Clinical presentation includes large kidneys and
hepatosplenomegaly. Patient often develops chronic
renal failure and/or portal and systemic hypertension.
The disease often progresses to end-stage renal failure
by adolescence, which is the predominant cause of
mortality.
4. Category 4 is juvenile ARPKD. The hallmark of the
juvenile form is pronounced hepatic involvement.
Renal insufficiency is generally absent or mild, with
less than 10% of the kidneys affected. The disease
has a wide range of age presentations, from 6 months
to 5 years. The presentation is characterized by
variable renal enlargement and hepatosplenomegaly.
Significant liver involvement results in portal
hypertension. Morbidity and mortality are often
secondary to the sequelae of portal hypertension,
including variceal bleeding and thrombocytopenia
or anemia secondary to hypersplenism. Mortality for
this type is lowest among the 4 categories, with
approximately 80% of patients surviving beyond the
age of 15 years.
Congenital Anomalies of Urorenal Tract 45
INCIDENCE
ARPKD has an incidence of 1 in 6,000 to 1 in 55,000
live births.
Notably in Finland, the incidence is reported to be
higher (1 in 1000).
CLINICAL FEATURES
Race: No information has shown a racial predominance.
Sex: Both sexes are affected equally.
Age: ARPKD may initially occur anytime between
perinatal period to five years of age depending on
classification.
Two constant features of the disease are kidney and
liver involvement of variable severity. Generally, renal
and hepatic disease manifest opposite degrees of severity.
Patients that develop severe kidney disease early in life
tend to succumb to renal failure before significant hepatic
disease can develop. On the other hand, patients with
a milder form of kidney disease tend to develop severe
hepatic complications later on in life. The main
characteristic of kidney involvement is dilatation of the
collecting system resulting in multiple cysts, which
manifests as progressive renal failure. Disease in the liver
is typically diffuse, presenting as portal and interlobular
fibrosis, dilatation and hyperplasia of bile ducts, or a
combination of both. Liver disease ultimately results in
portal hypertension.
ANATOMICAL BASIS
ARPKD results in bilaterally generally symmetrically
enlarged kidneys that maintain their reniform shape.
Beneath the capsule are scattered opalescent cysts from
dilated collecting ducts, usually 1–2 mm in diameter, but
sometimes larger. On sections, the renal parenchyma
resembles a sponge with ectatic, nonobstructed, radially
oriented collecting tubules that have areas of hyperplastic
cuboidal or low columnar lining epithelium. Interstitial
fibrosis develops but the glomeruli remain normal.
ARPKD results in dilated bile ducts with protrusions
from the walls and bridging tissue between the duct walls.
There are often increased numbers of ducts. There is
congenital hepatic fibrosis with increased connective tissue
in the enlarged portal tracts.
46 Uroradiology: Text and Atlas
Generally, there is a reciprocal relationship between
the degree of renal and hepatic involvement in individual
patients. Those with more severe renal involvement have
less severe hepatic disease.
PREFERRED INVESTIGATIONS
IVU It helps to differentiate ARPKD from ADPKD,
Glomerulocystic disease and renal dysplasia by demon-
strating bilateral and symmetrical enlargement of the
kidneys and ‘streaky/ chaotic/ Swiss-cheese’ nephrogram
as the contrast clears in the ectatic collecting ducts.
Ultrasonography
It is the primary modality for the evaluation of ARPKD,
especially during the perinatal and neonatal periods,
which characteristically shows bilateral renomegaly with
uniformly increased reflectivity.
CT and MRI
In older children, CT and MRI are often used to evaluate
liver disease.
MORTALITY/MORBIDITY
ARPKD accounts for 1.5% of children in renal replace-
ment therapy prior to the age of 15 and 0.6% of patients
treated because of end-stage real failure before the age
of 20 years.
ADULT POLYCYSTIC KIDNEY DISEASE (ADPKD)
INTRODUCTION
It is transmitted as an autosomal dominant trait and affects
approximately 1 in 1000 people. Cysts arise from the
nephrons and the collecting tubules. Islands of normal
parenchymal renal tissue are interspaced between the
cysts. Microdissection reveals that the cysts communicate
directly with the nephrons and collecting tubules.
Patients present with hypertension and progressive
renal failure after their third decade of life. Uncommonly,
autosomal dominant polycystic kidney disease (ADPKD)
appears in children, and it is rarely seen in neonates.
Of patients with ADPKD, 25–50% have associated
hepatic cysts, 9% have associated pancreatic cysts, and
5% have associated splenic cysts; pulmonary cysts occur
uncommonly. These extrarenal manifestations are not
found in neonates and children.
PATHOPHYSIOLOGY
ADPKD is an inherited condition comprising at least 3
phenotypically indistinguishable but genetically distinct
entities caused by mutations in 3 genes: PKD1, PKD2,
and PKD3. The gene is located on chromosome arm
16p and chromosome 4 in 90% of patients and is related
to spontaneous mutation in 10%. ADPKD is transmitted
as an autosomal dominant trait, with almost 100%
penetrance if patients live long enough. Because of the
variable expressivity and spontaneous mutation, a family
history is not found in nearly one half of patients.
Histologically, ADPKD is characterized by an
abnormal rate of tubule divisions, with hypoplasia of
portions of tubules left behind as the ureteral bud
advances. Cystic dilatation occurs in the Bowman’s
capsule, loop of Henle, and proximal convoluted tubule
interspersed with normal renal tissue. Thus, in distinction
to simple renal cysts in which the contents are
biochemically similar to plasma, the biochemical features
of the fluid content of cysts in ADPKD is closer to those
of urine, particularly when samples are taken from distal
nephrogenic cysts. Cysts in ADPKD are lined by flattened
or cuboidal epithelium. Stromal changes are nonspecific
and are those of renal failure; dystrophic calcification is
common.
With minimal disease, the kidneys are normal in size
and are smooth, and the cysts are discovered only on
cut pathologic specimens. As the size of cysts increases,
the kidneys enlarge, often asymmetrically, and the kidneys
may become bosselated and lose their reniform shape.
The age of patients at onset of cyst formation varies; 54%
appear by the first decade of life, 72% occur by the second
decade, and 86% occur by the third decade. By the age
of 80 years, evidence of cyst formation exists in all persons
who have the gene.
True unilateral disease is rare because most genetic
diseases involving paired organs are bilateral. Segmental
ADPKD also occurs rarely, although some doubt the
existence of segmental disease and suggest that it should
not be considered a forme fruste of ADPKD. Segmental
disease is not inherited and not associated with renal
failure. Rarely, ADPKD may be detected in utero, usually
in the third trimester, although the earliest diagnosis
recorded was at 14 weeks gestation.

With small cysts, ADPKD can be confused with
autosomal recessive polycystic kidney disease (ARPKD)
because the kidneys may be enlarged and echogenic.
Sometimes, the cortical cysts are large enough to be
demonstrated on ultrasonographic images, which can
confirm the diagnosis when cysts are demonstrated in
the fetus of a parent with the disease.
With progression of the disease, impaired renal
function ensues. Hypertension precedes renal failure.
Extrarenal manifestations include liver cysts in 25–50%
of patients, pancreatic cysts in 9%, and splenic cysts in
5% of patients. Other cysts reported include cysts of the
thyroid, parathyroid, lung, brain, pituitary gland, pineal
gland, ovary, uterus, testis, seminal vesicles, epididymis,
bladder, and the peritoneum. Aneurysms of cerebral
arteries (berry aneurysms) have been reported in 3–50%
of patients. A variety of cardiac and aortic abnormalities
have been associated with ADPKD, including aortic root
dilatation, aortic regurgitation, bicuspid aortic valves,
coarctation of the aorta, mitral regurgitation, and
abdominal aortic aneurysm.
Cysts vary in size from those barely visible to those
that are several centimeters in diameter. Cysts usually
contain clear straw-colored fluid, but hemorrhage into
1 or more cysts is common, which may change the gross,
biochemical, and histologic character of the fluid. Cysts
may become infected, and aspiration of the fluid may
reveal purulent contents. Incidence of renal cell carcinoma
is only slightly increased in patients with ADPKD; a greater
increased incidence is associated with cystic disease of
dialysis.
Approximately 50 cases of renal cell carcinoma have
been reported in association with polycystic kidneys; some
of the cases were associated with von Hippel-Lindau
disease and tuberous sclerosis. No correlation exists
between the severity of renal disease and the number
of liver cysts. Liver function usually remains normal, but
with longer survival of patients with ADPKD, liver function
abnormalities may occur, particularly in patients with
portal hypertension. An association between ADPKD and
congenital hepatic fibrosis has been described.
INCIDENCE
One in 1000 people carry the ADPKD trait. ADPKD is
the most common genetically linked renal disorder.
Congenital Anomalies of Urorenal Tract 47
CLINICAL FEATURES
Race: No race predilection exists.
Sex: No sex preponderance exists.
Age: Patients of any age can be affected, but the mean
age at diagnosis is 43 years. In rare cases, renal cysts
are incidentally discovered in people aged 70–90 years.
Although the disease probably begins in utero in most
patients, symptoms are unusual until the fourth or fifth
decade. With increasing use of cross-sectional imaging,
ADPKD is discovered incidentally in asymptomatic
patients in their 80s. However, the most common
presentation is a palpable mass, hypertension, abdominal
pain, and hematuria. Hypertension often predates renal
failure.
Renal failure ultimately affects most patients by the
time they are aged 60 years. Patients may present with
fever, dysuria, and leukocytosis due to urinary tract
infections. Renal and/or ureteric colic from calculi is a
known complication. Hemorrhage, which may be
intracystic or retroperitoneal, may present with hematuria,
abdominal pain and, rarely, massive hemorrhagic shock
or anemia. Polycythemia is a rare but known association
secondary to increased erythropoietin production. Rarely,
intracystic hemorrhage within a liver cyst may cause acute
abdominal pain, mimicking an acute cholecystitis.
Urinalysis may reveal proteinuria and hematuria.
PREFERRED INVESTIGATION
Plain radiographs offer limited information. Plain
radiographic findings are normal in the early stages of
ADPKD, but with enlargement of the kidneys, soft-tissue
masses displace the normal intra-abdominal organs.
IVU when multiple cysts are readily visible on USG the
IVU will show compression and displacement of calyces
by the intrarenal cysts. There is difficulty in identifying
the renal outline. Puddling of contrast medium on
IVU is differentiating feature of ADPKD from that of
ARPKD, especially in infants.
Ultrasonography is the modality of choice in the workup
of patients with ADPKD, and it is an ideal modality
for screening the family of patients. In earlier studies
in young children, intravenous urography and
48 Uroradiology: Text and Atlas
nephrotomography were shown to be slightly more
sensitive than ultrasonography.
CT scanning is as sensitive as ultrasound in the detection
of cystic disease, although problems may arise with
smaller cysts. CT appears to be more specific than
sonography in differentiating an obstructed renal pelvis
from a parapelvic cyst. CT scans also appear superior
to ultrasonographic images in helping assess
retroperitoneal rupture of a cyst and perinephric extension
of blood or pus from an infected cyst.
MRI is especially useful in patients who are allergic to
iodinated contrast media and in patients with
compromised renal function who are at risk for iodinated
contrast-induced renal failure. MRI also has advantages
in patients in whom hemorrhagic cysts are considered.
MRI is probably superior to other modalities in charac-
terizing complicated cysts (Figure 4.19).
RNI: A 99mTc DMSA scan will give info regarding the
differential function and will show photon-deficient
areas occupied by the cysts with uptake in the intervening
normal renal parenchyma. The kidneys have lost their
normal reniform appearances and the appearances can
be quite misleading for the unwary.
Angiography: Its role in the diagnosis of ADPKD is
limited. Although angiography has a high degree of
accuracy in the diagnosis of ADPKD, its specificity is low.
FIGURE 4.19: Coronal T2WMR: Bilateral polycystic
kidneys–ADPKD
Radionuclide studies have a complementary role in
the assessment of renal function in ADPKD. These studies
do not have the added hazard of an exposure to iodinated
contrast material.
Limitations of above Modalities in General
On plain radiographs, nephromegaly may occur because
of causes other than ADPKD. Similarly, curvilinear
calcification is not specific for ADPKD and may be found
in other types of cysts and in tumors and granulomas.
Cysts similar to those of ADPKD can occur in nongenetic-
related simple renal cysts and in von Hippel-Lindau
disease. These findings apply to intravenous urography,
ultrasonography, CT scanning, MRI, and angiography.
Cysts associated with ADPKD cannot always be diffe-
rentiated from multiple simple cysts and cysts associated
with von Hippel-Lindau disease or tuberous sclerosis.
MORTALITY/MORBIDITY
Renal failure affects most patients with ADPKD by the
time they are aged 60 years.
Hypertension predates renal failure. Complications
from hypertension secondary to ADPKD are similar to
essential hypertension. Patients who are normotensive
at presentation have a better prognosis in terms of
survival. Infections, hemorrhage, cyst rupture, and renal
calculus disease are recognized complications of ADPKD.
Results of experimental studies have suggested that cystic
kidneys become infected more easily than noncystic
kidneys. The urinary tract carries a particular risk of
serious infections in ADPKD, which adds considerably
to morbidity and mortality. Rarely, massive intracystic or
retroperitoneal hemorrhage can occur; these require
nephrectomy. Before the availability of renal dialysis and
renal transplantation, most patients died within 10 years
after the onset of symptoms. Liver and other extrarenal
cysts seldom cause symptoms; however, with longer
survival of patients with ADPKD, liver impairment may
cause increased morbidity and mortality rates. Rare
complications of hepatic cystic disease include cyst
hemorrhage, infection, portal hypertension, biliary obstru-
ction from cystic mass effect, and cholangiocarcinoma.
The variety of cardiac and aortic problems associated
with ADPKD may add to morbidity and mortality.

Approximately 10% of patients with ADPKD die from
a ruptured intracranial berry aneurysm.
MULTICYSTIC DYSPLASTIC KIDNEY (MCDK)
DEFINITION
A non-functional kidney, replaced by multiple cysts and
dysplastic tissue, can vary in size from .10-15 cm to only
1–2 cm. It is the second most common abdominal mass
in a neonate (Figure 4.20).
It probably due to atresia of ureter. Equal incidence
in males and female. Gross pathologic-surgical features
include Walls of cysts vary in thickness fibrotic, renal
stroma, may be quite large and bizarre.
By classic imaging appearance: 2 forms are generally
recognized:
1. Pelvoinfundibular MCDK more common type—results
from atresia of ureter or renal pelvis, cysts are remnants
of dilated calyces
2. Hydronephrotic type of MCDK occurs less frequently
—results from atretic segment of ureter, cysts are the
entire pelvocalyceal system.
FIGURE 4.20: Multicystic dysplastic kidney
(For color version see Plate 3)
Congenital Anomalies of Urorenal Tract 49
• Tend to involute with time, cysts shrink and residual
tissue does not have a reniform shape, typically not
surgically removed.
• A few reports of Wilms’ tumor occurring in MCDK
may change management.
• Up to 40% of patients with MCDK have contralateral
abnormality-PUJ obstruction and vesicoureteral reflux
are most common.
• Can be segmental in duplicated kidneys.
INCIDENCE
0.03% in autopsy series.
IMAGING FINDINGS
Sonography to document cystic nature and exclude
enlarging mass over time (potential for Wilms’ tumor)
Nuclear scintigraphy to document non-function and
confirm normal drainage of contralateral kidney.
Nuclear Scintigraphy
Best imaging clue: Nuclear scintigraphy documents
lack of renal function. If some excretion is present,
consider poorly functioning hydronephrosis. Initial blood
flow images show perfusion of the MCDK, but sequential
images document lack of any excretory function. Note
that 99mTc DMSA may localize to the renal cortex in MCDK
due to the presence of tubular cells, but this is different
than true excretion of radiopharmaceutical.
a. Longitudinal sonogram of MCDK showing cysts of
varying sizes and echogenic intervening fibrous
stroma.
b. Posterior images from 99mTc MAG3 scan showing
normal drainage of left kidney and absent function
on the right in a toddler with right-sided MCDK.
MAG3, DTPA, Glucoheptonate are typically agents
of choice.
CT/MR Findings
Typically an incidental finding on CT or MRI scans, cystic
kidney with some enhancement possible in solid
components, but no true excretion of contrast, cortex
replaced by cysts.
50 Uroradiology: Text and Atlas
Ultrasound
Multiple anechoic cysts of varying size, largest cyst is not
generally centrally located, echogenic fibrous tissue in
intervening septa.
INTRAVENOUS UROGRAPHY (IVP)
It will also confirm non-function, but seldom used in
pediatrics.
RETROGRADE URETEROGRAM (RUG)
It will show blind ending ureter, different from rapid
change in caliber of ureter and communication with
calyces seen in UPJ obstruction or other causes of hydro-
nephrosis.
DIFFERENTIAL DIAGNOSIS
1. Hydronephrosis: Calyces should communicate with
each other in hydronephrosis, look for connections
on ultrasound.
2. Congenital mesoblastic nephroma: Solid tumor
of infancy.
3. Wilms’ tumor: Can be difficult to separate by USG,
absent excretory function is key.
PROGNOSIS
Excellent when uncomplicated.
MEDULLARY SPONGE KIDNEY (MSK)
INTRODUCTION
It is a developmental abnormality occurring in the
medullary pyramids of the kidney. MSK is characterized
by cystic dilatation of the collecting tubules in 1 or more
renal pyramids in 1 or both kidneys.
Lenarduzzi first described MSK in 1939.
The etiology is unknown.
Most patients remain asymptomatic, and MSK is
detected incidentally on urograms unless it is complicated
by infection, stone formation, or hematuria. Most cases
are sporadic, but a few hereditary cases have been
reported.
MSK also has been documented in siblings and in
several generations of families. The disease occurs in
persons of all ages and is more common in males than
in females.
PATHOPHYSIOLOGY
The pathogenesis of MSK is unknown. Most authors
believe that MSK is a developmental defect affecting the
formation of the collecting tubules. Some authors believe
that MSK is a progressive degeneration of the collecting
tubules that occurs later in life. According to Osathanondh
and Potter, the primary abnormality is hyperplasia of part
of the medullary collecting tubules. The size of the kidney
may be normal or slightly enlarged. On pathologic
sections, multiple cysts representing dilated terminal
collecting tubules are seen, measuring from 1–7 mm. The
cysts usually communicate proximally with collecting
tubules and distally with papillary ducts or calyx.
Intercommunicating and noncommunicating cysts
are seen occasionally. Calculi may be seen within the
cysts.
INCIDENCE
The frequency of MSK in the general population has
been estimated to be 1 case per 5,000–10,000
population, and MSK is seen in approximately 0.5% of
patients examined by using intravenous urography (IVU)
for various reasons.
CLINICAL FEATURES
Sex: The sex predilection varies.
Sometimes, the frequency is reported to be higher
in males than in females, and sometimes, it is higher in
females.
Age: MSK usually is diagnosed in persons aged 10–30
years, although MSK has been reported in children as
young as 2 years.
Most patients with MSK remain asymptomatic
throughout life, and the condition is discovered
incidentally when IVU is performed for reasons other than
the assessment of MSK. Patients with MSK are usually
asymptomatic, although acidification or impaired concen-
tration of urine has been documented. Complications
such as infection, hematuria, and stone formation may
be the presenting complaint in approximately 10% of
patients.
The frequency of calculus disease is increased and
manifested by hematuria, renal colic, flank pain, fever,
and dysuria.
 Congenital Anomalies of Urorenal Tract 51

ASSOCIATED SYNDROMES

MSK has been associated with hemihypertrophy, Ehlers-

Danlos syndrome, adult polycystic disease, congenital
hypertrophic pyloric stenosis, Caroli disease, parathyroid
adenoma, anodontia, Beckwith-Wiedemann syndrome,
distal renal tubular acidosis, horseshoe kidney, Marfan’s
syndrome, renal artery stenosis, pyeloureteritis cystica,
and ureteral duplication.
When associated with MSK, Beckwith-Wiedemann
syndrome has a high rate of tumors, including Wilms’
tumor and hepatoblastoma. MSK has been reported to
cause growth failure in children due to incomplete renal
tubular acidosis type 1, and it accounts for hypertension
in pregnancy in 1% of patients.

PREFERRED EXAMINATION

Plain Radiograph FIGURE 4.21: Plain KUB X-ray: Nephrocalcinosis

It may demonstrate nephrocalcinosis. Although MSK

cannot be diagnosed by using plain radiographic findings
alone, the presence of linear and rounded medullary
calcifications may suggest the diagnosis. The specific
diagnosis of MSK cannot always be made with plain
radiographic findings alone because MSK is one cause
of nephrocalcinosis, which has a wide differential
diagnosis.
Findings: Plain radiograph findings may be normal or
may demonstrate nephrocalcinosis. Nephrocalcinosis is
characteristic of MSK, with several discrete pyramidal
medullary calcifications occurring in clusters. When
passed into the collecting systems, calculi may be seen
in the renal pelvis, ureter, or bladder. Renal size is usually
normal, but the kidneys can be enlarged if the condition
is associated with polycystic kidney disease (Figure 4.21).
IVU
The principal method for diagnosing MSK is IVU, in which
discrete linear papillary densities, characteristic of MSK,
are seen. IVU appearances depend on the type of tubular
changes present. Changes form a spectrum that ranges
from mild dilatation of the renal collecting tubules (often
called renal tubular ectasia), which shows discrete linear
opacities in 1 or more papillae through increasing severity
of tubular dilatation and cystic changes, to gross
deformities with multiple cyst and cystlike cavities of
various sizes with beaded or striated cavities extending
through the pyramid from tip to base.
In patients with full-blown MSK, calyces tend to be
broad, shallow, distorted, and widely cupped. If calculi
are present, they tend to be arranged in groups around
a calyx, similar to a cluster of grapes or a bunch of flowers.
Renal function decreases with subsequent poor depiction
of the kidney. In view of the high incidence of nephro-
lithiasis in MSK, many patients have ureteral calculi. In
these patients, the excretory urogram may show
obstruction, calyceal distortion or destruction, and
evidence of urinary tract infection.
USG
Ultrasonographic (USG) and CT findings are more
sensitive than plain radiographic findings in showing
medullary calcifications, but they are less specific than
IVU findings. The sonographic appearances of MSK are
also nonspecific because hyperechoic medulla with or
without shadowing has been documented in a large
variety of conditions.
Findings: USG findings demonstrate echogenic medullary
pyramids in patients with MSK, irrespective of the
presence of medullary nephrocalcinosis. The echogenic
52 Uroradiology: Text and Atlas
medulla may cast acoustic shadowing. The increased
echogenicity is seen in particular at the periphery of
each pyramid between the interlobar cortices. US
findings can demonstrate complications related to calculus
disease.
CT
Findings: CT can be helpful in confirming the presence
of nephrocalcinosis, when it is suggested on USG images,
and CT scans can demonstrate tubular ectasia. In MSK,
unenhanced CT scan findings may be normal or
demonstrate medullary nephrocalcinosis.
Enhanced scans may demonstrate contrast
accumulation within the papillae.
CT scans readily depict obstructive changes and help
identify complications such as interstitial infection and
abscess formation.
Ill-defined areas of low attenuation representing
interstitial infection can readily be distinguished from
normally enhancing renal parenchyma.
CT scans also can help in differentiating interstitial
infection from abscess formation because abscesses
appear as sharply defined low-attenuation areas with thick
walls.
CT scans can also help in assessing the perinephric
extension of abscesses, and they can guide percutaneous
drainage.
Although CT has a limited role in evaluating patients
with MSK, it plays a significant role in evaluating
complications such as infection or abscess formation, and
CT can be used to guide percutaneous drainage of these
collections (Figure 4.22).
MRI
MRI is insensitive in detecting calcification.
The role of radioisotope uptake imaging is to assess
renal function and to show the site of renal parenchymal
scarring. CT appearances of MSK are nonspecific.
MRI has a complementary role and is a useful
alternative in patients who are allergic to iodinated
contrast media.
MRI is poor in depicting calcification. The role of MRI
in MSK is yet to be defined, but MRI may provide an
alternative to IVU in patients who are allergic to
radiographic iodinated contrast medium.
FIGURE 4.22: CECT: MSK with medullary calcification
is marked by contrast
RNI
The role of radionuclide scans in MSK is limited to the
assessment of renal function and to the identification of
a focus of renal infection.
INTERVENTION
Radiologic intervention is seldom required; however,
percutaneous nephrostomy may occasionally be useful
in treating a ureteric obstruction due to a calculus.
Although urinary tract infection occurs in approxi-
mately one-third of symptomatic patients with MSK, renal
abscess is a rare complication of the disorder. The
diagnosis of renal abscess should be suspected in patients
with MSK and acute pyelonephritis which do not respond
to appropriate antibiotic therapy. CT scans may reveal
large abscesses that require percutaneous or open surgical
drainage or small abscesses that require prolonged high-
dose antibiotic therapy.
MORTALITY/MORBIDITY
Morbidity associated with MSK appears to be higher in
women than in men.
In the vast majority of patients, MSK is associated
with a normal life expectancy.
A few cases do progress, with deterioration of renal
function and eventual renal failure.
CALYCEAL DIVERTICULUM
INTRODUCTION
Calyceal diverticulum, also known as pylogenic cysts, is
typically a symptomatic and incidentally found on IVUs.
 Congenital Anomalies of Urorenal Tract 53

They are found in both males and females of all ages.

Calyceal diverticulums are composed of uroepithelium
lined pouches that extend from the collecting system into
the renal parenchyma.

TYPES
They can be of three types:
1. Type I originates from the minor calyx,
2. Type II originates from the calyceal infundibulum and
3. Type III from the renal pelvis.
These diverticuli may lead to urinary stasis, which
may predispose the patient to stone formation or urinary
tract infections. During an intravenous urogram, the
calyceal diverticulum will appear opaque later in the
pylographic phase. It typically remains radiopaque after
the remainder of the kidney has drained due to the slow
exchange of urine caused by a narrow communicating
neck. The diverticulum should have a round, smooth-
walled appearance. It should not be confused with a hydro
calyx that develops from an infundibular stricture and FIGURE 4.23: Retrocard ureter
has a squared off appearance.
A calyceal diverticulum is a lesion that results from TREATMENT
an out pouching of a portion of the collecting system
Management of symptomatic stone disease associated
that protrudes into the corticomedullary region. They can
arise in any part of the collecting system from a fornix with calyceal diverticula has changed from an open
to the renal pelvis. Size varies anywhere from a few surgical approach to include ESWL, percutaneous,
millimeters to several centimeters in diameter. They are laparoscopic or ureteroscopic techniques. The choice of
uroepithelial-lined cavities that communicate via a narrow therapy depends largely on the anatomic location of the
channel to a nearby calyx. They may be congenital, or diverticulum.
acquired lesions (Figure 4.23).
It is not uncommon to see calcified stones COMPLETE URINARY COLLECTING SYSTEM
characteristically layering in the dependent portion of the DUPLICATION
diverticulum. The stones that form within the diverticulum
INTRODUCTION
may pass and cause symptomatic renal colic but they
are typically confined to the diverticulum due to its narrow It can be complicated by upper pole moiety obstruction
neck connection to the distal collecting system. and lower pole moiety vesicoureteral reflux.
They are regions of urinary stasis and the dependent
sediment that eventually develops in a calyceal PATHOPHYSIOLOGY
diverticulum is referred to as “milk of calcium”. Larger
Partial duplication is caused by branching of the ureteral
stones may form that are confined to the diverticulum
bud prior to its connection with the metanephric blastema
and may be a source of chronic pain.
(“Y” ureter). The two ureters may join between the kidney
On CT, the diagnosis is made with delayed imaging
showing the diverticulum fill with contrast. Alternatively and the bladder or one will end in a blind pouch.
if stones are present, the patient can be rescanned in the When two separate buds arise from the mesonephric duct,
opposite position. If the stones settle dependently, and complete duplication occurs as each ureteric bud
are confined to the lesion, the diagnosis can be made separately joins the metanephric blastema. This forms
in the absence of delayed imaging. both upper and lower pole “moieties”.
54 Uroradiology: Text and Atlas
The Weigert-Meyer rule specifies the upper pole
moeity ureter enters the bladder inferior and medial to
the insertion of the lower pole moiety ureter. While
uncomplicated duplex kidney is considered a normal
variant, there are potential complications as in this case:
a. Ectopic ureterocele of ureter draining upper pole may
result in upper pole hydroureteronephrosis.
b. Vesicoureteral reflux into lower pole due to abnormal
development of lower pole ureter-bladder wall valve
mechanism.
Less commonly, the ectopic upper pole ureter may
insert distal to the urethral sphincter causing continuous
urinary dribbling/incontinence or an ectopic ureter may
reflux.
VARIETIES
Duplex kidney refers to two ureters draining one
kidney. Most common (1 in 160) anomaly of the upper
collecting system. Spectrum from bifid renal pelvis to
complete duplication. Incomplete form with bifurcation
of the ureter high (bifid renal pelvis), anywhere along
the ureter (bifid mid-ureter) or near the bladder (low bifid
ureter).
Incomplete duplication more common than complete
duplication. Weigert-Meyer rule applies if the duplication
is complete: Ureteral orifice of the upper pole moiety
inserts ectopically into the bladder medial and inferior
to its normal location and to the ureter draining the lower
renal segment. With complete duplication, the ureter
draining the lower pole has a more perpendicular course
through the bladder wall making it more prone to reflux.
The ectopic ureter from the upper pole is prone to
obstruction, reflux or both. If large, a ureterocele may block
the contralateral ureteral orifice and/or the urethral orfice
at the bladder neck. Ureterocele treatment is surgical.
Ectopic ureterocele is a cyst like protrusion into the
bladder lumen of the dilated submucosal distal portion
of an ectopic ureter. Associated with duplication, usually
with the upper pole moiety. Upper pole of the duplex
kidney is dilated and connects with a dilated, tortuous
ureter. There may be dilatation of the lower moiety due
to VUR or extrinsic PUJ obstruction of the lower pole
ureter by the crossing dilated upper pole ureter. At the
level of the bladder, the hydroureter terminates in a round,
thin-walled anechoic intravesical ureterocele.
Duplications are familial. Incomplete duplication
results in no increased incidence of disease. Complete
duplication results in higher incidence of UTI, VUR,
parenchymal scarring and obstruction. If no reflux or
obstruction, considered a normal variant.
CLINICAL FEATURES
Frequently discovered during evaluation of a urinary tract
infection in a child or prenatally as hydronephrosis.
Results in variable to normal function with malfunction
due to both dysplasia of upper pole cortex due to obstruc-
tion and/or lower pole reflux nephropathy.
ROLE OF RADIOLOGY AND IMAGING
On sonography, a duplex collecting system is seen as two
central echogenic renal sinuses with intervening bridging
hypoechoic renal parenchyma.
On CT, the two ureters can be followed on sequential
contrast-enhanced images as they exit the renal sinus and
extend to join each other or the bladder. With obstructed
systems, the hydronephrotic segment of the kidney and
the nonenhancing dilated ureter can be followed to its
point of termination. MRI is useful in that the ureteral
insertion can be display in multiple planes. Sonography,
especially in children, is ususally sufficient for diagnosis.
DIFFERENTIAL DIAGNOSIS
Renal ectopia, congenital ureteropelvic junction obs-
truction, megaureter.
TREATMENT
Endoscopic ureterocele incision (upper pole moeity’s
ureteral herniation into bladder) - relieves hydonephrosis
AND re-implantation of lower pole moiety ureter into a
more oblique course through bladder wall eliminating
continued reflux into lower pole.
DUPLICATED COLLECTING SYSTEMS
INTRODUCTION
Duplicated collecting systems can be defined as renal units
containing two pyelocalyceal systems associated with a
single ureter or with double ureters. The two ureters empty
separately into the bladder or fuse to form a single ureteral
orifice.

Duplicated collecting systems can be unilateral or
bilateral and occur in 15% of the population. Duplicated
systems can be associated with a variety of congenital
genitourinary tract abnormalities. Most patients are
asymptomatic and genitourinary tract abnormalities are
detected incidentally on imaging studies performed for
other reasons. Symptomatic patients usually have
complete ureteric duplication in which the ureters are
prone to developing obstruction, reflux, and infection.
Ureteropelvic obstruction is more common when a duplex
kidney exists and can be inherited in an autosomal
dominant pattern.
PATHOPHYSIOLOGY
During embryogenesis, if a single ureteral bud bifurcates
before bifurcation of the ampulla, a duplex kidney results
with bifid pelvis or bifid ureter (Figure 4.24). If two ureteral
buds arise from the Wolffian duct, a duplex kidney results
with complete ureteral duplication. The ureteral bud
associated with the future lower pole separates first from
the Wolffian duct and the orifice progresses superiorly
and laterally as a result of growth of the urogenital sinus.
The common excretory duct, with the remaining ureter
still attached, is taken up in to the urogenital sinus. The
orifice of the ureter draining the upper pole opens medial
and inferior to the orifice draining the lower pole.
A duplex kidney may be drained by a single ureter
or by two ureters that unite to form a single ureter or
drain separately. Usually, the lower pole system is
dominant; a large renal pelvis drains the lower pole
through many calices. The upper pole pyelocalyceal
system may have only a single calyx and a single
infundibulum and drain directly into the ureter.
Bifid ureters draining a duplex kidney join to form
a single ureter, which can be extravesical (common;
Y- shaped) or intravesical (V-shaped) and usually empties
into the bladder.
FIGURE 4.24: Development of complete ureteral duplication
Congenital Anomalies of Urorenal Tract 55
Rarely, a single proximal ureter divides distally to form
an inverted Y appearance. Usually, 2 ureteral orifices are
observed on the same side; rarely, one of the ureters can
be ectopic. Infrequently, the middle third of the ureter
may be duplicated, with a single proximal third and a
single distal third. Double ureters remain completely
separated and in approximately 85% of patients, the
upper pole ureter drains below and medial to the lower
pole ureter (Weigert-Meyer rule).
Certain potential abnormalities result from or are
related to duplicated systems. The following are well-
known examples:
• Upper pole hydronephrosis from stenosis of the upper
pole ureteral orifice
• Ectopic insertion of the upper pole ureter
• Ectopic ureterocele of the upper pole ureter
• Reflux involving the lower pole from maldevelopment
of the valve mechanism.
INCIDENCE
The incidence of duplex kidney appears to be 12-15%
in the general population.
CLINICAL FEATURES
Race: No racial predilection has been recorded.
Sex: No sex predilection is found among patients with
bifid collecting systems and partial ureteric duplication.
The presence of double ureters appears to be 10 times
more common in females. Duplex kidney with uterus
didelphys has been reported in identical twins.
Age: A duplicated collecting system is a developmental
anomaly and patient age at presentation varies depending
on the type of abnormality. Patients with duplex kidney
are usually asymptomatic and duplex kidney is detected
incidentally on imaging studies performed for other
reasons, unless complications arise.
Presentation in patients with duplicated collecting
systems varies depending on the type of anomaly. Patients
with duplex kidney are usually asymptomatic.
Ureteropelvic junction obstruction is more common when
duplex kidney exists. Giant hydronephrosis in a duplex
kidney can manifest as a huge abdominal and
retroperitoneal mass and, rarely, can cause hypertension.
56 Uroradiology: Text and Atlas
The incidence of vesicoureteric reflux, urinary tract
infection, and parenchymal scarring is increased in
patients with duplicated collecting systems; patients can
present with pyrexia and dysuria. Prolapsed ureterocele
associated with a duplicated ureter can cause urethral
obstruction in males and females. Patients with ectopic
insertion of the ureter with completely duplicated ureters
can present with urinary incontinence, particularly in
females. Males are always “dry” since the insertion is
proximal to the sphincter.
Because of the widespread use of antenatal
ultrasound, duplicated collecting systems are diagnosed
in utero.
An ectopic ureter observed in a patient with complete
ureteral duplication can present in the early stage,
especially in female patients, since the ectopic ureter may
insert below the sphincter or outside of the urinary tract
(e.g. vagina).
Duplicated ureter complicated by transitional cell
carcinoma occurs in the elderly population.
ANATOMICAL BASIS
When a single ureteral bud bifurcates before the ampulla
bifurcates, a duplex kidney with a bifid renal pelvis or
bifid ureter results. If two ureteral buds arise from the
Wolffian duct, a duplex kidney with complete ureteral
duplication ensues.
TERMS RELEVANT TO DUPLEX COLLECTING SYSTEMS
1. Duplex kidney: The duplex kidney has a single renal
parenchyma drained by two pyelocalyceal systems.
2. Upper or lower pole: The poles represent one
component of a duplex kidney.
3. Duplex system: The kidney has two pyelocalyceal
systems and is associated with single or bifid ureters
(partial duplication) or two ureters (double ureters)
that drain separately into the urinary bladder
(complete duplication).
4. Bifid system: Two pyelocalyceal systems join at the
ureteropelvic junction (bifid pelvis) or the 2 ureters
join before draining into the urinary bladder (bifid
ureters).
5. Double ureters: Two ureters open separately into the
renal pelvis superiorly and drain separately into the
bladder or genital tract.
6. Upper and lower pole ureters: The upper pole ureter
drains the upper pole of a duplex kidney while the lower
pole ureter drains the lower pole of a duplex kidney.
PREFERRED INVESTIGATIONS
Plain Radiography
Plain radiography makes no major contribution but a
renal mass may be apparent because the duplex kidney
is almost always longer than the nonduplex kidney.
Hydronephrotic upper or lower pole moiety in a duplicated
collecting system can also be observed as a renal mass.
Features: The duplex kidney is almost always longer than
the nonduplex kidney. In a duplicated collecting system,
hydronephrotic upper or lower pole moiety can be
observed as a renal mass.
Limitations: Plain radiographs can demonstrate a renal
mass, which is a nonspecific finding.
IVU/ Excretory Urography
IVU findings are almost always diagnostic in most patients.
Difficulty may arise when function is poor or absent in
one of the moieties.
Features: A duplex kidney is usually longer than the
nonduplex kidney.
Parenchymal thickness of one of the poles of the
duplex kidney is less than the thickness of the other pole.
The calyces are asymmetric.
An ectopic upper pole ureteric insertion can cause
a nonopacified segment. This mass effect results in the
“drooping lily” sign with the depression of the lower
pole pelvicaliceal system (Figure 4.25).
If the lower pole of the duplex kidney is poorly
functioning or nonfunctioning, the lower pole collecting
system may not opacify and no discernible parenchyma
surrounds it (nubbin sign). This may resemble a non-
duplicated kidney with a lower polar mass or renal infarct.
Reduction in the number of calyces, depiction of a
portion of the collecting system, and the presence of a
straight inferior border help differentiate a duplicate
collecting system from a renal mass.
Anomalies of the ureter, such as partial or complete
ureteral duplication, may be demonstrated.

FIGURE 4.25: Complete duplication of right PC system
hydronephrosis of lower pole calyces
Limitations: On excretory urography, an obstructed
nonfunctioning upper or lower pole may mimic a renal
mass.
MCU/VCUG
Ectopic ureter of a nonfunctioning moiety can be
demonstrated best using voiding cystourethrogram if
vesicoureteral reflux exists.
Features: The intravesical ectopic ureter of a nonvisualized
moiety is demonstrated better using voiding cystourethro-
gram.
Antegrade Pyelography
Antegrade pyelography is useful in patients with
hydronephrosis to demonstrate the presence of a second
ureter and to determine the level of ureteric termination.
Features: Antegrade pyelography: Antegrade pyelography
is useful in patients with hydronephrosis for demonstrating
the presence of a second ureter and to determine the
level of termination.
Ultrasound
Ultrasound is a noninvasive and extremely useful
examination, particularly in children. The sonographic
appearance of a duplex kidney is specific but not sensitive.
Congenital Anomalies of Urorenal Tract 57
Ultrasound findings provide excellent anatomic
information but do not necessarily differentiate a bifid
renal pelvis from a bifid ureter or two complete ureters.
A large Bertin column can mimic a duplex collecting
system on CT. It is valuable in evaluating an intravesical
ureterocele, either orthotopic or ectopic.
Features: The duplex kidney appears as two central echo
complexes with intervening renal parenchyma.
Hydronephrosis of one pole is suggestive of a duplex
kidney. Although hydronephrosis can occur in either pole,
it is more common in the upper pole. Occasionally, two
distinct collecting systems and ureters can be observed
on ultrasound images.
CT with Contrast
CT with contrast is superior to ultrasound and excretory
urography in diagnosing the nubbin.
Features: The intervening renal parenchyma in a duplex
kidney lacks a collecting system and major vessels and
is termed a faceless kidney. CT can help determine
whether an obstruction exists and can help assess the
renal parenchyma. CT can help determine whether
insertion of the duplicated ureter is intravesical or
extravesical. CT can demonstrate the collecting system
in the nubbin or mass effect of tissue at the pole.
CT scanning is superior to ultrasound and IVU in
diagnosing the lower pole nubbin. CT is helpful when
function is poor or absent.
Magnetic Resonance (MR) Urography
Magnetic resonance (MR) urography may be used as a
primary diagnostic method in assessing a duplicated
ectopic ureter and the complications associated with
duplex kidneys. Spatial resolution is a limiting factor.
Features: MR urography can provide information similar
to that of excretory urography when renal function is poor
or absent. An ectopic ureter extending from a poorly
functioning moiety of a duplex kidney invisible on other
imaging may be observed with MR urography.
MR urography may be used as a primary diagnostic
method in assessing a duplicated ectopic ureter and
complications associated with duplex kidneys.
Limitations: Availability of MRI is limited, the procedure
is expensive, and it requires sedation of patients with
58 Uroradiology: Text and Atlas
claustrophobia. However, MR urography is an extremely
useful technique in patients who have the probability of
an adverse reaction to radiopaque contrast media.
Scintigraphy
Scintigraphy is useful in the assessment of relative renal
function and detection of renal scars.
Features: Duplex kidneys appear as two separate
collecting systems on the same side of the body.
Scintigraphy may demonstrate reflux up the ureter in a
nonfunctioning duplex kidney with ureteral duplication.
Limitations: Scintigraphy can reveal differential
functioning. However, if functioning is markedly
depressed, imaging is limited.
Arteriography
Arteriography is an invasive procedure and is no longer
used to diagnose duplex collecting systems but may
occasionally be useful in planning nephron-sparing
surgery.
Findings: Invariably, two separate arteries arise, mostly
independently from the aorta. Hydronephrosis of a
moiety appears as a filling defect displacing arterial
branches.
Arteriography is an invasive procedure and is no
longer used to diagnose a duplex collecting system.
MORTALITY/MORBIDITY
Most cases of duplicated collecting system are detected
incidentally; however, the incidence of ureteropelvic
obstruction is increased with duplex kidney, hydronep-
hrosis, and pyelonephritis in patients with complete
ureteral duplication.
ECTOPIC URETER
INTRODUCTION
A ureter that does not terminate at the trigone of the
bladder, which is its normal location. The term is used
to describe a ureter that opens outside the bladder.
ASSOCIATED ANOMALIES
Eighty percent of ectopic ureters are associated with
complete ureteral duplication. With unilateral single
ectopia, a hemitrigone is found in the bladder. With
bilateral single ectopia (very rare), there is no trigone;
the bladder fails to completely develop.
INCIDENCE
Females to males 6:1 ratio.
EMBRYOLOGY
The ureteral bud fails to separate from the mesonephric
duct. Its orifice opens in a urogenital sinus or Wolffian
duct structures, such as the bladder neck, urethra, seminal
vesicles, vas deferens, or ejaculatory duct in males, and
bladder neck, vestibule, or urethra in females. Ureteral
ectopy into the uterus, vagina or cervix may also be seen.
CLINICAL FEATURES
In males, urinary infection and obstruction but not
incontinence may be experienced, since the the ureter
opens above the urogential diaphragm. By contrast,
urinary incontinence may be seen in females. In many
cases, the diagnosis may not be made until adulthood,
especially if incontinence is absent.
IMAGING
Urography will demonstrate upper moiety obstruction due
to a stenotic ectopic ureteral orifice in cases associated
with duplication. Cystoscopy and retrograde pyelography
may be used to confirm the diagnosis if the ectopic orifice
terminates within the urinary tract. Otherwise, ultrasound
or CT may be useful. If a single ureter is present, a
nonfunctioning dysplastic kidney will be seen on the side
associated with the ureteral ectopia.
URETEROCELE
INTRODUCTION
A ureterocele is a submucosal cystic dilation of the
terminal segment of the ureter.
CLASSIFICATIONS
A ureterocele may be classified most easily as:
1. Intravesical, defined by its presence entirely within
the bladder
2. Extravesical, defined by the permanent presence of
some portion of the ureterocele at the bladder neck
or urethra.

Other classification systems for ureteroceles are based
on the location of insertion of the ureter into the bladder:
1. Simple (orthotopic)
2. Ectopic
3. Cecoureterocele
4. Pseudoureterocele.
According to their morphology, ureteroceles may be:
1. Stenotic (obstructive ureteral orifice within the bladder)
2. Sphincteric (ureteral orifice at the bladder neck), or
3. Sphincteric stenotic (obstructive ureteral orifice at the
bladder neck)
4. In addition, they can also be cecoureteroceles
(extension of the ureterocele past the bladder neck
into the urethra and may cause bladder outlet
obstructions).
Ureteroceles are most commonly found in association
with complete ureteral duplication (80%), but they can
also be seen at the terminus of a single system. The
association of a fluid-filled structure within the bladder
leading to an ectopic dilated ureter and a hydronephrotic
upper pole of a kidney is the sine qua non of a
ureterocele associated with a duplicated system. The
function of the upper pole segment is variable depending
on the relative degree of obstruction caused by the
ureterocele.
A ureterocele associated with the upper pole moiety
is located medially and inferiorly to the lower pole ureter
inserting in a more superolateral location (Weigert-
Meyer rule).
Aphorism: UU-LR, i.e. upper moiety is associated with
ureterocele and obstruction and the lower moiety with
reflux, in which case the draining moiety is dysplastic.
Intravesical single-system ureteroceles are typically
associated with good renal function (>80% with excretory
function), whereas extravesical single-system ureteroceles
are seen with poor renal function (<30% with excretory
function), dysplastic kidneys, and bladder outlet
obstruction.
Increasingly, ureteroceles are detected on antenatal
sonograms. Initial findings often include hydronephrosis
and a fluid-filled structure within the bladder. Antenatal
findings must be correlated with results of postnatal
studies, including ultrasonography, cystography, and
Congenital Anomalies of Urorenal Tract 59
functional studies. Vesicoureteral reflux is present in 50%
of ipsilateral lower-pole moieties in duplex-systems and
10–25% of contralateral moieties in single and duplex
systems.
PATHOPHYSIOLOGY
The true etiology of ureteroceles is not known. A common
etiology is unlikely in simple and ectopic ureteroceles.
Several postulated theories for the etiology of ureteroceles
include the incomplete dissolution of the Chwalla
membrane during development, altered development of
the ureteral bud, inadequate muscularization, Schisto-
soma hematobium infection, and trauma.
Histologically, ureteroceles contain abnormal mus-
culature, with an incomplete patchy muscular coat.
Electron microscopy shows a paucity of muscle
bundles and smaller myocytes and an absence of thick
myofibrils.
CLINICAL FEATURES
Sex: Females are affected more commonly than males,
with a female-to-male ratio of 6:1. Interestingly, ectopic
single system ureteroceles are more common in males
and associated with additional congenital anomalies.
Age: Two distinct groups of patients present with
ureteroceles. Infants and children most commonly (60%)
present with ectopic ureterocele associated with a duplex
system. Large ureteroceles are commonly seen in very
young infants. On the other hand, adults are most likely
to present with a simple single-system ureterocele.
Ureteroceles are associated with obstructive uropathy.
Detrusor hypertrophy is often seen if the ureterocele is
associated with bladder outlet obstruction. Vesicoureteral
reflux is present in 50% of ipsilateral moieties in duplex
systems and 10–25% of contralateral moieties in single
and duplex systems. Renal dysplasia is seen in 40% of
resected duplex systems, with hydronephrotic atrophy and
renal scarring also commonly seen.
Ectopic drainage (outside of the trigone) in females
may result in incontinence because the ureter drains
beyond the bladder neck into the urethra, vagina, or
uterus. However, incontinence is not seen in males
because the ectopic ureter always inserts proximal to the
external sphincter.
60 Uroradiology: Text and Atlas
INCIDENCE
The incidence varies from 1 case per 500 population to
1 case per 4000 population. A predilection for ureteroceles
is well documented in Caucasians.
ROLE OF RADIOLOGY AND IMAGING
Functional studies of the renal system includes:
1. Intravenous pyelography
2. CT scanning, and
3. Renal scanning.
These contrast-enhanced studies help in delineating
the relevant renal anatomy, especially with regard to
potential renal duplications. They are also useful in
evaluating the differential renal function. Contrast-
enhanced studies help in identifying ureteroceles within
the bladder as a thin nonenhancing rim around contrast
enhancement within the ureterocele. These functional
studies often add supplemental information useful in the
treatment of patients with ureteroceles, but they are
typically not used as first-line imaging modalities for the
diagnosis of suspected ureteroceles.
CT scans, intravenous pyelograms, and renal scans
are less sensitive for ureteroceles, but they help in more
clearly delineating the functional anatomy of the kidneys.
Voiding Cystourethrography
VCUG/MCU should be performed in all newborns with
fetal hydronephrosis. Early imaging prior to complete
opacification of the bladder with contrast material may
show the ureterocele as a filling defect. VCUG defines
the degree of vesicoureteral reflux in both ipsilateral and
contralateral systems and also possible inferior displace-
ment of the lower pole as a large obstructed upper pole.
The drooping lily sign is a classic description of moderate–
to–high-grade reflux into a displaced lower pole.
In addition, VCUG may be performed to evaluate
the size, position, tension, degree of detrusor backing,
and compressibility of ureteroceles. Eversion of uretero-
celes on VCUGs may be seen as protrusions outside the
urethral or vesical wall.
VCUGs are used routinely to visualize the bladder
and evaluate the accompanying reflux. Larger uretero-
celes are clearly identifiable as areas of cystic lucency
within the bladder. VCUG is the diagnostic procedure
of choice for evaluating and grading the vesicoureteral
reflux. It also helps in therapeutic decision making.
Ultrasound
Radiologic evaluation of an ureterocele in an adult usually
includes a kidney-bladder ultrasonography. Ultrasono-
graphy can be the initial study performed, and it can
be used to detect prenatal ureteroceles. Ultrasonography
noninvasively depicts anatomic changes in the kidney
and bladder. Sonography should be performed with the
bladder empty and with it filled to eliminate
nonvisualization of ureteroceles due to either compression
of the bladder or the ureterocele. Ultrasonography is the
most sensitive test and often the only radiologic evaluation
required for the diagnosis of ureteroceles.
Limitations of techniques: Ultrasonography is the most
sensitive test for the detection of ureteroceles.
Ultrasonography may cause ureteroceles to be missed
if the patient’s bladder is empty or fully distended, if the
ureteroceles are small, or if the patient’s body habitus
precludes proper examination. Ultrasonographic findings
are relatively specific for ureteroceles because the other
etiologies of a cyst within a cyst are relatively rare.
Antenatal Ultrasonography
On antenatal sonograms, the typical presentation is that
of an enlarged hydronephrotic fetal kidney. Renal
duplication and/or ureteral duplication may be seen.
Intravesical cystic dilation or septa within the bladder
(which represent ureterocele walls) suggest that the
etiology of the hydronephrosis may be an ureterocele.
Such antenatal ultrasonographic findings warrant
comprehensive postnatal evaluation and confirmation of
the diagnosis.
Antenatal ultrasonography is increasingly becoming
the diagnostic modality for diagnosing prenatal
ureteroceles. Findings of a cyst within the bladder and
hydronephrosis are virtually diagnostic of a ureterocele.
However, any finding on antenatal sonography must be
confirmed with comprehensive postnatal ultrasonogra-
phic evaluation. Hydronephrosis may be associated with
ureteroceles, but it is not pathognomonic.

Renal/bladder Ultrasonography
The initial study performed for the evaluation of a neonate
with fetal hydronephrosis with or without a suspected
ureterocele should be renal and/or bladder ultrasono-
graphy. During every postnatal ultrasonographic
evaluation of antenatal hydronephrosis, examining the
bladder is imperative to avoid missing associated
ureteroceles. The sonographic finding of a well-defined
cystic intravesical mass within the posterior bladder wall
is suggestive of a ureterocele.
The classic description is that of a cyst within a cyst
(see Figures 4.1 to 4.3). Occasionally, the dilated
intramucosal section of the ureter may be visualized as
it inserts into the bladder and terminates in the ureterocele
(see Figures 4.4 to 4.6). Ultrasonography also defines
the degree of hydronephrosis, and it possibly depicts renal
dysplasia as cortical thinning. With their distinct echogenic
renal pelves, duplex renal systems may also be identified
on the initial ultrasonographic examination. This finding
should exclude any solid periureteric orifice mass in the
bladder, such as a pseudoureterocele.
Renal and/or bladder ultrasonography is highly
sensitive for the detection of ureteroceles and widely used.
Similar to all other imaging modalities, smaller uretero-
celes may be compressed and thus missed on sonograms.
Intravenous Urogram
The classic finding on an intravenous urogram (IVU) is
a round radiopacity in the bladder surrounded by a
radiolucent rim.
If function of the affected kidney is poor, the upper
pole system may not be seen. Very few calices may be
noted in the lower pole system, with a downward and
laterally displaced lower-pole moiety (drooping lily
sign). The lower-pole ureter may be displaced laterally
or looped around the dilated upper pole ureter near the
sacrum.
Defects in the lower urinary tract are more evident
in single-system ureteroceles subtending well-functioning
kidneys. The contrast agent–filled ureterocele may be
separated from contrast medium in the bladder by a thin
lucent halo of the ureterocele wall (spring-onion or
cobra-head deformity). Radiopaque stones within
Congenital Anomalies of Urorenal Tract 61
ureteroceles are often seen as opacities on the scout
image. On the other hand, radiolucent stones are often
seen as filling defects within the ureterocele during the
excretory phase of the urogram.
IVUs are not typically obtained in infants because the
procedure is more invasive and the results are less
informative. The reason is the failure of infant kidneys
to concentrate the contrast agent. IVUs are more
commonly performed in adults, in whom ureteroceles
may be serendipitously depicted.
CT
Widespread use of CT for diagnostic imaging has allowed
the functional and anatomic identification of ureteroceles
in a single study. CT scans without and with intravenous
contrast enhancement can be used to define the size,
shape, and location of the ureterocele (see Figures 4.11
to 4.14). Ureteroceles may be seen as cobra-head
deformities (see Figure 4.14). In addition, CT scans enable
identification of duplicated renal systems, the renal and
ureteral contours, the degree of hydronephrosis, the
cortical thickness of each moiety, and the functional ability
of the kidneys to excrete contrast material, as well as other
anatomic anomalies.
CT scans offer greater anatomic resolution of the entire
urinary tract, especially in complicated cases. Ureteroceles
can be identified accurately and consistently by using CT
scans.
MRI
It is not usually applicable, but it should be as effective
as the IVU (as with magnetic resonance urography with
or without contrast enhancement) and CT scanning.
RNI
Radionuclide renal scans obtained with dimethylsuccinic
acid, diethylenetriamine pentaacetic acid, or mercapto-
triglycylglycine may be useful in evaluating baseline renal
function in the ipsilateral and contralateral units. These
scans commonly demonstrate minimal or no function in
the upper-pole moiety of the duplicated system, with
ureteral obstruction at the point of the ureterocele. A single
intravesical system is typically associated with good renal
function.
62 Uroradiology: Text and Atlas
Renal radionuclide scanning is not used to detect
ureteroceles, but it may aid in therapeutic decision
making. Evaluation of the function of the affected renal
units may help in deciding whether partial or radical
nephrectomy is indicated.
DIFFERENTIAL DIAGNOSIS
Pseudoureteroceles, bladder diverticula, and mesonephric
duct cysts may all resemble the ureterocele as a cystic
lucency on the radiologic imaging, and they may
contribute to false-positive findings. A pseudoureterocele
is so named because it can mimic the appearance of a
ureterocele on VCUGs or IVUs. A pseudoureterocele can
be caused by etiologies such as edema due to impaction
or passage of calculi, radiation cystitis, and transitional
cell carcinoma. Because ureteroceles are compressible,
they can be missed when the patient’s bladder is full.
Small (<1 cm) ureteroceles may also be missed.
With IVU, bladder diverticula and mesonephric duct
cysts may all resemble ureteroceles as a cystic lucency
on the radiologic imaging, and they may contribute to
false-positives findings. Pseudoureteroceles can either
mimic an obstructed ureterocele (lucent filling defect) or
a non-obstructed ureterocele (lucent halo surrounding the
ureteral orifice), depending on the size of the abnormality
and degree of the obstruction. Rarely, a focal bladder
tumor can cause a similar appearance. Because
ureteroceles may change the size and shape, depending
on the degree of filling, they may not be visible in all
phases of the urogram. Finally, because the IVU depends
on kidney function for optimal visualization, the use of
IVU for diagnosing ureteroceles may be compromised.
INTERVENTION
Each patient with a ureterocele is clinically unique
regarding anatomy, pathophysiology, and renal function.
As such, treatment options must be individualized.
Treatment often involves surgical intervention. Prior to
surgical intervention, the anatomy of the urinary tract
must be delineated as clearly as possible. Ipsilateral and
contralateral renal function must be assessed, and
treatment should be initiated expeditiously. The 4 goals
of intervention include (1) control and elimination of
infection, (2) minimization of vesicoureteral reflux and
bladder outlet obstruction, (3) preservation of urinary
continence mechanisms, and (4) protection of renal
function.
In infants with symptomatic ureteroceles, antibiotics
should be administered to treat urinary tract infections.
Antibiotic prophylaxis is associated with a low incidence
of urinary tract infections, and it may be used to delay
surgical intervention until the bladder matures. Small
asymptomatic ureteroceles may be observed with careful
serial physical and ultrasonographic examinations.
Surgical options include endoscopic ureterocele
incision, and, depending on renal function, percutaneous
diversion, ureteropyelostomy, partial or total nephroure-
terectomy, or complete reconstruction.
In the endoscopic approach, a small endoscopic
incision is made inferiorly and medially on the anterior
wall of the ureterocele above its base at the bladder neck.
This minimally invasive method is associated with low
morbidity rates and represents an effective method of
decompression in infants. The endoscopic approach is
highly successful for small, single-system intravesical
ureteroceles. With this procedure, the reported incidence
of iatrogenic reflux and incontinence (<10%) is low, and
secondary procedures are often not needed (10–15%).
The endoscopic approach represents a good first-line
method for the acute management of symptomatic
ureteroceles.
Radiologic interventions for ureteroceles are
primarily temporizing maneuvers rather than definitive
procedures. Percutaneous nephrostomy drainage allows
decompression of a dilated renal pelvis prior to definitive
treatment of the ureterocele.
MORTALITY/MORBIDITY
The morbidity of ureteroceles may be largely attributed
to their ability to cause obstructive uropathy. The primary
obstruction is at the level of the ureterovesical junction.
Ipsilateral (50%) and contralateral (25%) vesicoureteral
reflux is common. As a consequence, urinary tract infec-
tions are a common finding in infants with ureteroceles.
Pyelonephritis and frank pustulant urosepsis may be
present. Hydronephrosis is a common finding in both
ipsilateral and contralateral renal units.
Untreated, ureteroceles may progress to renal scarring,
renal failure if both kidneys are affected with the sub-

sequent need for dialysis and kidney allograft
transplantation.
Prolapsed ureteroceles also may cause a functional
bladder outlet obstruction.
OTHER BLADDER ABNORMALITIES CAUSING
URETERIC OBSTRUCTION
1. Cystitis
2. Hemorrhagic, bullous, eosinophilic, radiation,
tuberculous, schistosomiasis, lupus, Wegener’s,
small fibrotic bladder
3. TCC, SCC, rhabdomyosarcoma, mesodermal
tumors, invasion or metastasis from gynecological
cancer, prostatic cancer
4. BPH
5. Neuropathic bladder
6. Congenital or secondary to outlet obstruction
Following ureteric catheterization, transurethral or
open procedures on bladder, including fulguration
7. Foley balloon
8. Tumor
9. Muscular hypertrophy, bladder diverticulum
Iatrogenic trauma
10. Miscellaneous.
VESICOURETERAL REFLUX (VUR)
INTRODUCTION
Hodson initially noted the association of vesicoureteral
reflux (VUR) with renal parenchymal scarring.
Normally the ureter enters the superolateral angles
of the trigone, penetrating the bladder wall at an oblique
angle, giving rise to an oval ureteric orifice.
This acts as a valve preventing urine refluxing from
the bladder into the ureter during micturation, the rise
in intravesical pressure tending to close the orifice.
In some children the ureter takes more direct course
in the bladder wall leading to a short intramural portion
and a round ureteric orifice, which predisposes to reflux.
Renal cortical scarring and dilatation of calyces may
eventually result if untreated.
PATHOPHYSIOLOGY
Reflux nephropathy is based on persistent reflux of sterile
or infected urine from the bladder to one or both kidneys
Congenital Anomalies of Urorenal Tract 63
via the ureters. Although sterile VUR may cause renal
scarring, most studies indicate that the appearance of
renal scarring or the extension of established renal scars
requires infection (Escherichia coli is the common
pathogen). The higher the grade of reflux, the greater
the likelihood of development of new or progressive
scarring in association with infection.
Intrarenal reflux, or the extension of VUR into the
collecting tubules of the nephrons that allows urinary
microorganisms access to the renal parenchyma, is
believed to be particularly important in the development
of renal scarring.
Radiologic evidence of renal scarring is noted in
30–60% of children with VUR, and VUR is present in
almost all children with severe renal scarring. A direct
correlation between the prevalence of scarring and the
grade of VUR has been demonstrated.
Although VUR occurs at a similar rate in boys and
girls, girls are at greater risk of developing reflux nephro-
pathy because of increased incidence of urinary tract
infection (UTI). In the absence of reflux and UTI, abnor-
malities of organ systems other than the genitourinary
tract do not place a child at increased risk for developing
reflux nephropathy.
INCIDENCE
The incidence of renal scarring in children resulting from
VUR is unknown. The prevalence of VUR in asympto-
matic children is less than 0.5%, but VUR is present in
29–50% of children with UTIs.
ANATOMICAL BASIS
Most VUR is considered primary because of incompetence
of the ureterovesical junction (UVJ), and it is not
secondary to either obstruction or infection. As the UVJ
matures to assume its adult 1.5 cm oblique path through
the bladder wall, VUR tends to decrease in severity and
eventually disappears just before puberty. An exception
is in patients with an anatomic abnormality, such as a
bladder diverticulum, into which the refluxing ureter
enters. Incompetence of the vesicoureteral junction
resulting from a lack of maturation is the most common
cause of vesicoureteral reflux in children. Obstruction and
infection rarely cause reflux. With maturation of the
64 Uroradiology: Text and Atlas
incompetent vesicoureteral junction, reflux usually
eventually resolves.
A small subgroup of children who have a
perpendicular ureteric insertion at the bladder wall with
a resultant golf-hole ureteric orifice. In these patients,
surgical correction is necessary to eliminate VUR. A
decision to perform a repair, either a ureteroneocysto-
stomy or a collagen periurethral injection is dependent
upon the appearance of the ureteric orifice. Nevertheless,
all patient are covered with appropriate antibiotics to await
the maturation of the intramural portion of the ureter
or undergo surgery to stop the reflux.
CLINICAL FEATURES
Sex: Reflux occurs at a similar rate in boys and girls;
however, the much higher incidence of UTI in girls places
them at greater risk for reflux nephropathy.
Age: In children, the occurrence of VUR decreases with
increasing age. The vesicoureteral insertion matures just
prior to puberty. The mature bladder wall intramural
portion of the ureter attains its 1.5 cm length.
Children with reflux nephropathy may be asymp-
tomatic, they may present with nonspecific symptoms
(e.g. failure to thrive, fever, poor food intake), they may
be acutely ill in association with acute pyelonephritis, or
they may present with renal failure with advanced renal
scarring associated with reflux nephropathy.
GRADES OF VUR
Vesicoureteric reflux is graded on a scale of 0–5.
Grade 0 indicates no reflux;
Grade 1 indicates reflux into the ureter but not reaching
the renal pelvis; grade 2 indicates reflux into the renal
pelvis and calices but without any dilatation; and
Grades 3, 4, and 5 indicate reflux to the renal pelvis and
calices with mild, moderate, and severe dilatation,
respectively (Figure 4.26).
ROLE OF RADIOLOGY AND IMAGING
Renal ultrasonography (RUS) and voiding cystourethro-
graphy (VCUG) are the preferred radiologic methods.
The two procedures provide complementary information.
RUS helps in evaluating the upper urinary tract (kidneys
and proximal portion of the collecting system) for
FIGURE 4.26: Grades of VUR (For color version see Plate 3)
anomalies, masses, calcification, hydronephrosis, and size
and can identify renal scarring if moderate to severe in
degree. VCUG helps in evaluating for vesicoureteric reflux
and the anatomy of the lower urinary tract (bladder and
urethra).
VCUG
Plain images offer no diagnostic information regarding
VUR and reflux nephropathy, although they can be used
to evaluate spinal anomalies and potential urinary tract
calculi, which rarely occur in this population. VCUG is
essential in evaluating lower urinary tract anatomy and
in identifying or excluding VUR.
With voiding cystourethrography, contrast material is
instilled in the urinary bladder via transurethral catheter
and demonstrates increased opacity in the ureters and
pelvicaliceal systems when VUR is present. VUR grading
(grades 0–5) is based on the distribution and degree of
associated upper urinary tract dilatation demonstrated
on VCUG.
Intravenous Urography (IVU)
It can demonstrate changes reflecting reflux nephropathy
and renal scarring, including the following:
1. Dilatation and deformity of one or more renal calyces
2. Loss of parenchymal thickness of a region of the
kidney (especially upper and lower poles)
3. Focal contour indentation typically adjacent to a
calyx, representing renal scarring (Figures 4.27A and
4.27B).
 Congenital Anomalies of Urorenal Tract 65

FIGURE 4.27B: USG pelvis: Dilated left lower

ureter due to VUR
FIGURE 4.27A: MCU: Bilateral highgrade VUR

With VCUG, rate of detecting VUR is high but

detecting chronic pyelonephritic scarring rate is low. With
IVU, sensitivity is moderate for detecting chronic
pyelonephritic scarring.

Ultrasonography
Findings: Alteration of renal contour and reduced
thickness to the renal parenchyma are the primary findings
of reflux nephropathy. Ultrasonography is excellent for
demonstrating upper urinary tract dilatation.
Echo-enhanced cystosonography performed by using
ultrasonographic contrast media is a new diagnostic
procedure with a major attribute in the exclusion of
ionizing radiation. Echo-enhanced cystosonography, in
limited experience, is reported to be as accurate as
radiographic VCU in the identification of reflux
(Fig. 4.27B).
CT scanning is not indicated in the evaluation of FIGURE 4.28: MRU: Bilateral high grade VUR
reflux nephropathy because of radiation dose, the need
for intravenously administered contrast material, and the RNI
potential need for patient sedation. However, CT scans 99m
Tc dimercaptosuccinic acid and 99mTc glucoheptonate
can demonstrate renal scarring and hydronephrosis but are scintigraphic agents with a high affinity for the renal
not VUR. cortex because they are concentrated by renal tubular
MRI is not routinely indicated in the evaluation of cells. As a result, they produce a relatively high level of
reflux nephropathy because of cost of the procedure and renal detail. Concern for acute pyelonephritis, the
the potential need for patient sedation. However, MRI assessment of renal cortical scarring, and the identification
can demonstrate renal scarring and hydronephrosis but of a malpositioned kidney are among the indications for
not VUR (Figures 4.28 and 4.29). cortical scintigraphy. The use of single-photon emission
66 Uroradiology: Text and Atlas
FIGURE 4.29: MRU: Bilateral primary megaureter
computed tomography increases sensitivity of the agents
to changes of renal scarring and acute pyelonephritis.
Reduced accumulation of a cortical imaging isotope
within the renal margins is an indication of renal scarring.
Radionuclide cystogram provides an alternative to VCUG
in identifying renal scarring. Cystograms have the primary
disadvantage of poor anatomic resolution but the
advantage of a lower radiation dose.
Degree of confidence is high with renal cortical
imaging performed by using technetium 99mTc dimercap-
tosuccinic acid.
Patient motion results in inaccurate imaging depiction
of isotope distribution and greater probability of
underestimating renal scarring (false-negative findings).
Hydronephrosis, anomalies such as ectopic and/or fused
kidneys, and renal masses or cysts may result in the overcall
of severity of renal scarring (false-positive findings).
Angiography
It does not play a role in the evaluation of reflux
nephropathy.
LIMITATIONS OF ALL MODALITIES IN GENERAL
Renal scarring is detected and identified better by using
nuclear medicine renal scanning with a cortical imaging
agent (eg, 99mTc dimercaptosuccinic acid) than with
ultrasonography.
Imaging with renal scanning may require sedation in
younger children. Sedation is increasingly requested,
although rarely necessary, for children undergoing VCUG.
MORTALITY/MORBIDITY
The incidence of renal scarring in children caused by VUR
is unknown. VUR is present in 29–50% of children with
UTIs.
MEGAPOLYCALICOSIS AND PRIMARY
MEGAURETER MEGAPOLYCALICOSIS
(OR CONGENITAL MEGACALYCES)
It is a non-obstructive enlargement of the calyces due
to underdevelopment of the medullary pyramids. This
entity is important because it can be confused with
obstructive or refluxing hydronephrosis. Distinguishing
characteristics include preservation of the renal cortex
and the size and morphology of the calyces. There is
increase in the number of calyces. Moreover, these calyces
are polygonal in shape and faceted in appearance. The
calyces have no definable papillary impressions on
excretory urography. There is a prompt nephrographic
phase but opacification of the pelvis and ureter may be
delayed because the volume of contrast required to fill
the calices is large.
It is caused by underdevelopment of the papillae. The
calyces are uniformly dilated with the medullary tip having
a semilunar shape which caps rather than projects as a
cone into the calyx. Consequently, the calyces have a
polygonal shape and have a mosaic or faceted appea-
rance. It is usually unilateral.
PATHOGENESIS
Faulty ureteral bud division, primary hypoplasia of
glomeruli in the juxtamedullary cortex, functional
infundibular achalasia due to maldevelopment of smooth
muscle fibers of the pelvocalyceal junction, and transient
collection system obstruction in utero caused by involuting
folds in the proximal portion of the fetal ureter.
ROLE OF RADIOLOGY AND IMAGING
Diagnosis should be considered only in patients without
prior or concurrent obstruction or vesicoureteral reflux.
Renal function is normal and this differentiates congenital
megacalyces from postobstructive atrophy (Figure 4.30).
 Congenital Anomalies of Urorenal Tract 67

atrophy from vesicoureteral reflux by demostrating normal

renal function without permanent loss of nephrons.
Radionuclide tracers like I-131-iodohippurate sodium or
99m
Tc-DTPA that measure excretion show marked
prolongation of the excretory phase with a normal diuresis
phase excluding obstruction.

PRIMARY MEGAURETER
It is a congenital abnormality resulting from an aperistaltic
juxtavesical segment of ureter. Ureteral peristaltic
contractions are focally uninhibited secondary to faulty
development of the surrounding periureteral musculature.
It is akin to achalasia of the esophagus and it represents
the second most common cause of hydronephrosis in
the fetus and newborn. Most patients are asymptomatic.
The left ureter is affected three times more often than
the right and the finding is bilateral in 15–40% of cases.
Urine transit is delayed above the affected segment,
FIGURE 4.30: IVU: Congenital megacalyces on right side
typically at the distal third of the ureter, resulting in massive
dilatation of some or all of the more proximal ureter.
Clinically, stasis of urine in the enlarged calyces Reflux of urine does not occur. The calyces retain their
predisposes the patient to infection and stone formation. normal appearance which distinguishes this from ureteral
During excretory urography, maximum opacification obstruction. Other key radiographic findings include
of the pelvocalyceal system is delayed in the affected smooth, tapered narrowing of the ureter, no reflux and
kidney(s) because of the dilutional effect of the large no stenosis. Nonpropulsive to-and-fro motion in the
volume of urine in the enlarged, but otherwise normal, dilated segments may be seen (Figure 4.31).
infundibula and renal pelvis. Other features include
normal to increased number of calyces, normal to
increased kidney length, and decreased parenchymal
thickness due to expanded calyceal volume, thinning of
the medulla and shallow or absent papillary tips.
Congenital megacalyces is not progressive. Stones and
infection complicate the urographic appearance.
Ultrasound and CT findings of dilated calyces and
decreased renal parenchyma thickness do not help diffe-
rentiate congenital megacalyces from other nonobstruc-
tive causes of a dilated collecting system. Angiographic
nephrogram confirms that the reduction in parenchymal
thickness is due only to a medullary deformity and that
the cortex retains its normal thickness of 0.5 to 0.8 mm.
MR also demostrates the normal thickness of the cortex.
Quantitative renal radionuclide studies with 99mTc-
FIGURE 4.31: IVU: Bilateral congenital megaureters seen as dilated
DTPA or -DMSA differentiate nonobstructive congenital lower ureters without dilatation of pelvicalyceal system or proximal and
megacalyces from postobstructive atrophy or pressure mid parts ureters
68 Uroradiology: Text and Atlas
Potential Complications
Recurrent urinary tract infections
Urolithiasis
Differential Diagnosis
Chronic ureteral obstruction. This misdiagnosis may occur
if megacalicosis co-exists with primary megaureter.
BLADDER EXSTROPHY
INTRODUCTION
It is a congenital birth defect that is the malformation
of the bladder and urethra, in which the bladder is turned
“inside out”.
Bladder exstrophy results from a deficiency in develop-
ment of the lower abdominal wall musculature leaving
the bladder open and its mucosa continuous with the
skin. This condition is associated with epispadias in which
the urethra is open dorsally and urethral mucosa covers
the dorsum of a short penis.
The bladder does not form into its normal round shape
but instead is flattened and exposed outside the body.
The lower portion of the bladder, a funnel-shaped bladder
neck, made up of muscles that open and close the bladder,
fails to form correctly. The urethra and genitalia are not
formed completely (epispadias) and the anus and vagina
appear anteriorly displaced. Additionally, the pelvic bones
are widely separated (diastasis). Rarely a vesicointestinal
fistual or prolapse (cloacal exstrophy) is seen in these
patients. The anus is ventral in position and may
occasionally be imperforate. The genitalia are consistently
involved. Rectal prolapse can occur due to poor pelvic
musculature.
PATHOPHYSIOLOGY
It is unknown what causes Bladder Exstrophy. The
problem occurs somewhere between 4–10 weeks of
pregnancy when various organs, tissues and muscles
begin to form layers that separate, divide and fold.
Bladder Exstrophy is a Surgically Correctable Birth Defect.
INCIDENCE
Bladder Exstrophy is noted in 1 of 30,000 to 50,000 live
births.
CLINICAL FEATURES
Bladder Exstrophy is more likely to occur in males than
females by approximately 2 to 1. The risk of having a
2nd child with bladder exstrophy is about 1 in 100 and
1 in 70 if one of the parents has bladder exstrophy.
ROLE OF RADIOLOGY AND IMAGING
On plain films 60% of cases show separated symphysis
with extrophy-epispadic anomaly. 25% are associated
with epispadic anomalies alone. Radiologic evaluation
is usually done postoperatively to exclude adencarcinoma
at the anastomosis site years after ureterosigmoidostomy.
Ultrasound, CT, nuclear cystography and IVU are helpful
tools.
ASSOCIATED ANOMALIES
Skeletal: Diastasis of the symphysis pubis correlates well
with the severity of the extrophy-epispadia complex. Over
60% of diastases are associated with this complex and
approximately 25% with epispadias alone.
Gastrointestinal: Umbilical and inguinal hernias.
Urinary: Ureteric obstruction; unilateral or bilateral
pelvicaliectasis due to ureterocele formation or fibrosis
at the ureterovesical junction.
MANAGEMENT
Ureteral diversion, bladder augmentation, and skin
grafting. Radiological assessment/monitory: mandatory
in the postoperative period, because adenocarcinoma
may develop at the anastomosis years after uretero-
sigmoidostomy. This complication is not uncommon.
CONGENITAL BLADDER DIVERTICULUM
If a congenital diverticula (hutch diverticula), the bladder
outlet obstruction is usually secondary to a congenital
urethral valve or urethral stricture. The congenital variety
of diverticula are typically seen in boys. These diverticula
are characteristically located at the ureteral insertions.
Often, vesicoureteral reflux is resultant. Bladder diverticula
most often occur as a result of outlet obstruction.
Occasionally, a congenital weakness in the bladder wall
adjacent to the ureteral orifice results in a diverticulum.
This is termed a “Hutch” diverticulum.

In children, outlet obstruction causing a diverticulum
is rare and can be seen with urethral valves. In men,
diverticula are associated with outlet obstruction from
urethral stricture, prostatic hypertrophy, prostatic
carcinoma etc. acquired diverticula are rare in women.
BLADDER DUPLICATION
Is rare and may be complete or incomplete.
Complete duplication demonstrates two bladders lying
side by side, separated by a peritoneal fold. Each bladder
has normal musculature and mucosa and receives the
ipsilateral ureter. Each also has separate urethral orifices
that may drain into a common urethra and single penis,
or there may also be complete duplication of the urethra
and penis. Lower GI anomalies are commonly associated.
Complete duplication may result from bifurcation of the
cloacal septum resulting in two bladders and urogenital
sinuses.
Incomplete duplication is less common. A bladder
septum may divide the bladder into two equal or unequal
chambers. Each chamber has a ureteric orifice but the
septum may be eccentrically located leading to ureteric
obstruction, and aplastic or hypoplastic kidney. There is
a common urethral orifice and the external genitalia are
not duplicated. The bladder septum may be multiple,
dividing the bladder into several compartments.
Agenesis of the bladder is incompatible with life as
it leads to death from obstruction and renal failure.
However, a few cases have been reported in children
(all female) who lived long enough to be diagnosed.
URACHAL ABNORMALITIES
INTRODUCTION
These run the spectrum from a patent urachus and
umbilical ligament in which urine can flow from the
bladder to the abdominal exterior via the umbilicus, to
urachal cyst and umbilical cyst.
ANATOMY/EMBRYOLOGY
As the bladder descends into the pelvis, its dome narrows
to form the urachus. Normally, this umbilical attachment
of the bladder becomes obliterated to form the umbilical
ligament. Anomalous regression of normal closure of the
Congenital Anomalies of Urorenal Tract 69
umbilical ligament can lead to urachal abnormalities.
These may include, in addition to a patent urachus, a
urachal cyst resulting from failure of closure of the urachus
at the bladder attachment, or an umbilical cyst resulting
from failure of closure at the umbilical attachment.
The urachus develops embryologically from the allantois
in the 5th gestational month. There is ventral
communication from the umbilicus to the cloaca, from
which arises the urinary bladder. There is usually complete
regression of this communication by mid-fetal life; the
structure persists in post-natal life as the median umbilical
ligament. There are four recognized types of urachal
remant conditions which result from complete or partial
failure of urachal obliteration. All but one type are typically
asymptomatic, except when exacerbated by infection or
tumor.
INCIDENCE
Male:female ratio of patent urachus is 3:1.
CLINICAL FEATURES/COMPLICATIONS
Clinical presentation of urachal cysts is usually during
adulthood because they are clinical silent until
infection supervenes. Calculi may form within urachal
cysts and will be seen on plain films as small punctate
calcifications above the bladder outline. An increased
incidence of adenocarcinoma arising within an urachus
has been reported.
VARIETIES OF ABNORMALITIES
Patent Urachus
The urachus may rarely remain completely or partially
patent, allowing for a fistulous tract between the bladder
and the umbilicus (patent urachus).
Urachal Sinus
For a blind ending tubular structure extending from the
umbilicus inferiorly (umbilical-urachal sinus).
Urachal Cyst
A non-communicating fluid collection along the urachus
(urachal cyst).
70 Uroradiology: Text and Atlas
FIGURE 4.32: IVU: Urachal FIGURE 4.33: Cystogram: Delineation of endometrial
diverticulum cavity posterior to bladder–uterovesical fistula
Urachal Diverticulum
For an outpouching along the superior aspect of the
bladder (vesicourachal diverticulum).
The most common (50%) urachal remant abnormality
is patent urachus. This is a pure congenital abnormality
that results in persistent vesico-urachal fistula. The next
most common type is the urachal cyst (30%). This results
in a preperitoneal cyst just posterior to the midline rectus
muscles, with normal regression of the umbilical and
vesical urachal tract. Next is the umbilical-urachal sinus
(15%), a persistence of the proximal urachus for few to
several centimeters distal from the umbilicus. Last is the
vesico-urachal diverticulum (5%), representing persistence
of the distal urachal-vesical communication (Figure 4.32).
Complications of these anomalies include
development of infection, stones, and carcinomas, most
commonly adenocarcinomas.
Urachal remnants tend to become infected, and have
a propensity to undergo malignant degeneration,
representing about 0.5% of all bladder carcinomas
(all histology). Although lined by transitional epithelium,
FIGURE 4.34: IVU: Prune Belly
syndrome
the vast majorities of malignancies are adenocarcinoma,
typically at the level of the bladder, and represent greater
than 40% of all bladder adenocarcinoma. Urachal
carcinoma is typically not differentiable from an infected
remnant, and differentiation from a primary bladder
dome neoplasm typically relies on demonstration of
tumor extending towards the umbilicus, out of the
perivesical region. There is an approximately 30%
recurrence rate after surgical resection, which is the
treatment of choice.
ROLE OF RADIOLOGY AND IMAGING
CT, ultrasound, and fluoroscopy are well-suited for
demonstrated diseases of urachal remnants.
Cystography will be sufficient to make the diagnosis,
especially relying on oblique views.
CONGENITAL UTEROVESICAL FISTULA
See Figure 4.33.
PRUNE BELLY SYNDROME
See Figure 4.34 and refer to Chapter 18 for discussion.
 Cystic Disease of Kidney 71

INTRODUCTION 2. Autosomal recessive

No single classification of cystic kidney disease is entirely • Autosomal recessive polycystic kidney disease
satisfactory but the following, based on genetic/nongenetic ARPKD)
disorders, is still the most widely acceptable. • Juvenile nephronophthisis.
Cystic disease of kidney can be broadly divided into: 3. Cysts associated with syndromes
1. Nongenetic cystic disease • Chromosomal disorders
2. Genetic cystic disease. • Autosomal recessive syndromes
• X-linked syndromes.
NONGENETIC CYSTIC DISEASES
PATHOPHYSIOLOGY
1. Cortical renal cysts
2. Cystic dysplasia or dysplasia. (Multicystic dysplastic Should divide the kidneys into unilateral or bilateral renal
kidney) disease; diffuse or localized cysts; size of the kidneys;
3. Multilocular cyst extrarenal manifestations, e.g. cysts in the liver or
4. Multilocular cystic Wilms’ tumor pancreas; evidence of portal hypertension, intracranial
5. Localized cystic disease of the kidney or cardiac abnormalities.
6. Parapelvic cyst The genetic disorders are often systemic and there
7. Calyceal cyst/diverticulum may be more than one abnormal chromosome causing
8. Medullary sponge kidney the disorder, e.g. autosomal dominant polycystic kidney
9. Acquired cystic kidney disease (in chronic renal failure). disease (ADPKD). Not all present in the newborn period.
The nongenetic conditions include both congenital and
GENETIC CYSTIC DISEASES acquired disorders.
1. Autosomal dominant The first imaging procedure should be a full US
• Autosomal dominant polycystic kidney disease examination, which remains the comer stone of imaging.
(ADPKD) However, in this difficult area there is an on-going need
• Tuberous sclerosis to integrate other renal imaging modalities such as IVU
• Medullary cystic disease and/or 99mTc-DMSA when certain differential diagnoses
• Glomerulocystic disease. are being considered. Other system imaging is usually
72 Uroradiology: Text and Atlas
also required, either to look for associated abnormalities,
e.g. brain scan for intracranial tubers, or for complications
of the disease.
US will immediately identify if the abnormal kidney
anatomy, that diseases is unilateral or bilateral,
symmetrical or asymmetrical. The size of the kidneys and
the presence or absence of dilatation of the collecting
system can be easily ascertained. Heavy reliance is placed
on the ultrasound examination in reaching a specific
diagnosis and it also has a role in directing further
appropriate imaging.
NONGENETIC ‘CYSTIC KIDNEY’ DISEASE
The terminology used is often imprecise and inaccurate
and one should be sure that colleagues are discussing
the same condition with the different terms.
CORTICAL RENAL CYSTS
Simple renal cysts occur in 50% of the population older
than 50 years. They are considered to be acquired lesions
that probably arise from obstructed ducts or tubules. A
simple cortical cyst represents the most common renal
mass lesion.
Incidence
Uncommon in children or young adults, but is seen by
IVP in upto 20% of men with prostatic enlargement. A
cyst in a child must be carefully differentiated from a cystic
Wilms’ tumor.
Pathology
The cyst wall is composed of fibrous tissue and is lined
by flattened cuboidal epithelium. The cyst contains serous
fluid and does not communicate with the collecting
system.
Clinical Features
Most cysts are asymptomatic and are detected as
incidental findings. Local pain may occur due to cyst wall
distention or spontaneous intracystic bleeding.
Occasionally, hematuria may occur and rarely, a large
cyst may obstruct the collecting system or cause
hypertension.
Role of Radiology and Imaging
Plain abdominal radiograph: Occasionally, one may
see a cortical bulge projecting into the perinephric fat.
Calcification in a cyst wall is seen in only 1% of cases.
Urography: A lucent mass may be seen within the renal
parenchyma. A cyst will be well defined with a sharp
interface with the surrounding normal renal cortex. It will
not enhance, nor will it distort the adjacent parenchyma.
However, a “beak” or “claw” sign may be seen if the
cyst extends beyond the surface of the kidney, and
represents the adjacent stretched parenchyma. If the cyst
is completely intrarenal, the thickness of its wall cannot
be assessed. Radiographs taken 1–2 minutes after IV
contrast injection optimally visualize a cyst.
USG: A simple cyst is a rounded homogenous mass
demonstrating a sharp interface with the surrounding
parenchyma. It is echolucent and shows enhanced
through transmission.
Ultrasound represents the most cost efficient modality
to confirm the presence of a simple cyst. When all the criteria
for a benign simple cyst are present by any modality, further
evaluation is not indicated (however, cysts are usually not
visualized well enough by IVP to make this determination).
Since CT is the gold standard for evaluation of renal masses,
it should be used to evaluate cysts when US has been
indeterminate or technically unsatisfactory due to overlying
bowel gas or the presence of obesity. Also, CT should be
the modality of choice if a urogram indicates that a mass
is complex or likely to be solid.
CT: The density of cyst fluid can be measured by this
modality; it should be near than of water. A value greater
than 15 Hounsfield units (HU) should raise suspicions
for a complicated cyst or even a solid mass. A cyst should
not enhance following contrast injection, although small
increases of 2–5 HU may normally be seen with contrast.
When evaluating wall thickness on CT, it is best to examine
a portion of the cyst that extends beyond the renal contour
and does not lie adjacent to the “beak”.
MRI: A cyst will be low signal intensity on T1, and very
high signal intensity on T2 weighted images. As on CT,
it will appear as a homogenous rounded mass with a

thin wall and sharp interface with the surrounding normal
renal parenchyma.
Angiography: It is not routinely used to evaluate a cyst.
On an angiogram, a cyst will be seen as an avascular
mass displacing adjacent blood vessels.
Complications
Spontaneous cyst rupture into the collecting system or
perinephric space may occur. This occurs due to buildup
of pressure within the cyst as a result of either intracystic
hemorrhage or a change in composition of the cyst fluid
(Figure 5.1).
Following rupture, the cyst may regress or disappear
completely. The patient may experience hematuria and
flank pain. Rupture is detected by IVP or retrograde
pyelography if it leads to communication with the
collecting system, in which case the cyst cavity may be
opacified. Management of a ruptured cyst is conservative.
In most instances, the communication with the collecting
system closes spontaneously.
Bosniak Classification of Cortical Renal Cysts
Many renal cystic lesions do not fulfill the criteria for simple
cysts listed previously. Such lesions vary from minimally
complicated simple cysts that usually do not require
surgery to cystic renal neoplasms that generally need
resection. Complicated cysts often result from bleeding
FIGURE 5.1: CECT: Small exophytic renal cortical cyst with
intracystic hemorrhage
Cystic Disease of Kidney 73
in a simple cyst. Bosniak has suggested the ~categoriza-
tion of cystic renal masses according to CT criteria in
an attempt to separate lesion~ that require surgery from
those that do not. The application of Bosniak’s classifi-
cation is most useful in evaluating and managing cystic
renal lesions.
Category I Lesions.
In Bosniak’s classification, category I lesions are classic
simple cysts.
Obviously they require no further evaluation or
management (Figure 5.2).
Category II Lesions.
Category II lesions are minimally complicated cysts that
also usually, do not require surgery.
Minimally calcified benign cyst; category II lesion. A
contrast-enhanced CT scan reveals fine linear calcification
in the cyst wall and septa. The lesion shows a thin wall,
and no focal nodules or areas of enhancement. It should
be monitored with serial imaging, provided that the follow-
ing CT criteria are fulfilled:
1. The lesion must be perfectly smooth, round, sharply
marginated, and homogeneous;
2. The lesion should not enhance with intravenous
contrast medium;
3. At least one fourth of the lesion’s circumference should
extend outside the kidney so that the smoothness of
some of the wall can be evaluated; and
FIGURE 5.2: CECT: Category I simple exophytic renal cortical cyst
74 Uroradiology: Text and Atlas
4. The lesion should be less than 3 cm in diameter.
Although most lesions meeting these criteria are
benign hemorrhagic cysts, cystic renal cell carcinoma
may rarely show similar characteristics on CT (Figures
5.3 and 5.4).
MRI may also help in characterizing high-density renal
cysts that do not fulfill all the preceding CT criteria or
FIGURE 5.3: CECT: Category II renal cortical cysts
FIGURE 5.4: CECT: Category
that show internal echoes on ultrasonography. Hemor-
rhagic cysts appear on MRI as sharply marginated,
smooth, round, homogeneous lesions. They have high
signal intensity on both Tl and T2 weighted sequences,
and they do not enhance after intravenous administration
of gadolinium DTPA. In addition, hemorrhagic cysts often
show fluid-iron levels on MRI, probably because of
dependent settling of methemoglobin containing
sediment.
Category III Lesions
Lesions in category III are more complicated cystic lesions.
They exhibit some findings seen in malignant lesions,
including thick, irregular mural or septal calcification,
numerous or thick (> 1 mm), irregular septa, and uniform
or slightly nodular wall thickening. Most of the category
III lesions are benign (e.g. Multilocular Cystic Nephromas
and hemorrhagic renal cysts); others are cystic renal cell
carcinomas. All such lesions should undergo surgical
exploration, unless the procedure is contraindicated
because of the patient’s advanced age or poor general
medical condition (Figure 5.5).
Category IV Lesions.
Category IV lesions are clearly malignant lesions with large
cystic components; they should be resected. They may
show marginal irregularity or solid vascular elements
(See Figure 5.2).
Summary
FIGURE 5.5: CECT: Multiseptate complex left renal cyst with
enhancing indistinct, irregular wall–category III Bosniak lesions

Briefly, the Bosniak classification of renal masses is as
follows: class I includes simple cysts; class II, minimally
complicated but overwhelmingly benign masses with thin
septa, hyperattenuation, or small amounts of mural or
septal calcification; class III, moderately complicated
masses with mural nodularity, thick septa, or irregular
or thick calcifications that often require surgical
exploration; and class IV, significantly complicated and
generally malignant masses with thick and irregular
enhancing regions and definite solid components.
DYSPLASIA/CYSTIC DYSPLASIA/ MULTICYSTIC
DYSPLASTIC KIDNEY (MCDK)
There is confusion over this condition because the terms
used by many nephrologists, radiologists, pathologists and
urologists have different meanings. From a purist’s
viewpoint, dysplasia is a histological diagnosis based on
abnormal metanephric differentiation, with persistence
of fetal kidney tissue in the form of nests of metaplastic
cartilage associated with primitive ducts. However, the
pediatric nephrologist or radiologist may use the term
as a generic description for a small, highly reflective,
poorly functioning kidney without establishing histology
by an invasive renal biopsy. From a management
perspective, all these kidneys function to some degree
even though function may be very poor in childhood.
Pathologically, renal cystic disease and renal dysplasia
are two distinct entities. This is true even though dysplastic
kidneys often are cystic and many types of cystic kidneys
demonstrate some dysplasia.
MEDULLARY SPONGE KIDNEY
Medullary sponge kidney is a term used to describe
changes found on intravenous urography which show
brush-like linear striations in the renal papillae, frequently
in association with renal calculi. It may be focal or involve
the whole of the kidney and usually is associated with
some enlargement of the kidney. It is not usually a disease
of childhood although isolated cases are sometimes seen
with hematuria, nephrolithiasis and infections.
On IVU the blush in the medulla related to the calyces
has a very similar appearance to that seen in the ARPKD
and at times may be indistinguishable if the entire kidney
is involved. The term renal tubular ectasia is more widely
Cystic Disease of Kidney 75
accepted as the correct term to describe these renal
changes in children. The ultrasound appearances of renal
tubular ectasia without calculi are simply an increased
echogenicity of the medullae in normal kidneys of normal
size. Periportal fibrosis is generally associated with ARPKD
but some rare cases have been described in association
with ADPKD.
CALYCEAL DIVERTICULUM
Introduction
Calyceal diverticulum, also known as pylogenic cysts,
is typically a symptomatic and incidentally found on IVUs.
They are found in both males and females of all ages.
Calyceal diverticulums are composed of uroepithelium
lined pouches that extend from the collecting system into
the renal parenchyma.
Calyceal diverticula, the result of anomalous budding
of the calyceal system, is also associated with stone
disease. In 10–40% of calyceal diverticula, stones are
present. These range from a few large calculi to many
tiny seed calculi and to the microscopic “milk of calcium”.
Types
They can be of three types:
1. Type I originates from the minor calyx
2. Type II originates from the calyceal infindibulum and
3. Type III from the renal pelvis.
These diverticuli may lead to urinary stasis, which
may predispose the patient to stone formation or urinary
tract infections. During an intravenous urogram, the
calyceal diverticulum will appear opaque later in the
pyelographic phase. It typically remains radioopaque after
the remainder of the kidney has drained due to the slow
exchange of urine caused by a narrow communicating
neck. The diverticulum should have a round, smooth-
walled appearance. It should not be confused with a
hydrocalyx that develops from an infundibular stricture
and has a squared off appearance.
A calyceal diverticulum is a lesion that results from
an outpouching of a portion of the collecting system that
protrudes into the corticomedullary region. They can arise
in any part of the collecting system from a fornix to the
renal pelvis. Size varies anywhere from a few millimeters
76 Uroradiology: Text and Atlas
to several centimeters in diameter. They are uroepithelial-
lined cavities that communicate via a narrow channel
to a nearby calyx. They may be congenital, or acquired
lesions.
It is not uncommon to see calcified stones charac-
teristically layering in the dependent portion of the
diverticulum. The stones that form within the diverticulum
may pass and cause symptomatic renal colic but they
are typically confined to the diverticulum due to its narrow
neck connection to the distal collecting system.
They are regions of urinary stasis and the dependent
sediment that eventually develops in a calyceal diver-
ticulum is referred to as “milk of calcium”. Larger stones
may form that are confined to the diverticulum and may
be a source of chronic pain.
On CT, the diagnosis is made with delayed imaging
showing the diverticulum fill with contrast. Alternatively
if stones are present, the patient can be rescanned in the
opposite position. If the stones settle dependently, and
are confined to the lesion, the diagnosis can be made
in the absence of delayed imaging.
Treatment
Management of symptomatic stone disease associated
with Calyceal diverticula has changed from an open
surgical approach to include ESWL, percutaneous,
laparoscopic or ureteroscopic techniques. The choice of
therapy depends largely on the anatomic location of the
diverticulum.
ACQUIRED CYSTIC RENAL DISEASE
This term usually refers to the cysts which develop in
the native kidneys of patients in chronic renal failure.
There is no underlying cystic renal disorder and no other
organ involvement. Acquired cysts can be found in up
to 22% of patients in chronic renal failure but their
frequency increases with duration of dialysis up to 90%
for those on dialysis for over 10 years. The incidence
is similar for those on hemo- and chronic peritoneal
dialysis. After successful transplantation, the cysts tend
to regress in size. The importance of maintaining
surveillance of these kidneys is because of a potential
for malignant change, namely renal cell carcinoma. The
cysts may also be complicated by hemorrhage or
infection. Diagnosis is easily reached with ultrasound.
GENETIC CYSTIC DISEASE
AUTOSOMAL DOMINANT POLYCYSTIC KIDNEY DISEASE
Autosomal dominant polycystic kidney disease (ADPKD)
is a renal cystic disorder which becomes manifest
frequently after the third decade of life. However, there
is considerable phenotypic variation.
Incidence is 1:1000 with two and possibly three
genetic loci. Families have the gene located on the short
arm of chromosome 16 (PKDI). The second gene is on
chromosome 4 (PKD2). The location of PKD3 has not
yet been found. Although this is inherited as a dominant
condition, nevertheless no family history is often encoun-
tered as spontaneous mutation seemingly accounts for
many cases.
ADPKD is a systemic disease with both renal and
extrarenal manifestations. In PKDl families, 64% of
children affected under the age of 10 years will have cysts
and 90% between the ages of 10 and 19 years will have
cysts 31. Extrarenal manifestations, such as cysts in the
liver, pancreas or spleen, are rarely seen in pediatric
patients. Subarachnoid hemorrhage due to intracranial
aneurysm is also rare in childhood. The occurrence of
subarachnoid hemorrhage tends to cluster in families and
routine screening in otherwise asymptomatic individuals
is not recommended. Congenital hepatic fibrosis is
generally associated with ARPKD but some rare cases
have been described in association with ADPKD.
The cystic abnormality differs from ADPKD in regard
to its localization into one part of the kidney and apparent
absence of cysts in the contralateral kidney. No family
history or pattern of inheritance has been reported. Some
of the earlier reported patients with unilateral ADPKD
almost certainly had this condition. It is suggested that
the family should be routinely screened for cystic kidneys
and the patient’s remaining kidney should be followed
up for life. The lesions do not appear to be progressive
in the few cases that have been reported and left in situ.
Hypertension has been documented and nephrectomy
is curative but the natural history is unclear.

ARPKD
It is the most common heritable cystic renal disease
occurring in infancy and childhood. It is distinct from
autosomal dominant polycystic kidney disease (ADPKD),
which tends to occur in an older population. The clinical
spectrum shows a wide variability, ranging from perinatal
death to a milder progressive form, which may not be
diagnosed until adolescence.
Blyth and Ockenden initially classified ARPKD into
four groups:
1. Perinatal,
2. Neonatal,
3. Infantile, and
4. Juvenile.
Cystic Disease of Kidney 77
IVU: It helps to differentiate ARPKD from ADPKD,
Glomerulocystic disease and renal dysplasia by demon-
strating bilateral and symmetrical enlargement of the
kidneys and ‘streaky/chaotic’ nephrogram as the
contrast clears in the ectatic collecting ducts.
Ultrasonography: It is the primary modality for the
evaluation of ARPKD, especially during the perinatal and
neonatal periods, which characteristically shows bilateral
renomegaly with uniformly increased reflectivity.
CT and MRI: In older children, CT and MRI are often
used to evaluate liver disease.
For rest of the genetic cystic diseases of kidney, please
refer Chapter 4.
78 Uroradiology: Text and Atlas
UROLITHIASIS
INTRODUCTION
2.
Passage of a urinary stone is the most common cause
3.
of acute ureteral obstruction and affects as many as 12%
4.
of the population. The pain may be some of the most
5.
severe pain that humans experience, and complications
6.
of stone disease may result in severe infection; renal
failure; or, in rare cases, death.
PATHOPHYSIOLOGY
In patients with stone disease, more than 1 of 3 general
mechanisms is likely to be active. These include the
following:
1. the possible presence or abundance of substances that
promote crystal and stone formation; TYPES OF RENAL CALCULI
2. a possible relative lack of substances to inhibit crystal 1. Calcium stones account for 75–85% of urinary
formation; and
3. a possible excessive excretion or concentration of
salts in the urine, which leads to supersaturation of
the crystallizing salt. The greater the degree of super-
saturation, the greater the rate of growth of the calculi.
PREDISPOSING FACTORS
1. Stasis or anatomic factors can also contribute to the
development of stone disease. These include
ureteropelvic junction (UPJ) obstruction, horseshoe
or ectopic kidney, autosomal dominant polycystic
kidney disease, and vesicoureteral reflux.
Medullary sponge kidney
Renal tubular acidosis (RTA)
Immobilization
Hyperoxaluria
Other secondary causes:
• Milk-alkali syndrome
• Steroids
• Cushing syndrome
• Hypervitaminosis D
• Paraneoplastic Syndromes
• Multiple myeloma.
stones. Approximately one half of calcium stones are
composed of a mixture of calcium oxalate and calcium
phosphate. They demonstrate intermediate fragility
to extracorporeal shock wave lithotripsy (ESWL).
Approximately three eighths of calcium stones are
formed of only calcium oxalate dihydrate. These may
be spiculated, dotted, mulberry, or jackstone in
appearance. Usually, these stones are fragile in
response to ESWL. The remaining one eighth of
stones are composed of calcium phosphate (apatite)

or calcium monohydrate. These stones are the densest
and, consequently, the least responsive to ESWL.
Calcium stones have numerous causes. Approxi-
mately 85% of calcium stones are idiopathic, or
primary. Idiopathic hypercalciuria occurs in more than
one half of patients with calcium oxalate stones. Most
causes of hypercalciuria are absorptive. Increased
absorption in individuals after a normal diet causes
an elevation of serum calcium levels and a suppression
of parathyroid function as an abnormal response to
vitamin D. Approximately 10% of cases of primary
hypercalciuria are renal in origin. The inability of the
kidney to conserve calcium results in low serum
calcium concentrations, which stimulate parathor-
mone secretion.
The remaining 15% of calcium stones are secon-
dary to some discernible etiology. Most commonly,
they result from hyperparathyroidism, which is found
in 5-10% of patients with stones. In this situation,
hypercalcemia and increased absorption lead to
hypercalciuria. Patients with the stones are treated with
surgical removal of the parathyroid adenoma or
hyperplasia. Calcium stones can also occur in
approximately 15% of patients with sarcoidosis in
whom the production of activated vitamin D by
macrophages is abnormal.
2. Magnesium ammonium phosphate (struvite)
stones account for approximately 10–20% of urinary
stones. These stones are lucent but complex with
calcium phosphate. On occasion, they enlarge and
branch (staghorn*). Although they fragment easily,
patients with these stones usually are treated with
percutaneous fragmentation and extraction because
of the large size of the stones and, usually, the presence
of infection. Struvite stones are caused by urea-splitting
bacteria such as Proteus, Klebsiella, and Pseudomonas
species. However, as many as one half of patients
have an underlying metabolic cause for stone disease;
*“Staghorn calculi” resembles antlers of a stag. Composition: Struvite
>> cystine or uric acid. Usually associated with recurrent urinary tract
infections from bacterial pathogens that produce alkaline urine (thus,
F>M cases). Staghorn can be disrupted if infection complicates
obstruction related to the stone. Renal enlargement from pyonephrosis
or xanthogranulomatous pyelonephritis may produce a fragmented
staghorn.
Calculus Diseases of Kidney 79
therefore, metabolic evaluation is indicated.
Combined obstruction and infection frequently cause
renal destruction and, potentially, renal failure if both
kidneys are affected.
3. Uric acid stones account for 5–10% of urinary
stones. These small smooth stones usually appear
radiolucent on conventional radiographs but opaque
on CT scans. Predisposing factors include acidic
concentrated urine, excess urinary uric acid, small-
bowel disease or resection, gout, and cell lysis (e.g.,
resulting from treatment of leukemia or from
starvation). Treatment and prevention for these stones
is alkalinization and dilution of the urine.
4. Cystine stones account for only approximately 1%
of urinary stones. These ground-glass stones, which
result from cystinuria (a rare autosomal recessive
metabolic disorder), are homogeneous; less opaque;
and less fragile than other stones, especially if they
are smooth.
5. Xanthine stones are relatively radiolucent stones.
6. Several other less common forms of urolithiasis
may produce stones that appear relatively lucent, even
on CT scans. Inspissation of indinavir, an anti-
retroviral protease inhibitor used to treat HIV infection,
may cause stones that appear lucent on CT scans.
7. Matrix stones formed from inspissated mucoproteins
in patients with a chronic Proteus infection may demo-
nstrate soft tissue attenuation on CT scans. Stones
can also be caused by metabolic byproducts and drugs
(e.g. sulfa drugs, salicylates, triamterene ephedrine).
8. Orotic acid stones are rare to occur.
INCIDENCE
Renal calculi occur in 5–12% of the population, and they
are bilateral in 10–15% of patients. The prevalence of
urinary lithiasis is as high as 2–3% in the general
population. A slightly lower prevalence of urinary stones
is found in less developed countries, possibly because
of diets lower in protein.
CLINICAL FEATURES
• Acute ureteral obstruction by stone causes severe
colicky (intermittent) flank pain that can radiate
throughout the groin, testicles, back, and periumbilical
region.
80 Uroradiology: Text and Atlas

• Some patients with renal calculi may have no

symptoms at all
• Hematuria
• Occasionally, recurrent infection may result in
pyelonephritis or abscess. Stones can result in renal
scarring, damage, and renal failure.
• They are also more prevalent in highly developed
countries, possibly as a result of a higher protein diet.
• Sex: Males are at a greater risk than females, with
a male-to-female ratio of 3:1 (except for struvite stones
and in black populations).
• Age: Stones the peak age for development is in
persons aged 40–60 years.

DIFFERENTIAL DIAGNOSIS

1. Appendicitis (Figure 6.1)

2. Cholecystitis, acute
3. Cholelithiasis
FIGURE 6.1: KUB film: Appendicolith
4. Colon, diverticulitis
5. Crohn disease
29. Wilms tumor
6. Duodenum, ulcers
30. Xanthogranulomatous pyelonephritis.
7. Epididymitis
8. Gastric ulcer ROLE OF RADIOLOGY AND IMAGING
9. Gout The goals of imaging are to determine the presence of
10. Meckel diverticulum stones within the urinary tract, evaluate for complications,
11. Midgut volvulus estimate the likelihood of stone passage, confirm stone
12. Nephrocalcinosis passage, assess the stone burden, and evaluate disease
13. Obstructive uropathy, acute activity.
14. Ovarian torsion When acute flank pain suggests the passage of a
15. Ovarian vein thrombosis urinary stone, many methods of examination can be used.
16. Pancreatitis, acute Often, conventional radiography is initially used to screen
17. Pancreatitis, chronic for stones, bowel abnormalities, or free intra-abdominal
18. Papillary necrosis air. Radiographs can also be used to monitor the passage
19. Pelvic inflammatory disease/Tubo-ovarian abscess of visible stones.
20. Renal cell carcinoma IVU (excretory urography) provides important physio-
21. Renal vein thrombosis logic information regarding the degree of obstruction.
22. Retroperitoneal fibrosis Ultrasonography (USG) is useful in young or pregnant
23. Testicular torsion patients and in patients allergic to iodinated contrast
24. Transitional cell carcinoma material. USG is also helpful in problem solving.
25. Tuberculosis, Genitourinary tract All of these methods have become less useful with
26. Ureterocele the advent of more sensitive and specific nonenhanced
27. Ureteropelvic junction obstruction, congenital CT scanning. When CT is available, it is now considered
28. Vesicoureteral reflux the examination of choice for the detection and
 Calculus Diseases of Kidney 81

localization of urinary stones. Almost all studies conducted in patients undergoing screening or follow-up observation
to date show that IVU provides no additional clinically for stones.
important information after nonenhanced CT is Typically, phleboliths are round or oval, and they may
performed. As a result of the higher radiation dose of demonstrate a central lucency. However, they are often
CT, conventional or digital radiography should be used difficult to distinguish from ureteral calculi. Phleboliths
to monitor the passage of stones if radiographic follow- in the pelvis are usually located lower than and lateral
up studies are indicated and if the stone is visible on to the ureter, but they overlap with the ureter. Because
conventional radiographs. gonadal veins parallel the upper ureters, contrast
enhancement may be needed to opacify the ureter and
Conventional Radiography demonstrate the extraurinary location of phleboliths in
Conventional radiography is often performed as a the gonadal veins.
preliminary examination in patients with abdominal pain Although 90% of urinary calculi are opaque on
possibly resulting from urinary calculi. These images abdominal radiographs, the sensitivity for the prospective
should be obtained before contrast material is adminis- identification of individual stones is only 50–60%, and
tered to prevent obscuring calcifications within the the specificity is only approximately 70%. Approximately
collecting system or calyceal diverticula. Conventional 10% of stones are radiolucent on conventional
radiographs should include the entire urinary tract, and, radiographs.
often, 2 images are required.
Limitations
Stones are often found at key points of narrowing
Because of the higher radiation dose with CT,
such as the UPJ, the ureterovesical junction (UVJ), and
conventional or digital radiography should be used to
the point at which the ureter crossing the iliac vessels.
monitor the passage of stones if radiographic follow-up
An addition site is on the right side where the ureter passes
is believed to be indicated and if the stone is visible on
through the root of the mesentery.
conventional radiographs. Pregnant or pediatric patients
Calcium stones as small as 1–2 mm can be seen.
Cystine stones as small as 3–4 mm may be depicted,
but uric acid stones are usually not seen unless they have
become calcified.
An erect or posterior oblique radiograph obtained on
the side of the calcification may help in distinguishing
urinary stones from extraurinary calcifications. This view
can also depict calcifications that are projected over the
sacrum or transverse processes on the frontal view.
(Figure 6.2).
Preinjection renal tomography may depict additional
stones, and it can be used to confirm the relationship
of stones to the kidneys.
Because stones are more visible with a lower peak
kilovoltage (kVp), maintaining a maximum of 60–80 kVp
is best, if possible. Larger patients may require a higher
peak kilovoltage for acceptable exposure and scatter. In
this situation, compression of the abdomen and
collimation is critical.
Mild bowel preparation may be helpful for increasing FIGURE 6.2: KUB film: Multiple small ‘gravel’ calculi in right
the sensitivity of conventional radiography for small stones kidney, right lower ureter and in the right ureterocele
82 Uroradiology: Text and Atlas

may be imaged with US first to avoid radiation exposure.

The rare false-negative finding is usually due to reader
error or a protease-inhibitor CT-lucent stone. False-
positive results are usually due to phleboliths adjacent
to the ureter. In some cases, intravenous contrast material
may be needed to opacify the ureter.

Intravenous Urography
IVU is useful for confirming the exact location of a stone
within the urinary tract. IVU depicts anatomic abnorma-
lities such as dilated calyces, calyceal diverticula,
duplication, UPJ obstruction, retrocaval ureter, and others
that may predispose patients to stone formation or alter
therapy. Because contrast agents can obscure stones in
the collecting system, scouting the entire urinary tract prior
to their administration is critical.
When an acute urinary stone is the primary conside-
ration, compression may not be used to increase sensi-
tivity for detection of low-grade obstruction. A caveat is
that the contralateral kidney may have an abnormality
that requires ureteric compression for adequate exami-
nation. In rare cases, the use of compression has been
associated with forniceal rupture.
When a stone causes acute obstruction, an obstructive
nephrogram may be present. This may be prolonged and
hyperopaque, with increasing opacity over time. The
nephrogram of acute obstruction is usually homogeneous,
but may also be striated or occasionally not visible on
radiographs.
Other signs include delayed excretion, dilatation to
the point of obstruction, or blunting of the calyceal
fornices. Immediately after the passage of a stone, residual
mild obstruction or edema can be detected at the UVJ.
Delayed images may be needed to opacify to the point
of the obstruction, but using gravity to position the more
opaque and more distal contrast material–laden-urine is
also possible by placing the patient in a prone or erect
position.
Extravasation of urine at the fornices may result in
pyelosinus or pyelolymphatic extravasation, which is often
first indicated by blurring of the calyceal fornices. Greater
extravasation may outline the collecting system, and the
contrast may dissect into the perinephric space; however,
if the urine is not infected, this is usually clinically insignificant.
FIGURE 6.3: IVU: Large right lower ureteric calculus with nonfunctioning
right kidney with focal caliectasis at upper pole of left kidney
Limitations
IVU is the traditional examination for the assessment of
urinary stone disease, and it does provide physiologic
information related to the degree of obstruction. The
radiation dose is generally smaller than that of CT, but
it is of the same order of magnitude. Intravenous contrast
is required, with resultant risks of an allergic reaction or
nephrotoxicity. IVU is less sensitive than CT, especially
for small or nonobstructing stones (Figures 6.3 to 6.5).
Ultrasonography
On sonograms, stones are demonstrated as bright
echogenic foci with posterior acoustic shadowing. Stones
are visualized fairly well with USG in the kidneys and
the distal ureter at or near the UVJ, especially if dilatation
is present. USG is good for the visualization of
complications such as hydronephrosis (or other signs of
obstruction); however, some patients with acute
obstruction have little or no dilation.
In particular, USG is helpful in evaluating those with
renal insufficiency or contraindications for the use of
contrast media; however, USG is often skipped in favor
of nonenhanced CT.
 Calculus Diseases of Kidney 83

or after forniceal rupture. Absence of the ureteral jet, as

visualized with color Doppler on the symptomatic side,
is presumptive evidence for a high-grade obstruction in
a well-hydrated patient.
USG is very insensitive for stones, especially stones
smaller than 2 mm, stones at the UPJ, or stones in the
mid ureter. Fowler et al suggest that USG has a sensitivity
as low as 24%, compared with nonenhanced CT.
Furthermore, estimations of stone size may not be
accurate. Compared with nonenhanced CT, USG is more
dependent on the operator’s ability and more time
consuming.
Limitations: USG has limited sensitivity for smaller stones,
and does not depict the ureters well. It should be used
mainly in patients who are young, those who are
pregnant, or those undergoing multiple examinations (eg,
patients with spine injury).
FIGURE 6.4: Lateral view (overlapping of PCS on spine)

CT
With a sensitivity of 94–97% and a specificity of 96–
100%, helical CT is the most sensitive radiologic
examination for the detection, localization, and
characterization of urinary calcifications; therefore, helical
CT is considerably more effective than IVU.
Helical CT scans frequently depict non-obstructing
stones that are missed on IVU (Figure 6.6).
CT is faster and no contrast agent is needed in most
patients.

FIGURE 6.5: IVU: Filling defect of calculus seen in

left lower ureter with mild left hydronephrosis

In addition, USG is good for characterizing lucent

filling defects that are visualized as stones on IVU.
However, USG does not provide direct physiologic
information regarding the degree of obstruction.
Doppler imaging may demonstrate a high resistive index FIGURE 6.6: Non-contrast spiral CT scan section
in acute obstruction, but this may not occur immediately showing small nonobstruction bilateral renal calculi
84 Uroradiology: Text and Atlas

To discern between phleboliths and urinary stones,

FIGURE 6.7: Non-contrast CT: Left staghorn calculus
CT easily differentiates between non-opaque stones
and blood clots or tumors (compared with IVU, which
may depict only a filling defect) (Figure 6.7).
In addition, helical CT is better than USG or IVU in
detecting other causes of abdominal pain. In fact, in most
studies, IVU added little or no information.
Rarely, pure matrix stones may demonstrate soft-
tissue opacity on CT scans, and indinavir stones appear
lucent. However, all other stones appear opaque on CT
scans.
50 ml of low-osmolar contrast agent should be
administered. After 3–5 minutes, a 5 mm helical scan
is obtained through the area of concern. Fewer contrast-
enhanced studies are needed with increasing experience.
Soft tissue around the rim of a calculus can differentiate
it from a phlebolith. A phlebolith may have a comet tail
of soft tissue extending from it; this finding differentiates
it from a calculus. On CT scans, phleboliths do not have
radiolucent centers, as often seen on plain radiographs
(Figures 6.8 and 6.9).
When contrast-enhanced scans are required to
evaluate pain not related to stones, routine abdominal
and/or pelvic CT should be performed. In this situation,
100-150 ml of a low-osmolar oral and rectal contrast agent
is used, and a 5 mm helical CT scan is obtained with

CT Protocol for Calculus Disease

Because stones in the collecting system may be obscured
by contrast material, nonenhanced CT is usually
performed. Helical CT is important to avoid missing
stones because of section misregistration. A 5 mm helical FIGURE 6.8: Non-contrast CT: Calculus in right lower ureter

technique with a pitch of 1.5:1 or less is preferred,

although some radiologists choose to use a pitch of as
much as 2:1. The kidneys and, if possible, the entire
abdomen should be scanned during a single breath hold
to prevent section misregistration.
Because patients with stones are often young and
because stone disease may recur, minimizing the radiation
dose is critical. A fairly high level of noise as a result of
the inherently high contrast levels is tolerable in most
patients.
Reported radiation doses for CT are 2.8–4.5 mSv
compared with 1.3–1.5 mSv for a 3-image IVU. However,
the uterine dose is approximately 0.006 Gy for 4 image
FIGURE 6.9: Non-contrast CT: Tiny right UVJ
IVU compared with 0.0046 Gy for nonenhanced CT. calculus pouting in bladder

a pitch of 1.5:1. Patient selection determines the number
of examinations needed.
Stones at the UVJ may be difficult to distinguish from
stones that have already passed into the bladder. If the
distinction changes therapy, a repeat scan through the
UVJ in the prone position may be helpful. Stones that
have already passed into the bladder will drop into a
dependent location.
CT findings
1. Stones in the ureter
2. Enlarged kidneys
3. Hydronephrosis (83% sensitive, 94% specific)
4. Perinephric fat stranding ± fluid (82% sensitive, 93%
specific)
5. Ureteral dilatation (90% sensitive, 93% specific)
6. Soft-tissue rim sign (good positive predictive value
with a positive odds ratio of 31:1)
7. White pyramid sign absent.
The amount of perinephric fluid is correlated with the
degree of obstruction seen on IVU, and as with the
obstruction, the amount of fluid is correlated with the
likelihood of stone passage. Normal hyperattenuating
renal pyramids sometimes are seen. These indicate that
significant obstruction is not present. However, this finding
has been seen with proven ureteral calculi and is often
absent in patients without stones. For this reason, the
usefulness of IVU is limited. If contrast material is adminis-
tered, a delayed or hyperattenuating nephrogram may
also be visible on CT scans if the ureter has an obstruction.
Conventional radiography may be helpful in visua-
lizing larger stones, once they are identified on CT scans,
to provide a baseline to follow passage of the stone. If
kidney, ureter, and bladder radiographs fail to depict the
stone, CT may be needed to follow its passage.
Approximately 40–55% of stones are not visible on
abdominal radiographs. Almost no stones with attenua-
tion values of less than 200 HU are visible, and repeat
CT scans are usually required if passage of the stone is
to be followed. Cystine and urate stones have an
attenuation of 100-500 HU; calcium stones usually
demonstrate attenuation higher than 700 HU. Consi-
derable overlap exists in the CT attenuation values of
calcium stones.
Individual CT signs are associated with varying
degrees of confidence, as noted in CT findings above.
Calculus Diseases of Kidney 85
Limitations
Nonenhanced CT results are usually diagnostic, but if
contrast material is needed, actions can be taken to
decrease the risk of an adverse reaction in patients. The
patient can be premedicated with steroids and histamine
blockers. Use of low-osmolar contrast agent also helps.
Use of iodinated contrast agents should be avoided in
patients who have had previous life-threatening reactions.
Nonenhanced CT is usually sufficient with the aid of USG
and MRI as problem-solving tools. Nuclear scintigraphy
may also be helpful in confirming obstruction.
Usually, in patients with renal insufficiency,
nonenhanced CT is sufficient. Very poor renal function
results in a failure to opacify the collecting system. As
in pregnant patients, USG, MRI, and scintigraphy can
be useful as problem-solving tools
MRI
Stones are not directly visible on MRIs because they
produce no signal. However, they may be indirectly
visualized as a filling defect in the ureter or collecting
system on heavily T2-weighted images or on gadolinium-
enhanced T1-weighted images. MRI can be useful as a
problem-solving tool if the use of iodinated contrast
material or radiation is contraindicated (e.g. during
pregnancy).
RNI
Nuclear medicine studies may demonstrate the retention
of activity in the cortex or collecting system when the
obstruction is ongoing. Nuclear medicine tests are useful
in determining differential renal function for treatment
planning and for assessing how much renal function might
return after the obstruction is relieved. For example, a
kidney with very little function might be removed if very
little function persists after a trial of drainage. Occasionally,
confirming the obstruction with nuclear medicine studies
is useful if the administration of iodinated contrast material
is contraindicated.
INTERVENTION
Retrograde or antegrade pyeloureterography may be
indicated if the collecting system cannot be opacified
otherwise. This becomes much less useful as a diagnostic
86 Uroradiology: Text and Atlas
examination when CT is available. Retrograde stent
placement is indicated if obstruction is present with
proximal infection (pyonephrosis). Stent placement is
performed to prevent sepsis and irreversible renal
damage. If retrograde stent placement is unsuccessful,
nephrostomy or antegrade stent placement serves as a
reliable backup.
SPECIAL CONSIDERATIONS
In the diagnosis and treatment of kidney stones, special
concerns exist in patients who are pregnant, in those who
have contraindications to the use of contrast media, and
in those with renal insufficiency.
Pregnancy does not predispose patients to stone
formation; however, stone formation is a complication
in as many as 0.05% of pregnancies, and the diagnosis
may be difficult to establish with imaging because of the
displacement and obscuration of organs by the enlarged
uterus and fetus. Consider using USG first in a pregnant
patient, especially in the first trimester. IVU can be used,
but the views should be limited to scout and 10 to 30
minute images if possible. CT can also be useful, and
the radiation dose may be justified (especially if the clinical
picture is confusing), because any fetal damage is unlikely
at the typical radiation doses. Minimize the dose by
increasing the pitch and decreasing the milliamperage.
MRI may be a useful tool for problem solving.
MORTALITY/MORBIDITY
Passage of a renal stone is the most common cause
of acute ureteral obstruction. When this occurs, pressure
in the collecting system and renal blood flow acutely
increase, followed by decreased blood flow after 1–2
hours. Hematuria usually occurs. This can be intermittent
or persistent and microscopic or gross. However, as many
as 10% of patients with acute stones may not have
hematuria.
Acute ureteral obstruction by stone causes severe,
colicky (intermittent) flank pain that can radiate
throughout the groin, testicles, back, or periumbilical
region. Some patients with renal calculi may have no
symptoms at all. Stones smaller than 4 mm pass
spontaneously in approximately 80% of patients. Stones
that are 4–6 mm pass in approximately 50% of patients,
whereas stones larger than 8 mm pass in only
approximately 20% of patients.
Occasionally, recurrent infection may result in
pyelonephritis or abscess. Stones can cause renal scarring,
damage, or even renal failure if they are bilateral.
In 10% of patients, stones recur within 1 year. This
percentage increases to 50% within 10 years.
RADIOLUCENT UROLITHIASIS
The prevalence of urolithiasis is approximately 2 to 3
percent in the general population, and the estimated
lifetime risk of developing a kidney stone is about 12%.
The classic presentation of renal colic is excruciating
unilateral flank or lower abdominal pain of sudden onset
that is not related to any precipitating event and is not
relieved by postural changes or nonnarcotic medications.
With the exception of nausea and vomiting secondary
to stimulation of the celiac plexus, gastrointestinal
symptoms are usually absent. Approximately 75% of
urinary calculi are composed of calcium oxalate, calcium
phosphate, or a mixture of the two. Phosphate-containing
stones account for about 15% of urinary calculi, with
struvite (magnesium ammonium phosphate) being the
most common. Uric acid stones account for approximately
5 to 10% of urinary calculi.
The radiodensity of ureteral calculi also clearly affects
their visibility on plain radiographs. In general, calcium
phosphate stones have the greatest density, followed by
calcium oxalate and magnesium ammonium phosphate.
Cystine calculi are only mildly radiodense. Uric acid stones
and matrix stones are usually entirely radiolucent. It has
been estimated that most (85–90%) of all renal stones
are radiopaque.
There are several modalities used to make the
diagnosis of urolithiasis. With its increasing availability
and technical superiority, helical CT has been shown to
be more accurate than KUB radiography, IVU, and US
for the diagnosis of ureteral calculi. It has been proposed
that because of its safety, speed, cost-effectiveness,
accuracy, and ability to assess other potential causes of
flank pain, nonenhanced helical CT should replace IVU,
in most instances, as the most effective study used for
the diagnosis of ureteral calculus disease. Furthermore,
essentially all stones, including uric acid stones, appear
dense on CT.

The primary use of CT in suspected renal stone disease
is to differentiate stones from other causes of filling defects.
Uric acid, xanthine, and cystine stones that are radiolucent
on plain film are appropriately identified as high density
on CT, with densities of 100 to 600 Hounsfield units (H).
Uroepithelial tumors usually range from 8 to 30 H
unenhanced, whereas blood clots are typically 50 to
65 H with or without contrast. In other cases of
obstruction, CT demonstrates the dilated collecting
structures, delayed excretion of contrast agent, as well
as calculi, tumor, or extrinsic masses.
In addition to its sensitivity, a helical CT of the entire
urinary tract can be performed in 30 seconds, allowing
a diagnosis to made much faster than urography,
sonography, or radiography. CT for flank pain identifies
an alternative diagnosis up to 50% of the time, and
typically exposes the patient to less than half the radiation
of an intravenous urogram with nephrotomography.
A circumferential rim of ureteral tissue (tissue rim sign)
is seen around 90% of stones less than 4 mm in diameter,
helping distinguish stones from phleboliths. Secondary
signs such as unilateral hydronephrosis, unilateral
hydroureter, unilateral perinephric stranding, and
unilateral nephromegaly may also be seen. In fact,
hydroureter with ipsilateral stranding around the kidney
or ureter has a positive predictive value of 98% for the
presence of ureteral stone, and the absence of these two
findings has a negative predictive value of 93%.
Stones >4 mm in the upper ureter are less likely to
pass spontaneously, and are often associated with
intractable nausea, vomiting, and fever.
In the case of giant hydronephrosis, defined as the
presence of more that one liter in the collecting system,
nephrectomy is often performed due to severe renal
failure. Giant hydronephrosis is seen more on the left
than the right, and more commonly in males than females.
Typical etiologies include PUJ obstruction, congenital
abnormalities, or stones. The first diagnosis is often
erroneous, with entities such as ovarian cysts or hepatic
cysts considered initially.
NEPHROCALCINOSIS
INTRODUCTION
This was a termed coined by Albright in 1934 to describe
the deposition of calcium salts in the renal parenchyma
Calculus Diseases of Kidney 87
in hyperparathyroidism. The term has now acquired more
of a radiologic concept and is used to describe diffuse,
fine, renal parenchymal calcification that is radiologically
demonstrable. This appearance is different from that of
calcification within the lumen of the collecting system,
ureter, and bladder, which represents nephrolithiasis.
Many causes of nephrocalcinosis have been added
since the original description. These include the several
causes of hypercalcemia and hypercalciuria. Nephrocal-
cinosis can be subdivided into the cortical type, which
is classically the result of acute tubular necrosis (ATN),
and the medullary type, which may be an extension of
cortical nephrocalcinosis or seen in isolation with several
metabolic disorders. In nephrology, the term nephrocal-
cinosis is applied only to the medullary type. Nephrocal-
cinosis can be demonstrated on plain radiographs,
sonograms, or CT scans. CT is the most accurate and
sensitive technique and therefore the modality of choice.
It can be unilateral or bilateral.
PATHOPHYSIOLOGY
Disorders of Calcium Metabolism
Disorders of calcium metabolism, such as hypercalcemia
and hypercalciuria, may induce the formation of calcium
renal stones and deposition of calcium salts in the renal
parenchyma (nephrocalcinosis). The extensive deposition
of calcium may lead to chronic tubulointerstitial disease
and renal insufficiency. The first signs of damage induced
by hypercalcemia are seen at the intracellular level, in
the tubular epithelial cells. This results in mitochondrial
distortion, and eventually, calcium deposits can be
demonstrated within the mitochondria, the cytoplasm,
and the basement membrane.
Calcified cellular debris results in occlusion of the
tubules, leading to obstructive atrophy of the nephron,
nonspecific inflammation, and interstitial fibrosis.
Impaired urine drainage through calcified tubules may
result in areas of cortical atrophy leading to scared
cortices. Functional abnormality of urine concentration
is the earliest detectable renal change. This effect is related
to decreased chloride transport in the ascending thick
segment of the nephron.
Other defects of tubular function, such as tubular
acidosis and salt-losing nephritis, may also occur.
88 Uroradiology: Text and Atlas
The continuing and unchecked deposition of calcium
eventually leads to chronic renal insufficiency. Nephrocal-
cinosis may be complicated by renal stone formation,
which adds another element to the causation of renal
insufficiency secondary to an obstructive uropathy. The
histologic findings include calcium phosphate or calcium
oxalate crystal deposits that mainly appear in the renal
interstitium, but deposits may also be seen within the
renal tubules. Special stains, such as von Kossa and
Pizzolato stains, can be used to specifically depict these
deposits.
CAUSES OF CORTICAL NEPHROCALCINOSIS
1. Acute cortical necrosis: This can follow placenta
abruptio, placenta previa, septic abortion, transfu-
sion reactions, burns, snake bite, severe dehydra-
tion, shock, severe heart failure, and abdominal
aortic surgery. In children, the condition may follow
dehydration, fever, sepsis, and hemolytic uremic
syndrome.
2. Chronic glomerulonephritis
3. Alport syndrome
4. Prolonged hypercalcemia and/or hypercalciuria
5. Poisoning and toxicity (e.g. Ethylene glycol
(antifreeze) poisoning)
6. A severe form of primary hyperoxaluria
7. Methoxyflurane anesthesia toxicity
8. Rejected renal transplants can give rise to cortical
necrosis.
9. Sickle cell disease is a rare cause of cortical nephro-
calcinosis. Sickle cell disease is related to infection.
10. Vitamin B6 (pyridoxine) deficiency can be associated
with xanthurenic aciduria related to deficiency of
phosphate dependent enzyme kynureninase.
Vitamin B6 (pyridoxine) deficiency is another cause
of secondary hyperoxaluria. It is a rare cause of
cortical nephrocalcinosis.
CAUSES OF MEDULLARY NEPHROCALCINOSIS
1. Hyperparathyroidism
2. Medullary sponge kidney
3. Tuberculosis of the kidneys
4. Renal tubular acidosis
5. Renal papillary necrosis
6. Immobilization
7. Milk-alkali syndrome
8. Hypervitaminosis D
9. Sarcoidosis
10. Nephrocalcinosis has been described in 16% of
preterm infants. On univariate analysis, gestation
age, male sex, duration of ventilation, oxygen
dependency, duration and frequency of gentamicin
treatment, toxic gentamicin/vancomycin levels, low
fluid intake, and postnatal dexamethasone were
significantly associated with nephrocalcinosis.
11. Nephrocalcinosis has been described in premature
infants treated with high doses of furosemide for
prolonged periods because of congestive heart
failure secondary to patent ductus arteriosus or
pulmonary disease. Both nephrocalcinosis and
nephrolithiasis may occur. These complications
occur 11–50 days after the commencement of
furosemide therapy. The addition of chlorothiazide
to furosemide prevents further calculi formation, and
it may also lead to the dissolution of existing stones.
Therefore, preterm infants who are taking furo-
semide should be regularly screened with renal
ultrasonography. Long-term furosemide abuse
can also cause medullary nephrocalcinosis in
adults.
12. Hyperoxaluria
13. Miscellaneous causes
14. A variety of conditions can cause bone destruction
associated with hypercalcemia and hypercalciuria.
These include bony metastases, multiple myeloma,
Paget disease, Cushing disease, and both
hyperthyroidism and hypothyroidism (though the
incidence associated with hypothyroidism is low).
Chronic paraneoplastic hypercalcemia may also
cause nephrocalcinosis.
15. Sickle cell anemia is a rare cause of nephrocal-
cinosis. A variety of radiographic renal abnormalities
have been associated with sickle cell disease,
including renal enlargement, thickening of the renal
cortex, focal hypertrophy, papillary necrosis, and
changes associated with infection.
16. Ochronosis (alkaptonuria) is an autosomal recessive
disorder involving deficiency of the enzyme homo-
gentisic acid oxidase. It is a rare cause of nephro-
calcinosis; renal stone formation is more common.

INCIDENCE
Regarding cases of nephrocalcinosis and nephrolithiasis
in children, 64% are associated with an underlying
structural renal lesion or urinary tract infection, 10% are
associated with hypercalcemia or hypercalcuria, 6% are
associated with cystinuria, and 20% are idiopathic.
Oxalosis and miscellaneous conditions may be involved.
In adults, 40% of cases of medullary nephrocalcinosis
are attributed to hyperparathyroidism, and 20% are
attributed to RTA. The remaining 40% are divided among
the other multiple causes. Conversely, 5% of patients with
hyperparathyroidism have nephrocalcinosis. The
medullary type accounts for 95% of all nephrocalcinosis,
whereas 5% represent cortical nephrocalcinosis. In 70%
of patients with RTA type I, both nephrocalcinosis and
nephrolithiasis eventually develop.
CLINICAL FEATURES
Sex: Both sexes are equally affected.
Age: All age groups can be affected, but the disease is
more common in childhood than at other times.
The clinical presentation is determined by the
underlying etiology of nephrocalcinosis. Most cases are
asymptomatic, and nephrocalcinosis is identified as a
radiologic abnormality. Renal tubular disorders may be
first diagnosed on biochemical examination of the urine,
which often reveals glycosuria, aminoaciduria, and
phosphaturia. Polyuria and polydipsia may be the
presenting features, with loss of the concentrating ability
of the renal tubules.
Anatomy: The basic unit of renal function is the nephron
(Figure 6.1). The nephron consists of the glomerulus; the
proximal convoluted tubule, the loop of Henle; and the
distal convoluted tubule, which finally drains into the
collecting ducts. Anatomically, the glomerulus and
proximal convoluted tubules are placed in the renal cortex,
while the descending loop of Henle enters the medullary
tissue. The ascending loop goes back to the cortex, where
it drains into the distal convoluted tubule. Finally, the
distal convoluted tubule drains into the collecting ducts,
which again enters the renal medulla and drains into the
calyx.
Calculus Diseases of Kidney 89
Each normal kidney contains about 1,250,000
nephrons. The gross anatomic renal functioning unit is
the lobule consisting of the medullary pyramid with its
base oriented toward the renal cortex, the apex oriented
toward the calyx. Its sides are covered by renal cortical
columns. At the glomerulus, all the constituents of plasma
are filtered, except the cellular elements, and the plasma
proteins and are transported via of tubules to the renal
sinus. In healthy adults, 180 L of filtrate is formed per
day. About 80% of the filtrate is reabsorbed in the
proximal convoluted tubule, and 20% is absorbed in the
distal tubular structures, dependent on antidiuretic
hormone (ADH).
Disorders of calcium metabolism, such as
hypercalcemia and hypercalciuria, may cause extensive
deposition of calcium within the renal tubules, and chronic
tubulointerstitial disease and renal insufficiency may
result. Calcified cellular debris results in occlusion of the
tubules, leading to obstructive atrophy of the nephron,
nonspecific inflammation, and interstitial fibrosis.
Impaired urine drainage through calcified tubules may
result in areas of cortical atrophy, leading to scared
cortices. Functional abnormality of urine concentration
is the earliest detectable renal change (osmolality). This
is related to decreased chloride transport in the ascending
thick segment of the nephron. Other defects of tubular
function, such as tubular acidosis and salt-losing nephritis,
may also occur.
PREFERRED INVESTIGATIONS
Most cases of nephrocalcinosis are asymptomatic and
usually identified on plain abdominal radiographs.
Planar radiography provides a useful adjunct to plain
radiography. Findings: Plain radiographic detection is not
possible until the attenuation of renal parenchyma
exceeds 100 HU. The calcification resolution also depends
on the size of the stones (those <2 mm are rarely
detected), the spatial resolution of the recoding technique,
and contrast factors. The characteristic cortical calci-
fication occurs within a few weeks after the onset of acute
cortical necrosis. When cortical nephrocalcinosis first
appears, the kidneys are still enlarged because of
inflammatory edema of the kidneys. With time, the
kidneys atrophy.
90 Uroradiology: Text and Atlas
Morphologically, three types of calcification have been
described. The most prevalent is a single cortical, calcified,
and thin peripheral band, often with calcified extensions
into the necrotic septa of Bertin (placed perpendicular
to the cortical calcification). The medullary pyramids are
usually spared, retaining the attenuation of the soft tissue.
Initially, this pattern of nephrocalcinosis may be difficult
to recognize because calcification is faint. However, the
kidney margins appear well defined and appear penciled
in.
The second pattern seen with cortical nephrocalcinosis
is the appearance of hyperattenuating tram lines. These
lines may be continuous. More often, they are interrupted,
reflecting more patchy distribution of cortical necrosis.
The third pattern is a more diffuse distribution of punc-
tate calcification. This punctate pattern of calcification
is thought to represent necrotic calcified glomeruli and
tubules.
Medullary nephrocalcinosis typically produces clusters
of stippled calcifications, mainly within the regions of the
renal pyramids.
Most conditions that cause medullary nephrocalcinosis
can also result in nephrolithiasis. Some nephroliths may
represent extruded deposits from the renal parenchyma.
The radiologic demonstration of both nephrocalcinosis
and nephrolithiasis also helps in determining their etiology
and thus significantly contributes to the management of
the disease. Planar conventional tomography provides
a cheaper alternative to CT, and it may be a useful adjunct
to conventional radiography.
Findings
In medullary calcinosis, the margins of the pyramids are
echogenic, while the center of pyramids remains
echolucent. The pyramids are well visualized as rounded
or echogenic structures. The pyramids may be densely
echogenic, and shadowing may be shown. These findings
may be evident on sonograms before they are seen on
plain radiographs.
Ultrasonography
This is noninvasive, ideal for use in young children, quick
to perform, and accurate. Early in its course, medullary
nephrocalcinosis can be seen as echogenic pyramids
before nephrocalcinosis can be identified on plain
abdominal radiographs.
Findings: In medullary calcinosis, the margins of the
pyramids are echogenic, while the center of pyramids
remains echolucent. The pyramids are well visualized as
rounded or echogenic structures. The pyramids may be
densely echogenic, and shadowing may be shown. These
findings may be evident on sonograms before they are
seen on plain radiographs.
Computed Tomography
Nonenhanced CT scans can also depict nephrocalcinosis,
and its apparent sensitivity and accuracy make it the
modality of choice.
Findings: CT is said to be the most sensitive modality
in the diagnosis of nephrocalcinosis. CT depicts
nephrocalcinosis at an early stage of the disease, it
provides a better picture of the density and extent of
nephrocalcinosis, and it may depict other changes such
as renal cysts. In one small series of 13 patients,
intravenous urograms showed medullary sponge kidneys
(24 kidneys), and nonenhanced CT scans showed
papillary calcifications in 11 kidneys. In 5 of these kidneys,
the calcifications were not detectable on plain
radiographs. Hyperattenuating papillae (55–70 HU)
without calcification were found in 4 other kidneys.
Hyperoxaluria is characterized by nephrocalcinosis on
radiologic examination, and it is associated with
nephrolithiasis and calcium oxalate crystal deposition in
multiple extrarenal organs. CT is a sensitive modality for
the detection of systemic oxalosis (e.g., in the liver and
heart), in addition to nephrocalcinosis. Bilateral
attenuating rings in the renal medulla have been depicted
on nonenhanced CT scans in a patient with marked
hypercalcemia and suspected hyperparathyroidism.
MRI
MRI is rarely required to diagnose nephrocalcinosis since
it does not depict calcium, as such.
Renal cortical calcification causes increased cortical
echogenicity with complete shadowing in severe cases.
Secondary pyramidal fibrosis may occur; these may cause
echogenic pyramids.

RNI
Findings: The role of nuclear medicine is confined to
assessing renal function by means of isotope renography,
particularly when renal surgery is being considered.
Intervention: Extracorporeal shock wave lithotripsy
(ESWL) may be indicated in cases of intrapelvic renal
Calculus Diseases of Kidney 91
stones (nephrocalcinosis). Parathyroidectomy may be
required to control hypercalcemia caused by hyperpara-
thyroidism. This technique is good for stones smaller than
5 mm, satisfactory for stones 5–10 mm, and rarely used
for stones larger than 10 mm because of the possibility
of the debris load causing steinstrasse.
92 Uroradiology: Text and Atlas
ACUTE URINARY OBSTRUCTION
INTRODUCTION
Acute obstructive uropathy is a commonly encountered
condition in day to day clinical practice. Unilateral
obstruction to urinary outflow typically occurs, with little
if any change in measured renal function in a healthy
individual. However, the less common bilateral form
results in measurable changes in kidney function.
PATHOPHYSIOLOGY
In a normally functioning kidney, urine formed within
the tubular system empties into the calyces, where
pacemaker sites generate peristaltic activity to propel urine
into the pelvis. Urine is conveyed into the ureter, where
further peristalsis moves it in boluses into the bladder.
The collecting system has a baseline pressure of 0–10
cm water, with peristaltic waves producing pressures in
the range of 20–60 cm water.
In acute obstruction, the pressures within the collecting
system and ureters above the point of obstruction can
increase dramatically. Pressures in excess of 80 cm water
may be generated. Intratubular pressure also is elevated,
leading to progressive renal impairment in the face of
continued obstruction. The kidney attempts to maintain
excretory function by mechanisms for urine resorption,
termed renal backflow. This includes pyelosinus backflow,
the most important in acute obstruction. Urine extravasa-
tes from a rupture of a calyceal fornix into the perinephric
spaces where it is resorbed, thus decompressing the
collecting system. Pyelovenous (a unique pathway),
pyelotubular, and pyelolymphatic backflow are other
compensatory mechanisms.
The degree of obstruction is an important determining
factor in the development of nephropathy, with impairment
of function occurring in a more complete obstruction.
Complete recovery of function occurs when the obstruction
is relieved in 7 days. However, permanent loss of function
occurs if the obstruction continued for around 50 days.
Acute obstruction also produces alterations in blood
flow, leading to ischemia. The renal capsule is a fixed
container, and only with longstanding obstruction will the
kidney significantly enlarge. Angiography may reveal
slight splaying apart and compression of arteries.
However, there is marked compression of the intrarenal
veins, giving them a spidery appearance.
These effects are believed to be the result of interstitial
edema secondary to increased hydrostatic pressure within
the tubules. Other factors that are involved in the
development of dysfunction include the health of the
kidney preceding the insult, as well as coexisting illnesses.
Of special significance is a superimposed infection that
can cause a rapid deterioration in renal function.
 Obstructive Diseases of Kidney 93

INCIDENCE 3. Sloughed papillae secondary to papillary necrosis

Unilateral obstructive uropathy is predominantly the result occasionally may cause symptoms and signs of acute
of urolithiasis, which has an annual incidence of 1 in obstruction.
1000. Approximately 12% of the population will develop 4. Less commonly, in patients with diabetes and in
calculi before age 70 years. The less common bilateral debilitated patients, fungal balls from Candida or
form has an estimated incidence of 1 in 10,000 in the Aspergillus may produce obstruction.
general population. 5. Ureteral ligation is a well-recognized complication of
Ureteral injury occurs as a complication of gynecologic abdominal and pelvic surgery, especially gynecologic
surgery in approximately 2% of patients. With abdominal interventions. In addition, distal ureteral ischemia may
radical hysterectomy, a 10–15% incidence rate has been result during pelvic lymphadenectomy, as small blood
reported. vessels are stripped along with the lymphatics.
6. Pelvic trauma, both penetrating and blunt, may
produce obstruction to urine outflow from rupture of
ETIOLOGY
the ureter or compression from a retroperitoneal
1. The most common cause for acute obstructive hematoma.
uropathy is an impacted calculus. In most of the 7. Extrinsic compression from an abscess or
patients, the level of obstruction is at the ureterovesical inflammatory mass in patients with appendicitis,
junction; in the remainder of patients, the ureteropelvic pancreatitis, or Crohn’s disease also has been reported
junction or mid ureter are the points where calculi (Figure 7.1).
tend to lodge. Most calculi contain calcium, combined
with oxalate and/or phosphate. While metabolic
disorders such as hyperparathyroidism can contribute
to stone formation, idiopathic hypercalciuria occurs
in about half of patients with stones. Magnesium
ammonium phosphate (struvite) stones are the next
most common type, and are observed most frequently
laminated with calcium apatite. They form in the
alkaline environment created by urease-splitting
bacteria, especially Proteus species, and commonly
produce the ‘staghorn’ appearance of the
pelvocalyceal system. Uric acid stones are less
common. Hyperuricemic conditions such as gout only
account for a small minority of patients. An acidic
environment is necessary for uric acid stones to form.
These stones, along with the less common xanthine
and matrix calculi, appear radiolucent on plain
radiographs. Cystine stones are less opaque than
calcium stones and may be difficult to demonstrate
on plain radiographs.
FIGURE 7.1: Causes of obstruction to urinary tract
2. Intraluminal obstruction also may be the result of
blood clots and mucosal edema. These may occur CLINICAL FEATURES
with passage of calculi but also can occur following A patient with a calculus lodged in the urinary tract can
instrumentation of the ureter, trauma, or anticoagulant present with acute, colicky flank pain that radiates to the
therapy. groin. Initial management usually involves pain control
94 Uroradiology: Text and Atlas
and aggressive hydration. Patients generally are treated
as outpatients unless a complicated course necessitates
hospitalization.
With other causes of acute obstruction, no symptoms
may be present. If bilateral obstruction is present, anuria
or oliguria is the earliest indication. Often, especially in
inadvertent ligation of a single ureter, no detectable
change in urine output occurs. As a result, it remains
unrecognized for 10–30 days postsurgery, at which time
flank pain and fever alert the physician to this
complication.
Sex: Urolithiasis occurs in a male-to-female ratio of 3:1.
Iatrogenic ureteral injury, mainly ligation, is more
common in women, as it is most frequently observed
with gynecologic surgery. With the other etiologies, the
relative incidence likely is variable.
Age: Renal calculi usually appear in the third decade,
with a recurrence rate in untreated patients of 50% in
10 years.
ANATOMICAL BASIS
The kidney is divided into a cortex and medulla. The
renal pyramids are located within the medullary portion;
they contain the loops of Henle and collecting ducts. At
the apical portion of the pyramids, cone-shaped papillae
convey urine from the distal collecting ducts into the minor
calyx. The peripheral projection of a minor calyx termed
the fornix produces the characteristic cup-shaped
appearance.
The minor calyces are arranged into 3 groups, the
upper, lower, and interpolar groups. Anterior and poste-
rior calyces are found within each group. Approximately
4–6 minor calyces converge into a major calyx or
infundibulum, which in turn forms the renal pelvis. The
fat-containing renal sinus envelops the entire collecting
system.
The pelvis tapers smoothly into the ureter at the
ureteropelvic junction (UPJ). The ureter travels inferiorly
along the psoas muscle, crossing over medially, anterior
to the iliac bifurcation. It then descends posteriorly and
laterally, inserting into the posteroinferior bladder wall
at the level of the trigone. At the ureterovesical junction
(UVJ), the ureter is most narrow; it also narrows at the
UPJ, the area overlying the iliac bifurcation and where
the right ureter passes through the root of the mesentery.
ROLE OF RADIOLOGY AND IMAGING
A. KUB and IVU
In general, the sensitivity of plain radiography in detecting
ureteral calculi to be approximately 45% and recommen-
ded that noncontrast helical CT replace the kidneys,
ureters, bladder (KUB) film as the initial and possibly only
imaging study. While CT appears to have replaced plain
radiography and IVU in the initial evaluation of acute
flank pain, these modalities remain involved in the follow-
up evaluation of stone disease as well as surgical and
interventional planning.
Features on plain film and IVU: The plain abdominal
radiograph or KUB film has long been the initial imaging
study of choice in patients presenting with symptoms of
acute flank pain. Calculi may have a variable appearance
on radiographs depending on their chemical composition,
especially the percentage and distribution of calcium
within them. They may appear homogeneously dense
and smooth to laminated and jagged.
While 90% of stones contain calcium, the sensitivity
of plain films has been reported at only 50–60%, with
a specificity of 70%. Therefore, in many centers, plain
radiographs are deferred in favor of CT in the acute
setting. In some instances, renal and ureteral calculi are
detected on plain abdominal radiographs obtained for
another reason.
Most noncalcified stones, blood clots, and most other
intraluminal obstructive causes are radiolucent; therefore,
they are not seen on abdominal radiographs. In trauma,
the presence of pelvic fractures and soft tissue mass in
the abdomen or pelvis may alert the radiologist to the
possibility of ureteral injury, a rare complication, or
obstruction from a large hematoma.
IVU, also termed excretory urography, came into
clinical existence in the 1920s as a method of evaluating
the structure and function of the kidney and urinary tract.
It served as both a screening and diagnostic imaging study
in patients with acute renal or ureteral colic, demonstrating
calculi and the presence of obstruction fairly accurately.
Since 1995, noncontrast helical CT has superseded IVU

in this setting, at least as a screening study. Obstructive
uropathy demonstrated on unenhanced helical CT often
requires no further imaging studies. An estimated 15%
of helical CT studies require radio-opaque contrast media
to confirm or exclude pelvic calcifications as stones or
phleboliths. However, IVU may be performed if findings
are equivocal or a noncalculus etiology is suggested.
IVU begins with a scout or preliminary radiograph.
Additionally, oblique scout radiographs may be obtained.
Pre-injection linear tomograms are helpful when the bowel
pattern obscures the areas of interest. Following the
administration of the contrast agent, coned films and
tomograms are then obtained, with the intervals and total
number of films being quite variable. In a normal kidney,
opacification of the renal parenchyma is observed within
1 minute. Within the next 2 minutes, the pelvocalyceal
system may be seen, followed by the ureters approxi-
mately 5–10 minutes post-injection.
In an obstructed kidney, delayed accumulation of
contrast is seen, resulting in a nephrogram that is initially
of lower density. Progressive concentration of contrast
within the renal cortex and medulla occurs, producing
the classically described “obstructive nephrogram” that
may persist for some duration. Striations may occasionally
be seen in the parenchyma, representing contrast material
within dilated tubules (Figure 7.2).
FIGURE 7.2: IVU: Striated nephrogram on left side
Obstructive Diseases of Kidney 95
The pelvocalyceal system may not opacify for hours
or at all, depending on the severity of obstruction.
Dilatation proximal to the obstructing process may be
seen as hydronephrosis and hydroureter, which may be
minimal in the acute situation. A standing column of
contrast may be observed proximal to the obstruction.
Pyelosinus extravasation of contrast and mild clubbing
of the calyces also may be seen.
On an IVU, the findings of a persistent nephrogram
and delayed passage of contrast through the urinary
system indicate with a high degree of confidence that
an obstruction is present. IVU is best performed following
a screening study that produces either negative or
equivocal results.
D/D of a Persistent Nephrogram
1. Pre-renal (15%)
a. Renal artery stenosis
b. Hypotension
2. Renal (70%)
a. Glomerulonephritis
b. Acute tubular necrosis
c. Papillary necrosis
d. Renal vein thrombosis
e. Acute interstitial nephritis
3. Post-renal (15%)
a. Obstruction.
Both false positives and false negatives are quite
common, as the sensitivity and specificity of plain
radiographs is poor. Small calcified stones, radiolucent
stones, clots, and mucosal edema are not visualized. In
addition, a large patient body habitus and overlying bowel
may obscure even densely calcified stones, resulting in
a false-negative interpretation.
Most false positives occur because of the presence
of other calcific densities within the perceived or expected
areas of the kidney and ureter. While gallstones usually
are multiple and have a faceted appearance, they may
be seen overlying the right kidney and, even on oblique
films, be indistinguishable from renal calculi. In the pelvis,
phleboliths often are misinterpreted as ureteral calculi.
The radiolucent center of a phlebolith may not always
be present to help differentiate the two.
96 Uroradiology: Text and Atlas
As reported in the literature, IVU sensitivity in the
evaluation of acute flank pain varies from 52–87%. The
detection of calculi as a cause for obstructive uropathy
depends on multiple factors, including stone size and
location as well as the degree of obstruction. As a result,
false-negative studies are not uncommon in the
urographic evaluation of calculi.
The presence of a standing column of contrast does
not always indicate the site of obstruction, as it may be
seen in normal individuals.
UROGRAPHIC FINDINGS IN ACUTE OBSTRUCTION
1. Spontaneous pyelosinus extravasation (up to 24% of
patients
2. Increasingly dense ‘obstructive’ nephrogram’
2. Modest kidney enlargement (50% of patients)
3. Delayed caliceal opacification
5. Minimal to modest pelvicaliectasis.
Limitations: Plain radiography and IVU have similar
drawbacks, including lower sensitivity because of
superimposition of bone and other calcified structures
and obscuring bowel pattern. They are limited by stone
size (<4 mm) and patient habitus. IVU, although
providing both anatomic and physiologic information,
has the added disadvantage of being time consuming
and dependent on administration of contrast material,
with its potential complications. It is also dependent on
renal function, as the use of the test is greatly diminished
when the serum creatinine concentration is elevated when
the patient has both intrinsic renal disease and an acute
obstruction.
UROGRAPHIC FINDINGS IN CHRONIC OBSTRUCTION
1. Renal size: Large in partial obstruction and small in
complete obstruction
2. Nephrographic density: Normal or decreased (may
increase with acute-on-chronic obstruction)
3. Parenchymal thickness: Reduced with or without
‘Crescents’, ‘soap-bubbles’, ‘rims’, or ‘shells’
Hydronephrosis
4. Pyelogram: ‘Negative pyelogram’ on nephrogram
phase (Black pyelogram) and/or ‘Ball’ pyelogram
5. Ureter: Dilatation and tortuosity (low obstructions) and
mucosal striations may be seen.
FIGURE 7.3: Right hydronephrosis due to small VUJ calculus
B. Ultrasound
In the evaluation of acute flank pain, ultrasound (USG)
is limited primarily to pregnant patients. While USG
demonstrates renal calculi, it is poor at detecting ureteral
stones.
Features on ultrasound: The hallmark of obstruction
on USG is the presence of hydronephrosis (Figure 7.3).
Prominent anechoic structures within the renal sinus
represent a dilated pelvocalyceal system. Renal calculi
also may be demonstrated as echogenic foci with or
without shadowing. This finding depends on the size of
the calculi, with smaller stones blending into the echogenic
renal sinus. Ureteral calculi and ureterectasis are detected
less often. While UPJ and UVJ stones may be observed,
mid ureteral stones are extremely difficult to detect.
Limitations: USG evaluates the ureters and detects
calculi poorly. The accuracy of USG in diagnosing
obstruction in the setting of acute flank pain was found
to be approximately 66%. This is directly related to the
anatomic nature of the examination, which relies mainly
on the presence of hydronephrosis to make the diagnosis.
In early obstruction, up to 36 hours, no dilatation of the
collecting system may be present, and a false-negative
study may result.
The reported sensitivity of USG in the detection of
a ureteral stone and associated obstruction is 60-70%.
As a result, USG is not routinely used in the evaluation
of acute renal or ureteral colic. However, it is an important
screening examination in pregnant patients with acute
flank pain and in acute renal failure. The gravid uterus
causes ureteric obstruction and a ureteric stone may be
missed.

C. Color Doppler
It has been suggested as a method of indirectly deter-
mining obstruction by measuring the resistive index in
renal arteries and evaluating the direction and magnitude
of ureteral jets. Also twinkling artefact is a helpful Doppler
sign in cases of obstruction due to calculus disease.
Features on color Doppler imaging: Doppler
sonography is an additional tool that may be employed
when radiation exposure is undesirable, such as in
pregnant patients. The RI, which is a measure of
impedance to renal blood flow, may be raised when
obstruction to urine outflow exists. In most centers,
obstruction is indicated by an RI greater than 0.70 or
a difference of greater than 0.10 between the kidneys.
However, any process causing decreased perfusion will
result in an elevated RI. Ureteral jets also may be
evaluated; these may be absent or decreased in frequency
in acute obstruction.
False positives/negatives: The presence of obstruction
is inferred by visualizing a dilated collecting system. This
may be minimal or even absent in acute obstruction. In
addition, ureteral calculi are not well demonstrated. The
false-negative rate is as high as 35% in patients with
uropathy secondary to a calculus lodged in the ureter.
Technical limitations to the study, such as patient obesity,
bowel gas, and operator skill, also may result in a false-
negative study.
The false-positive rate is approximately 10% in
patients with urolithiasis. The source of such errors
includes vascular calcifications that may simulate a
calculus. Peripelvic cysts, an extrarenal pelvis, or even
a normal collecting system may be misinterpreted as
representing hydronephrosis. Doppler sonography can
help by readily distinguishing renal hilar vessels from a
slightly dilated collecting system.
D. Unenhanced Spiral Computed Tomography
The advent of helical CT has dramatically altered the
diagnostic imaging approach to patients presenting with
acute flank pain. Unenhanced helical CT has both
a high sensitivity of 95-98% and a high specificity
of 96-100% in detecting ureteral calculi in the
acute setting. Both calcified and noncalcified calculi
Obstructive Diseases of Kidney 97
may be identified, along with the location and size of
the stone. Secondary signs of obstructive uropathy,
including hydronephrosis, white pyramid sign, rim sign,
perinephric and periureteral stranding, as well as
ureterectasis, are well demonstrated on CT.
Several recent reports compare unenhanced helical
CT with intravenous urography (IVU), the established
criterion standard in evaluating the genitourinary system.
Advantages of NCSCT are many. CT has been shown
to be more sensitive in detecting and characterizing
ureteral calculi and at least as sensitive in demonstrating
the presence of obstructive uropathy. Additionally, CT
may be performed rapidly, in approximately one third
the time of an IVU study, and does not require the use
of IV contrast material. The ability to diagnose noncalculus
etiologies, as well as evaluate other intra-abdominal
pathologies that may mimic renal colic, affords CT an
invaluable advantage.
Features on CT:
On unenhanced helical CT, calcified calculi appear
as in radiographs as opaque densities within the
genitourinary tract. Interestingly, calculi that are
radiolucent on plain film also are of high attenuation on
CT. Researchers have reported that Hounsfield values
may be used to differentiate the types of calculi, as this
can provide the clinician information concerning an
underlying metabolic disorder as well as influence
treatment decisions. However, the overlap in Hounsfield
values among the different stones makes this of limited
use.
These values become important in determining the
presence of an intraluminal blood clot, which appears
dense on CT but has a lower attenuation value than
calculi. An exception to the normal high attenuation of
calculi recently has been described in a small percentage
of HIV-positive patients being treated with Indinavir, a
protease inhibitor. As the stones are of soft tissue
attenuation, they are not detected on non–contrast-
enhanced CT.
As mentioned previously, unenhanced helical CT is
not a physiologic imaging study, and the sole finding of
a stone is inadequate to make the diagnosis of obstruction.
Therefore, secondary signs of obstruction as detected on
98 Uroradiology: Text and Atlas

CT are necessary to confirm the diagnosis and obtain

an idea concerning the severity of obstruction. In the
presence of ureteral calculi, proximal ureterectasis is the
most commonly seen indirect sign. This also may be
observed with other causes of intraluminal obstruction.
Dilatation of the pelvicalyceal system is seen on CT
as anterior and medial bulging of the renal pelvis, which
is of low attenuation compared to the surrounding renal
parenchyma. Renal enlargement also may be observed
in some patients. Perinephric fat stranding, representing
engorged lymphatics and/or edema, is seen as linear
wispy densities in the normally low-attenuation fat.
Moderate-to-severe perinephric stranding generally
corresponds to the degree of obstruction present.
Periureteral stranding densities often are seen, again
representing edema in the surrounding fat. Other signs
of obstruction include the rim sign, which refers to the FIGURE 7.4: Coronal reconstruction: Severe right hydronephrosis
soft tissue attenuation halo around an intraureteral due to stricture in mid ureter

calculus, ureteral wall edema, and blurring of the renal

sinus fat. One or more of these secondary signs usually
is present, and the predictive values of the individual signs
have been reported in the literature. Ureterectasis, hydro-
nephrosis, and periureteral and perinephric stranding
each have a positive predictive value of approximately
90%.
Hydronephrosis and perinephric stranding may be
the only signs of obstruction in patients with inadvertent
ligation of the ureters, while the presence of an intra-
abdominal hematoma in a posttraumatic setting or an
inflammatory mass in a patient with abdominal pain
indicates a possible etiology (Figure 7.4). FIGURE 7.5: Sagittal section on CT: Pyelosinus extravasation
The administration of IV contrast material in the above
situations may help delineate the ureter and determine The largest source of false-positive errors in
if the obstruction is indeed secondary to extrinsic unenhanced helical CT results from phleboliths in the
compression. In many patients, IVU or direct visualization pelvis. On CT, the radiolucent center is not present to
help differentiate them from stones, and some stones have
of the urinary tract is needed to establish the diagnosis.
a lucent center. The false-positive rate in most studies
Contrast-enhanced CT in obstruction produces is approximately 4%. Administration of IV contrast may
findings similar to that first described with IVU, revealing help by outlining the ureter and separating it from
a prolonged parenchymal phase (Figure 7.4). The extraluminal densities.
persistent nephrogram, which appears either as a homo- The absence of secondary signs of obstruction, as may
geneous or mottled density kidney, results from delayed occur in early obstruction, can result in a false-negative
passage of contrast into the collecting system. Pyelosinus study, especially when no intraluminal or extraluminal
extravasation is well demonstrated on CT as areas of cause may be seen. The incidence of false negatives is
contrast material within the renal sinus fat (Figure 7.5). reported to be 0–6%.

Limitations: An inherent limitation of unenhanced
helical CT is in providing functional information. The
severity of obstruction may be inferred by the presence
of perinephric stranding, which is believed to result from
forniceal rupture or inflammation in the perirenal fat from
high calyceal pressures. The absence of this finding as
well as the other signs of obstruction does not exclude
a significant obstruction.
Performing a contrast-enhanced CT may provide
greater physiologic information by demonstrating an
obstructive nephrogram and pyelosinus extravasation of
contrast material. An important consideration in choosing
this modality is the significant radiation dose to the patient,
compared to an intravenous pyelogram (IVP). This
disadvantage restricts its use, especially in pregnant and
pediatric patients.
In patients with ureteral calculi, stone size alone
determines initial treatment of patients, with no correlation
found between severity of obstruction as suggested by
CT and the decision to treat conservatively or perform
an intervention. The authors therefore suggest nonen-
hanced helical CT is adequate for the initial diagnosis
and treatment of patients with stone disease.
E. Radionuclide Scan
In nuclear medicine, the passage of radionuclide agents
through the urinary tract is monitored with a gamma
camera. Outlines of the kidney and ureter are generated
and a point of obstruction may be evident. More
importantly, it provides physiologic information regarding
the function and dynamics of the urinary system. The
technique of choice in the evaluation of obstruction is
diuresis renography, which is performed with technetium
99m
Tc labeled mercaptoacetyltriglycine (99mTc MAG3) in
most centers.
Diuresis renography: is not performed routinely in
acute ureteral colic, as CT usually provides the necessary
information. However, it may be important in documen-
ting return of renal function in patients where urological
intervention is required. Renography with Lasix is useful
in determining whether pelvocalyceal system dilatation,
often observed on a screening study such as USG, is
obstructive or nonobstructive in nature.
Obstructive Diseases of Kidney 99
Limitations: Doppler sonography is both operator
dependent and time consuming. Determination of
ureteral jets and the resistive index has not been adopted
into widespread clinical use for acute obstruction because
of technical limitations and questionable accuracy. Most
pathologic processes decrease renal perfusion, thus
increase the resistive index (RI).
Features on RNI: Scintiscans and time-activity curves
before and after administration of a diuretic (furosemide)
are obtained over a period of approximately 35 minutes.
In a normal renogram, initial increased activity is seen
as tracer accumulates within the kidney. As tracer moves
into the collecting system and ureter, the activity in the
kidney starts to drop. In kidneys with dilated collecting
systems, an up-slope in the time-activity curve occurs as
tracer is retained within the kidney.
Administration of furosemide in a nondilated kidney
results in a washout of tracer activity from the collecting
system, reflected as a down-slope on the time-activity
curve. T½ is defined as the time taken for reduction of
activity by 50%; a normal T½ is less than 10 minutes
with 99mTc MAG3.
In a kidney with collecting system dilatation, a
decrease in activity with furosemide indicates a
nonobstructive cause of dilatation. In an obstructed
kidney, no response is observed following the injection
of furosemide. A prolonged T½, greater than 20 minutes,
is highly indicative of obstruction. In addition, the
scintiscans, while providing the data for the time-activity
curve, also may indicate the site of obstruction past which
little or no activity is seen.
To make this study definitive, renal function must be
at least partially preserved. The glomerular filtration rate
(GFR) must be greater than 15 mL/min for an obstructive
time-activity curve to be judged accurate. In patients
where the GFR is less than 15 mL/min, no response to
the administration of furosemide is observed. No washout
of activity occurs regardless of the presence or absence
of obstruction. Thus, the study is deemed indeterminate
and further workup or intervention is required to make
the diagnosis.
Limitations: Diuresis renography, a physiologically
driven study, depends on renal function. If marked
100 Uroradiology: Text and Atlas

impairment of bilateral renal function is present, an

indeterminate study results. In patients who are
dehydrated, the expected response to the diuretic may
not be evident, leading to an inconclusive study.

F. MRU
Ultrafast T1 and T2 weighted techniques such as spoiled
gradient echo (T1) and single-shot fast spin echo (T2)
recently have been reported to be highly sensitive and
specific for determining the presence of both ureteral
calculi and acute obstructive uropathy. However, as with
US, in magnetic resonance urography (MRU) the degree
of dilatation must be sufficient to use the native urine
as a contrast agent (Figure 7.6).
Limitations: The use of MRU in the acute setting of
flank pain also is limited. Studies comparing MRU to CT
and IVU reveal that it misses small calculi and mild
dilatation. In addition, it is time consuming, expensive,
FIGURE 7.6: Left UVJ edema
and currently is limited to special situations, such as
pregnant patients.
in patients with staghorn calculi, which are commonly
INTERVENTION
infected and do not respond as well to other treatments.
Most calculi smaller than 6 mm in diameter pass In patients with obstructions with evidence of infection
spontaneously. Pain control and hydration usually are and/or sepsis, emergent percutaneous nephrostomy tube
all that is required in an uncomplicated situation. Larger placement serves to decompress the collecting system.
stones as well as stones lodged in the proximal ureter
are less likely to resolve on their own and require SPECIAL CONCERN DURING PREGNANCY
intervention. Treatment choice depends on the location Pregnant patient with acute flank pain from ureteral
and composition of the stone, presence of infection, obstruction presents a unique diagnostic and therapeutic
preceding treatment, and anatomy of the urinary tract. challenge. The incidence of an obstructing stone is
The placement of a ureteral stent by the urologist often approximately 1 in 1500 pregnancies. Compression from
is the primary intervention for ureteral calculi. If the the gravid uterus also may result in an obstructive
obstruction is not relieved, endourologic procedures such uropathy.
as retrograde ureteroscopy and lithotripsy may be The diagnostic imaging approach to these patients
attempted. Extracorporeal shock wave lithotripsy (ESWL) begins with an abdominal US to demonstrate the presence
commonly is performed on renal and ureteral calculi with of hydronephrosis. Remember that mild hydrouretero-
success but is contraindicated in obstruction, unless a nephrosis is observed in normal pregnant patients.
urinary diversion procedure allows for passage of the Transvaginal and transrectal US may be used to detect
stone fragments. distal ureteral calculi. Doppler sonography plays an
In ureteral obstruction, the interventional radiologist important role, using the RI and ureteral jets to diagnose
performs USG and/or fluoroscopic-guided percutaneous obstruction.
nephrostomy. As it provides access to the collecting Where USG does not provide a diagnosis, MRU or
system, nephroscopy, lithotripsy, and removal of large IVU may be the next step in imaging. MRU, if available,
renal calculi are possible. It is the treatment of choice is preferred, as no ionizing radiation exposure occurs.

One can make the diagnosis of an obstructing calculus
by the presence of a filling defect with associated
perinephric or periureteral edema. Alternatively, an
extremely limited IVU may provide the necessary
information. The limited IVU consists of a preliminary
film followed by a single postcontrast exposure to
demonstrate the point and cause of obstruction. However,
the gravid uterus with the fetus can obscure a
nonpregnancy cause of hydronephrosis.
As in other patients with ureteral calculi, management
is conservative, as most stones will pass with hydration.
In patients with persistent symptoms, placement of a
ureteral stent or percutaneous nephrostomy is needed
to relieve obstruction. This also may be necessary in
patients with obstruction secondary to a gravid uterus,
where conservative measures such as postural changes
may be ineffective.
CHRONIC URINARY OBSTRUCTION (IVU SIGNS)
MORTALITY/MORBIDITY
Morbidity is related to the etiology, degree, and duration
of the obstruction. A stone that lodges in the urinary tract
is associated with excruciating pain and discomfort.
Concurrent infection may produce both localized
sequelae, such as perinephric abscess, and systemic
manifestations including sepsis. Mortality can result
from untreated superimposed infection. As the kidney
has no pain receptors, it is only with pressure distension
of the capsule, the site of the receptors, that pain is
appreciated.
As opposed to the rim sign of hydronephrosis (in which
a rim of renal parenchyma enhances around a markedly
dilated renal pelvis and collecting system, with
enhancement of the cortical columns also frequently
seen), the crescent sign describes the appearance of
concentrated contrast material in the collecting tubules.
The collecting tubules are arranged parallel to the margin
of the dilated calyx, producing a thin line of contrast
material that resembles a crescent. The change in tubule
orientation from vertical to near horizontal is thought to
be the result of incomplete obstruction that produces a
gradual dilatation of the collecting system.
It is important to distinguish the crescent sign from
the rim sign of hydronephrosis since the former indicates
Obstructive Diseases of Kidney 101
recoverable renal function, even in the presence of severe
dilatation of the collecting system.
ADDITIONAL NOTE ON URETERAL OBSTRUCTION
Ureteral obstructions are commonly divided into intrinsic
and extrinsic causes. Intrinsic causes include stones and
strictures, extrinsic causes include pregnancy, tumor,
fibrosis, or iatrogenic. Patients often present with flank
pain. CT often will demonstrate the cause of the ureteral
obstruction (i.e. calcification, tumor) and will often
demonstrate secondary signs including hydronephrosis.
Patients will often have a delayed and persistent
nephrogram depending on the grade of obstruction.
Treatement involves re-establising the patency of the
ureter often through stenting. Decompression can also
be obtained through percutaneous nephrostomy.
THE DIFFERENTIAL DIAGNOSIS OF
HYDRONEPHROSIS
It includes both obstructive and non-obstructive causes.
In the child, the most common cause of a dilated renal
collecting system is ureteropelvic junction obstruction
usually from intrinsic dysfunction of the ureteral muscle.
Other causes of the obstruction include ureterovesicle
junction obstruction, ureterocele and posterior ureteral
valve.
NON-OBSTRUCTIVE CAUSES
1. Vesicoureteral reflux,
2. Congenital megaureter,
3. Eagle-Barret syndrome and
4. Polymegacalicosis (or congenital megacalyces)
5. Pregnancy
6. Raped ureter.
The distinction between obstructive and non-
obstructive causes can be made by diuresis renography
where the mechanically obstructed renal collecting system
shows prolonged retention of radioactivity.
DIFFERENTIAL DIAGNOSIS OF PRENATAL
(FETAL) HYDRONEPHROSIS
UNILATERAL PATHOLOGY
1. Renal pelvic dilatation
2. VUR
102 Uroradiology: Text and Atlas
3. Megaureter (with or without reflux)
4. Multicystic dysplastic kidney
5. Complicated duplex kidney
6. Upper moiety dilatation - either ureterocele or ectopic
drainage
7. Lower moiety dilatation - usually VUR but rarely renal
pelvic dilatation only.
BILATERAL PATHOLOGY
1. Bilateral renal pelvic dilatation
2. Bilateral VUR
3. Bilateral megaureter (with or without reflux)
4. Bladder pathology, e.g. neurogenic bladder
5. Bladder outlet pathology (posterior urethral valves)
6. Bilateral complicated duplex kidneys
7. Multicystic kidney on one side and cystic dysplastic
kidney on opposite side.
Renal pelvic dilatation (RPD) can be defined
postnatally as a kidney which on USG examination has
calyceal dilatation plus a dilated renal pelvis which
measures greater than 10–15 mm in its AP diameter and
there is no USG evidence of a dilated ureter. This has
been termed PUJ obstruction or PUJ stenosis in the past.
The identification on antenatal USG is that of an AP renal
pelvis which is greater than 50% of the longitudinal length
of the kidney. This equates to approximately a 5 mm
pelvis at 20 weeks gestation and a 10 mm pelvis in the
third trimester or at full term. RPD is commonly unilateral
but may be bilateral; the importance of this distinction
is that if it is unilateral then there is no urgency in terms
of investigation. The implication of this dilatation from
a management aspect is unclear since no natural history
studies have been undertaken.
All these infants are asymptomatic and their treatment
has changed from operating early on most infants in the
1980s to a position where only about 25% now undergo
surgery in some teaching institutions. There are more
children who are currently being followed expectantly so
that a body of experience is building up suggesting both
how to investigate and when to operate on these children.
The problem arises from the fact that the mere presence
of isolated calyceal and renal pelvic dilatation does not
necessarily imply an obstruction that requires surgery.
Obstruction is not easily defined physiologically but
the best definition may be a restriction to urine flow that,
left untreated, will cause progressive renal deterioration.
The effects of obstruction are recognized as hydronep-
hrosis, parenchymal atrophy and impaired renal function.
These changes are the results of obstruction but do not
define or predict the potential for progressive renal
deterioration.
 Renal Infections 103

CLASSIFICATION The most common organisms are gram negatives. E. coli

ACUTE INFECTIONS is the most frequent organism, with Proteus, Klebsiella,
Staphylococcus saprophyticus, and Enterococcus being
1. Acute pyelonephritis
less common.
2. Pyonephrosis
3. Renal abscess Role of Radiology and Imaging
4. Emphysematous pyelonephritis.
The role of imaging is generally to define underlying
CHRONIC INFECTIONS pathologies like:
1. Xanthogranulomatous pyelonephritis • Obstruction
2. Renal tuberculosis • Reflux,
3. Schistosomiasis • Calculus
4. Malakoplakia. And to rule out complications like:
• Abscess
ACUTE INFECTIONS • Emphysematous pyelonephritis
• Changes consistent with chronic infection.
ACUTE PYELONEPHRITIS
IVP, CT, USG, can be normal in up to 75% of cases.
Introduction IVU
It is an infection of the upper urinary tract that usually • Enlarged kidney
occurs when colonic bacterial ascend from the lower • Striated nephrogram.
urinary tract to invade the renal parenchyma.
CT Findings
Causative Organism • Renal enlargement (edema); (Figure 8.1)
Acute pyelonephritis can be caused by hematogenous • Areas of decreased perfusion/enhancement; (Figure 8.2)
spread of bacteria or ascending urinary tract infections. • Stranding of the perirenal fat;
It may be a multifocal process and involve one or both • Striated nephrogram with contrast enhanced studies.
kidneys. It will usually respond to appropriate antibiotics. A striated nephrogram appears as alternating linear
104 Uroradiology: Text and Atlas
FIGURE 8.1: Enlarged, inhomogenously enhancing right kidney with
patchy low density nonenhancing areas involving its parenchyma—
Acute pyelonephritis
FIGURE 8.2: Focal nephromia in right kidney
FIGURE 8.3: Left striated nephrogram–Acute pyelonephritis
FIGURE 8.4: Subcapsular perinephric infective collection
lucency/density parallel to tubules and collecting ducts
due to stasis of contrast material in dilated ducts
on a background of edematous renal parenchyma
(Figure 8.3).
• Perinephric collection can occur (Figure 8.4).
Differential diagnosis for a striated nephrogram:
(Pneumonic CHOIR C)
• Contusion;
• Hypotension;
• Obstruction (ureteral);
• Intratubular obstruction;
• Renal vein thrombosis;
• Cystic diseases of kidney (infantile PCKD, medullary cystic
disease, medullary sponge kidney).
PYONEPHROSIS
Pyonephrosis refers to infection in an obstructed kidney
or accumulation of pus in an obstructed PC system.
Pyonephrosis can result in rapid destruction of the renal
parenchyma and must be treated promptly by relief of
obstruction by ureteral stent or nephrostomy tube
placement and antibiotics.
Ultrasound classically demonstrates a dilated
collecting system filled with layering echogenic ‘‘pus and
debris” (Figures 8.5 and 8.6).

FIGURE 8.5: PUJ obstruction with pyonephrosis—note
internal echoes
FIGURE 8.6: Right hydronephrosis with pyonephrosis
and fungal balls
The preferred examination is CECT. On CT, patients
with pyonephrosis may have increased pelvic wall
thickness, inflammatory changes in the perinephric far,
and, in rare cases, layering of IV injected contrast agent
anterior to the pus in the dilated renal pelvis. PCS gas
in the absence of a history of urinary tract instrumentation,
is uncommon but strong diagnostic indicator of
pyonephrosis.
RENAL ABSCESS
If inadequately treated, acute pyelonephritis may progress
to tissue necrosis, resulting in renal abscess.
Features:
• On CECT, renal abscess usually have attenuation
valves of about 30HU with or without peripheral rim
Renal Infections 105
enhancement (due to enhancement of the distinct
rounded and thick walls), a feature that distinguishes
abscess from fluid density renal cysts. Their contents
do not enhance.
• Alternatively abscesses may be ill-defined and
surrounded by zones of decreased parenchymal
enhancement, representing inflammation that has yet
not progressed to necrosis.
• Occasionally gas/air is found in it.
• Focal thickening of the adjacent fascia and stranding
in adjacent perinephric fat are common.
A perinephric abscess may ultimately result if the
infection extends out through the renal capsule.
EMPHYSEMATOUS PYELONEPHRITIS (EPN)
Introduction
It is a life-threatening, fulminant, necrotizing upper urinary
tract infection associated with gas within the kidney and/
or perinephric space. Gas confined to the renal pelvis
should be called emphysematous pyelitis, and gas
confined to the perinephric space should be called
perinephric emphysema.
D/D of Air/Gas in PCS (Pelvi Calyceal System)
1. Retroperitoneal perforation of an abdominal viscus
2. Psoas abscess secondary to gas-forming organisms
3. Reflux of air from the bladder
4. Fistulae (as may occur with xanthogranulomatous
pyelonephritis)
a. Bronchorenal
b. Enterorenal
c. Cutaneorenal
5. Air in a focal renal abscess (not life-threatening)
Incidence
EPN is rare, but the frequency is higher in patients who
are immunocompromised, especially in patients with
diabetes, who account for 87–97% of patients.
Predisposing Factors
1. EPN is usually a rapidly progressive and life-
threatening infection that is seen most commonly in
persons with diabetes.
2. EPN in a solitary, polycystic, transplanted kidney has
been described recently, with a rare association with
106 Uroradiology: Text and Atlas
xanthogranulomatous pyelonephritis. Often, multiple
conditions are associated with EPN, such as poorly
controlled diabetes, acidosis, dehydration, and
electrolyte imbalance.
3. Females are affected twice as often as men, and
mortality rates can be as high as 80%.
4. Obstructive uropathy, urinary calculi, calyceal stenosis,
and neoplasms are significant predisposing factors.
Etiological Agents
The infecting organisms usually consist of mixed flora,
including:
1. Escherichia coli (68%),
2. Klebsiella pneumoniae (9%),
3. Proteus mirabilis and
4. Other organisms include Pseudomonas; Enterobacter;
Candida; and, rarely, Clostridia species.
Pathophysiology
EPN is an acute and chronic necrotizing pyelonephritis
with multiple renal abscesses. Mixed acid fermentation
of glucose by Enterobacteriaceae bacteria is the major
pathway of gas formation.
Types of EPN
Two subtypes of EPN based on CT appearances have
been described.
Type I EPN (33% of patients) is characterized by
parenchymal destruction with either absence of fluid
collection or presence of streaky or mottled gas radiating
from the medulla to the cortex. A crescent of subcapsular
or perinephric gas may be present. The absence of fluid
collection implies a poor immune response. The mortality
rate is high at 66%.
Type II EPN (66% of patients) typically has a confined
bubbly intrarenal gas pattern, probably within abscesses
associated with renal and perinephric fluid collection, and
gas within the renal pelvis. The mortality rate in type
II is 18%.
Conversion from type I EPN to type II EPN has been
described. Wan et al have shown that serum creatinine
levels are the most reliable predictors of the outcome in
patients with EPN. By calculating likelihood ratios,
patients with creatinine levels greater than 1.4 mg/dL and
platelet counts of 60,000/mm3 or less are at high risk.
The posttest probability of death increases from 69% to
92% in type I EPN and 18% to 53% in type II EPN.
Patients with creatinine levels of 1.4 mg/dL or less and
platelet counts greater than 60,000/mm3 are at much
lower risk. The posttest mortality risk in these patients
decreases from 69% to 27% and from 18% to 4% for
type I EPN and type II EPN, respectively.
Clinical Features
Patients usually present with chills, fever, flank pain,
lethargy, and confusion. Septicemic shock may occur. A
crepitant mass may be present. Often, bacteriuria, positive
blood culture results, and leukocytosis are present. Patients
are usually quite ill, but occasionally, the symptoms are
mild, belying the severity of the disease. This is particularly
the case in persons with long-standing diabetes. The
condition is bilateral in 5-7% patients.
Age: The average age of patients with EPN is 54 years.
Sex: The male-to-female ratio is 1:2.
Preferred Investigations
Plain abdominal radiography is the initial examination
of choice because it better depicts air in the renal collecting
system and it is much more specific than ultrasonography.
However, in practice, sonography may be the initial
examination performed.
Features: Plain radiographs may show bubbles of gas
within the region of the renal bed and in the upper renal
collecting system. These may be diagnostic in the
appropriate clinical setting.
Gas within the collecting system without evidence of
renal parenchymal gas may be seen in patients with
diabetes and does not have the same ominous prognosis.
Limitations: Plain radiographs are good for depicting air
within the renal collecting system, but nonspecificity is
a problem because of the superimposition of gas from
the bowel. Moreover, gas in the retroperitoneum and gas
within a renal or perinephric abscess may mimic EPN.
IVU: Intravenous urography may be necessary if renal
intervention is contemplated.

Features: Intravenous urography shows significant renal
enlargement associated with delayed or absent excretion.
Acute renal edema with obliteration of the renal pelvis
can be seen.
Limitations:
USG:
Ultrasonography is usually the first imaging modality for
assessing renal pathology, but confirmation and better
assessment entails the use of CT.
Findings: Intrarenal gas causes high-amplitude echoes
within the renal sinus/renal parenchyma associated with
dirty acoustic shadowing.
Ring-down artifacts may result from air bubbles
trapped in fluid.
Shadowing from gas bubbles in the perinephric space
may be seen. These make visualization of the kidney
difficult.
Perinephric fluid, if any, tends to be obscured by gas.
Limitations: USG is limited because gas within the kidney
and/or renal pelvis mimics renal calculi and produces
artifact due to reverberation echoes and shadowing.
Computed tomographic (CT) findings are diagnostic
of the presence of air within the renal tract, and CT also
elegantly depicts the renal and perirenal anatomy and
the spread of infection to the perinephric tissues.
CT is the most reliable and sensitive modality
in diagnosing EPN.
Features:
CT is the examination of choice for diagnosing
EPN.
Intraparenchymal, intracalyceal, and intrapelvic gas
and extension into perinephric space are readily identified
on nonenhanced CT scans.
Mottled areas of low attenuation extend radially along
the pyramids.
Occasionally, pus may be seen extending into the renal
veins.
Limitations: CT scans do not always depict other causes
of intrarenal air, such as reflux of air from the bladder,
Renal Infections 107
bronchorenal, and enterorenal, or cutaneorenal fistulae.
These may occur with xanthogranulomatous pyelone-
phritis and focal renal abscesses.
MRI
MRI is not the modality of choice in the diagnosis of EPN.
When CT is available, it should be used instead.
Features: MRI is not the modality of choice in the diagnosis
of EPN. MRI findings reported are a signal void on both
T1-weighted and T2-weighted images. Perinephric and
intraparenchymal fluid collections are demonstrated well
on MRIs.
RNI: Because function is depressed or even absent on
the affected side, radionuclide studies are more
appropriate for assessing renal function, particularly if
surgery is indicated.
Findings: Radionuclide studies are nonspecific; therefore,
they have a limited role in the evaluation of EPN.
However radionuclide study is an excellent modality for
assessing differential function when nephrectomy is
contemplated. Scintigraphy has been used to evaluate
responses to antimicrobial therapy.
Limitations: The sole limitation of radionuclide imaging
is its lack of availability. Otherwise, it is an excellent
modality, and it does not result in false-positive or false-
negative diagnoses.
Intervention
Treatment involves aggressive antibiotic therapy, drainage
procedures to relieve obstruction, and prompt nephrec-
tomy in life-threatening situations.
With early diagnosis and the aggressive and prompt
administration of antibiotics, therapeutic success may be
achieved in selected patients. Percutaneous nephrostomy
and percutaneous perinephric drainage may preclude
nephrectomy in some patients. Occasionally, drainage
procedures alone are successful; however most patients
require immediate surgical intervention.
Treatment
It involves aggressive antibiotic therapy, drainage
procedures to relieve obstruction, and prompt nephrec-
tomy in life-threatening situations.
108 Uroradiology: Text and Atlas
Mortality/Morbidity
The mortality rate is 60–75% with antibiotic therapy and
21-29% after antibiotic treatment and nephrectomy.
When the infection extends into the perinephric space,
the mortality rate increases sharply to 80%.
Summary
Emphysematous pyelonephritis (EPN) is a severe
infection of kidneys with accumulation of gas in the renal
parenchyma. The infection can be fatal if left untreated.
The mortality rate is 60-75% with antibiotic therapy and
21–29% after antibiotic treatment and nephrectomy.
When the infection extends into the perinephric space,
the mor tality rate increases sharply to 80%.
EPN is a rare condition, with a mean age of 55 years,
and range of 19-81 years. Women are affected more often
than men. Ninety-five percent of patients have diabetes,
and of those, most are uncontrolled. Other factors include
immunocompromised state and ureteral obstruction/
calculi. Other cases have been reported in patients with
polycystic kidneys and end stage renal disease.
Interestingly, the left kidney is affected more commonly
than the right.
Escherichia coli is isolated in 66% of patients and
Klebsiella species are reported in 26%. Proteus,
Pseudomonas, and Streptococcus species have been also
been reported.
Patients typically present with fever, abdominal or
flank pain, thrombocytopenia, acute renal failure, shock,
altered sensorium, nausea and vomiting, or dyspnea.
Laboratory data reveal leukocytosis with a left shift,
pyuria, infected urine, thrombocytopenia, an elevated
creatinine level, and positive results from blood culture.
Renal ultrasound images often reveal high echogenic
areas (air) with dirty shadowing. Hydronephrosis and
perinephric fluid may also be seen. CT scan will show
kidneys with a streaky and mottled or bubbly appearance.
Rimlike or crescent-shaped areas of gas may be found
in the perinephric area. Gas may also accumulate in the
adjacent structures, i.e. renal vein, inferior vena cava or
along the psoas muscle.
Fluid resuscitation and treatment with systemic
antibiotics are cornerstone to initial patient management.
Aggressive medical management and prompt surgical
intervention are also key. Although nephrectomy offers
the best outcome, a trial of conservative treatment with
drainage should be considered.
CHRONIC INFECTIONS
XANTHOGRANULOMATOUS PYELONEPHRITIS (XGPN)
Introduction
It represents an unusual suppurative granulomatous
reaction to chronic infection, often in the presence of
chronic obstruction from a calculus, stricture, or tumor.
XGPN is characterized histologically by the presence of
foamy lipid-containing macrophages (xanthoma cells),
diffuse infiltration with plasma cells, and histiocytes.
XGPN is more common in women than in men;
female patients with XGPN usually have a history of
recurrent or chronic urinary tract infections. Presenting
symptoms may include pyuria, flank pain, fever, dysuria,
pyuria, hematuria, proteinuria, or microscopic hematuria.
A palpable flank mass may be present, which may be
tender or demonstrate costovertebral angle tenderness.
XGPN is rare in children.
Forms
Two forms of XGPN are described:
1. Diffuse or global form (83–90%)
2. Focal form (10–17%).
XGPN has been termed the great imitator because
it may be misdiagnosed as a renal neoplasm, especially
if the lesion is focal.
Pathophysiology
XGPN almost always occurs unilaterally, and to the
author’s knowledge, only 1 patient with bilateral disease
has been described. The kidney is involved either globally
or focally. Changes of XGPN have been described in
kidneys destroyed as a result of pyonephrosis; in renal
cell carcinoma; in transitional cell carcinoma; and, rarely,
in a renal cyst. These focal pathologic changes are
detectable only by using histologic analysis, and they
usually do not appear on images.
On gross examination, the focal form of disease
usually is seen as a renal mass. On cut sections, the mass
appears as a yellowish white, solid or semisolid structure

that is indistinguishable from renal cell carcinoma. In
global disease, the kidney is enlarged, and indurated or
thickened perinephric fat is associated. The renal pelvis
is dilated and often contains staghorn calculus. Soft,
yellow nodules replace the corticomedullary junction, and
the calyces are filled with pus and debris.
Microscopically, both the focal and global forms
appear similar, with diffuse infiltration by plasma cells,
histiocytes, and lipid-laden foam cells. The foam cells
contain neutral fat and cholesterol (ester granules) that
test positive for periodic acid-Schiff (PAS) stain. PAS
staining is useful in differentiating these cells from the
clear cells found in renal cell carcinoma.
Laboratory testing frequently shows an elevated
erythrocyte sedimentation rate, leukocytosis, elevated
gamma-globulin levels, and anemia. Proteinuria and
pyuria are frequent. Urine cultures may reveal Proteus
mirabilis, Escherichia coli, Staphylococcal aureus, and
Klebsiella, Pseudomonas, and Enterobacter species. Urine
cultures may show negative results in 30–39% of patients
despite positive results from the kidneys. Occasionally,
different organisms may be isolated from urine and from
the removed kidney, underlining problems with
antimicrobial therapy.
Abnormal results in liver function tests are found in
as many as 50% of patients, and these are occasionally
associated with hepatomegaly. The cause of the liver
abnormalities is not known, but results of liver function
tests return to normal after treatment. Inflammation
resulting from XGPN may extend into the perirenal space,
pararenal space, ipsilateral psoas muscle, colon, spleen,
diaphragm, posterior abdominal wall, and skin.
Stages
XGPN has been described in three stages, as follows:
Stage 1: The lesion is confined to the kidney.
Stage 2: The pathologic process extends to the Gerota
space.
Stage 3: The process spreads to the paranephric space
and other retroperitoneal structures.
Incidence
In the USG: XGPN is found in 1–18% of patients in whom
Renal Infections 109
the kidneys require nephrectomy because of inflammatory
conditions.
Clinical Features
Sex: The male-to-female ratio is 1:3–4.
Age: Patients typically present at the age of 45–65 years,
but individuals of all ages may be affected, including
infants.
The typical patient is a middle-aged obese diabetic
female with a staghorn calculus, recurrent fever, dysuria,
and flank pain unresponsive to antibiotics. Other
symptoms include dysuria, pyuria, hematuria, proteinuria,
or microscopic hematuria. A palpable flank mass may be
present, which may be tender, or the patient may exhibit
costovertebral angle tenderness. XGPN is rare in children.
Frequently, urinary symptoms, fever, and flank pain
are absent, and minimal, if any, leukocytosis is found;
therefore, excluding renal cell carcinoma is difficult on
clinical grounds. Abnormal results in liver function tests
are reversible in as many as 50% of patients and
occasionally are associated with hepatomegaly. Patients
(40%) are often symptomatic for 6 months before XGPN
is diagnosed; however, the reported duration of symptoms
prior to presentation is extremely variable, extending from
3 days to 8 years.
Role of Radiology and Imaging
Classic excretory urographic triad of XGPN:
1. Obstructing stone
2. Renal enlargement
3. Nonexcretion of contrast material from the involved
kidney.
Plain KUB radiograph
Radiographic findings confirm the presence of renal
calculi.
A plain scout radiograph obtained before intravenous
urography typically shows a staghorn calculus.
Further smaller calcifications may be seen scattered
throughout the renal area, and a soft-tissue mass may
be identified.
If present, perinephric extension may produce ill-
defined renal margins, and a large soft-tissue mass may
be seen occupying the renal fossa.
110 Uroradiology: Text and Atlas
A thickened Gerota fascia is occasionally demon-
strated.
IVU
After the administration of contrast material, findings
depend on the morphologic type of XGPN. An absent
nephrogram or focally absent nephrogram may occur.
On nephrotomography, some opacification of the
kidney may occur, and a mass may be seen. A central
opacified mass may correspond to a xanthoma.
When the inflammatory process extends into
perinephric tissues, the renal outline is obscured.
Inflammation from XGPN may extend into the perirenal
space, pararenal space, ipsilateral psoas muscle, colon,
spleen, diaphragm, posterior abdominal wall, and/or skin.
This inflammation may obscure the renal outline.
Focal disease may appear as any other renal space-
occupying lesion, especially when it is not associated with
a calculus. The focal lesion usually shows no function
or a patchy nephrogram; this may be associated with
splaying and stretching of the calyces.
Retrograde pyelography
It may show a complete obstruction at the ureteropelvic
junction, infundibulum, or proximal ureter.
If a focal, solitary noncystic lesion is seen. The
differential diagnosis is that of a solid mass.
Ultrasonography
Is the initial examination in most patients of any age who
have urinary symptoms.
Findings:
Renal ultrasonographic findings demonstrate an enlarged
kidney that tends to maintain the reniform shape.
Loss of corticomedullary differentiation occurs.
Parenchymal calcification is uncommon, but when
present, it appears as central echogenic foci with
associated acoustic shadowing.
The renal pelvis is small due to fibrosis, but hypoechoic
dilatation occurs in calyces, which have an echogenic
rim.
The renal parenchyma is replaced by hypoechoic
masses, which frequently have low-level internal echoes.
Sound transmission is usually not enhanced because
the hypoechoic areas are not simple fluid-filled spaces.
Renal cortical tissue is markedly thinned and may have
scattered cystic collections representing abscesses.
The obstructing calculus usually does not create
shadowing.
Although the ultrasonographic features are not specific
to XGPN, the failure to depict a normal kidney associated
with a staghorn calculus suggests the diagnosis. Ultrasono-
graphic results are not routinely helpful in identifying renal
calculi, and sonography is less sensitive than other
modalities in demonstrating extrarenal spread.
CT Scans
It demonstrates retroperitoneal involvement more clearly
than do other images.
Findings: CT is the most useful investigation for the
preoperative assessment of XGPN. CT findings depend
on the morphologic type of XGPN.
In diffuse disease, CT scans may show a staghorn
calculus within a nonfunctioning kidney.
Although the reniform shape is maintained, the renal
parenchyma is destroyed and is replaced by low-attenua-
ting masses. The attenuation values in these masses vary
from –10 to 30 HU, depending on the lipid content.
The renal sinus may not be identifiable.
Fine calcifications are occasionally discerned within
the xanthomatous masses.
Small gas collections are sometimes seen in intrarenal
abscesses.
The Gerota fascia is invariably thickened and
identified.
Extrarenal extension of XGPN is well depicted on CT
scans and has been described both in the diffuse form
and the focal form.
Enhanced CT images show ring enhancement in areas
of granulation tissue; the xanthomatous tissue does not
enhance.
Definition of cortical renal abscesses is improved on
enhanced images.
In focal XGPN, a large mass is identified in an
otherwise functioning kidney. The mass usually is low
attenuating and fails to enhance on CT scans; however,
rim enhancement may be seen.
Calculus is often associated with the central portion
of the mass.

None of the features described above are characteristic
of XGPN, but they are sufficiently typical of the diffuse
form of XGPN to suggest a preoperative diagnosis in the
appropriate clinical setting especially by low CT values.
Focal disease cannot be diagnosed with confidence by
using radiologic images, and they should be regarded
as malignant until proven otherwise. The importance of
urine cultures in assessing an unexplained renal mass
cannot be overemphasized.
MRI
Documented findings include the presence of a large mass
in the renal fossa that appears multiloculated. Abscesses
and calyces demonstrate intermediate signal intensity on
T1weighted images and high signal intensity on T2
weighted images. Calcification and renal calculi appear
as signal voids. MRI appears to be extremely sensitive
in outlining perinephric spread. Residual parenchyma in
the unaffected kidney may appear normal.
MRI findings have been inconsistent, with varying
degrees of signal change described in areas involved by
the inflammatory process compared with normal
uninvolved renal tissue. In general, CT findings appear
to be more helpful than those obtained with other
modalities.
Angiography
It is occasionally performed to characterize a focal renal
mass further and to plan surgery. CT angiography and
magnetic resonance angiography are replacing conven-
tional techniques.
The features described in global disease include
stretching of segmental and/or interlobular arteries around
large avascular masses, similar to those seen in hydro-
nephrosis. Attenuation occurs in major renal arteries, and
peripheral vessels lack arborization. Inhomogeneity of the
nephrogram may mimic hydronephrosis. In the late
arterial phase, hypervascularity or arterial blush may be
noted around the periphery of the masses due to
granulation tissue.
The focal form of XGPN is usually hypovascular.
Intrarenal veins are stretched and compressed by
inflammatory renal masses. The renal vein may be
Renal Infections 111
encased or occluded, but inferior vena cava thrombosis
has not been described.
Angiography no longer plays a diagnostic role in
XGPN, although the authors occasionally use angio-
graphy to characterize focal renal masses or to plan
surgery. The invasive catheter technique is being replaced
with CTA and MRA with reformatting images.
Isotopic renography
It is useful in demonstrating relative renal functions prior
to surgery.
Limitations of the Modalities in General
No radiologic features are characteristic for XGPN, but
in the diffuse form, some CT and ultrasonographic fea-
tures may be sufficiently typical to suggest a preoperative
diagnosis in the appropriate clinical setting. Focal disease
cannot be diagnosed with confidence radiologically and
should be regarded as malignant until proven otherwise.
Differential Diagnosis
1. Renal fungal infections
2. Hydronephrosis
3. Avascular tumor (on angiography)
4. Pyonephrosis
5. Cystic renal carcinoma
6. Lymphoma
7. Renal tuberculosis.
Intervention
Needle biopsy may be helpful in differentiating XGPN
from other renal masses. Percutaneous nephrostomy may
be necessary to treat patients presenting with acute
septicemia due to an obstructive form of the disease
associated with pyonephrosis.
Treatment
The treatment of patients with XGPN usually involves
intensive antimicrobial therapy, but surgery is invariably
required to completely eradicate the infection and the
accompanying calculus and/or obstruction. Kidney-
sparing surgery may be undertaken in patients with focal
disease.
112 Uroradiology: Text and Atlas
RENAL TUBERCULOSIS
Introduction
The genitourinary tract is the second most common site
for tuberculous infection after the lungs. The infection
almost always affects the kidneys during the primary
exposure to infection but does not present clinically. The
spread to the kidneys usually is hematogenous from the
lungs, bone, or a GI tract focus. The true incidence of
renal tuberculosis may be underestimated since radiologic
findings may be absent and diagnosis is made by urine
culture. Genital tuberculosis is usually secondary to renal
tuberculous infection.
Renal involvement may be indolent, with a latency
period of more than 20 years after the primary infection
to the appearance of urinary tract symptoms of hematuria
and stone disease. In patients with renal tuberculosis,
treatment involves antituberculous drugs, with surgical
excision as an adjunct to antituberculous therapy. The
urine can be free of bacteria in less than 72 hours but
anatomic changes can progress as part of the healing
process. Females with genital tuberculosis may present
with infertility, menstrual disorders, and pain. Pregnancy
is unusual in the presence of genital tuberculosis. When
pregnancy occurs, spontaneous abortion or ectopic
pregnancy usually results. As a result of the lack of clinical
features, diagnosis of genital tuberculosis may be difficult.
Pathophysiology
Tuberculosis of the kidneys usually spreads by a
hematogenous route from pulmonary disease, although
it occasionally may be secondary to tuberculosis of the
GI tract or bone. By the time of diagnosis of renal
tuberculosis, the primary source of pulmonary infection
may be inactive or calcified. True prevalence of renal
tuberculosis is underestimated since radiologic signs may
be absent. Moreover, tubercle bacilli are found in 7–29%
of urine samples in patients with extrarenal tuberculosis.
The initial renal focus is usually a small tubercle in the
glandular and cortical arterioles. With the passage of time,
these lesions progress to form necrotizing lesions. The
disease spreads to the renal tubules and renal medulla
in which further tubercles develop, usually at the turn
of the loop of Henle, coalescing into larger necrotic
irregular cavities. The cavities usually communicate with
the renal collecting system, generally a calyx, with
formation of fistulae and stricturing. Eventually, the kidney
may become fibrotic and scarred.
The course of renal tuberculosis may be indolent, with
the appearance of few, if any, symptoms. Presentation
is usually late and symptoms usually occur as a result
as nonspecific urinary tract infection. Constitutional
symptoms usually do not occur or are sparse. Renal
tuberculosis is bilateral although radiologic findings are
asymmetric and unilateral in 25% of patients. Ultimately,
the kidney becomes atrophic, scarred, densely calcified,
and nonfunctioning (autonephrectomy) if not
appropriately treated. Ureteric involvement occurs as a
descending infection secondary to kidney infection.
Tubercles may involve the transitional epithelium, causing
mucosal granulomas that project into the ureteric lumen.
Eventually, fibrosis occurs in the ureter. These pathologic
processes can be demonstrated radiologically by the
appearance of a beaded, saw-toothed, corkscrew, or
pipestem ureter depending on the stage of disease.
Usually, the upper and/or lower third of the ureters are
involved. The vesicoureteric junction may become fixed
and patulous, allowing vesicoureteric reflux. The kidneys
are always involved when ureteric tuberculosis is present.
Bladder tuberculous infection is almost always
secondary to renal involvement. Initially, interstitial cystitis
occurs, eventually causing bladder mucosal ulceration and
thickening of the bladder wall. End-stage disease causes
scarring and bladder fibrosis, resulting in diminished
capacity of the urinary bladder. Bladder wall calcification
is uncommon. Bladder tuberculosis may be complicated
by fistulae or sinus tract formation, although these
complications are rare.
Tuberculosis of the seminal vesicles usually occurs as
a result of hematogenous spread. Descending infection
is unusual. The same pathologic processes occur as within
the bladder (ie, mucosal tuberculomas, ulceration,
fibrosis). Calcification is present in only 10% of patients.
Unlike seminal vesicle tuberculosis, tuberculosis of the
prostate is usually secondary to descending infection from
the kidney. However, the kidneys may occasionally
appear normal, suggesting subclinical infection or a

hematogenous prostatic infection. The tuberculous
cavities or abscesses may discharge into the surrounding
tissues forming sinuses or fistulae to the perineum or
rectum, eventually resulting in a watering-can perineum.
The scrotum and urethra may be involved, although
rarely. Urethral involvement may be complicated by
urethral strictures.
Tuberculosis may cause chronic epididymitis and
epididymoorchitis. Tuberculous granulomas may develop
within the testes and epididymis and rarely may be
complicated by abscesses and discharging sinuses.
Thickening of the scrotal wall and tunica albuginea and
moderate hydrocele also may be observed occasionally.
Female genital tuberculosis is invariably secondary
to tuberculosis elsewhere, and spread may be hemato-
genous, via the lymphatic system, or by direct spread
from adjacent organs. Patients usually present with
infertility, menstrual irregularity, and pain. Pregnancy is
rare in the presence of genital tuberculosis and is often
complicated by ectopic pregnancy or spontaneous
abortion.
Incidence
The urogenital tract is the second most common site of
tuberculosis after the lung. Renal tuberculosis is associated
with active pulmonary tuberculosis in 4–8% of patients.
Genitourinary tuberculosis appears to be fairly common
in developing countries.
Clinical Features
Race: Incidence of renal tuberculosis varies throughout
the developing world where the infection is common. The
disease is more common in higher socioeconomic groups,
similar to the pattern found in Europe. Renal tuberculosis
is uncommon in tropical Africa despite the fact that other
forms of tuberculosis are common. High prevalence is
observed in Eastern Europe, Asia and, particularly,
Bangladesh, India, and Pakistan. On the Indian
subcontinent, renal tuberculosis is associated with
diabetes.
Sex: Males are affected more often than females.
Age: Individuals of any age can be affected, but most
patients present younger than 50 years.
Renal Infections 113
Renal tuberculosis may remain dormant for many
years after the kidneys become seeded during the primary
tuberculous infection. With reactivation, one or more renal
abscess is produced. Patients usually become
symptomatic, with extension of the disease to the renal
pelvis and ureters causing hydronephrosis. Specific
symptoms may be lacking until the hydronephrotic kidney
becomes secondarily infected.
Symptoms of frequency and urgency of urination and
dysuria may ensue, with development of tuberculous
cystitis. However, long before patients become
symptomatic, sterile pyuria, albuminuria, and hematuria
are present but cultures for pyogens demonstrate negative
results. Diagnosis usually is achieved using imaging,
cystoscopy, and culture of acid-fast bacilli from early
morning urine specimens. Needle aspiration biopsy is a
last resort when urine cultures are negative.
Preferred Examination
Plain KUB
Plain radiography may provide a clue to the diagnosis
and may guide further imaging.
Since the type and distribution of calcification may
be suggestive of tuberculosis, CT scans (with the ability
to depict calcification) may be helpful.
IUV
While intravenous urography remains the primary
modality used to image patients with renal, ureteric, and
bladder tuberculosis, findings of urinary tuberculosis are
also detectable on ultrasound, CT scan, or MRI.
While intravenous urography is the primary modality
for imaging renal tuberculosis, CT scans clearly reveal
changes of renal tuberculosis, particularly in advanced
disease. Changes such as calcification, calyceal dilatation
without a hydropelvis, parenchymal loss, and extrarenal
spread are well depicted.
Radiological Findings
Findings in the kidneys
IVP is abnormal in 85–90% cases and gold standard in
diagnosis of Renal TB Distinctive features of Renal TB
on IVU:
114 Uroradiology: Text and Atlas
1. Moth-eaten Calyx “smudged” papillae (the earliest
sign) and diminished excretion of contrast, focally
or generally.
2. Hydrocalicosis with infundibular strictures (most
common sign)
3. Caliceal truncation
4. Phantom calyx/amputed calyx
5. Kerrkink sign (kinking of renal pelvis)
6. Parenchymal calcifications (amorphous/granular/
curvilinear/punctate/confluent tooth paste) involving
entire kidney (putty kidney)
7. Cavities communicating with collecting system
8. Nonfunctioning kidney with dystrophic calcification
9. Lobar calcification (unique feature)
10. Putty kidney (Tuberculous pyonephrosis)
11. Autonephrectomy
12. Nephrolithiasis
13. Signs of extrarenal active or inactive tuber-
culosis may be apparent, such as osseous or
paraspinal changes of tuberculosis and old healed
calcified splenic, hepatic, lymph node, and adrenal
granulomas. Chest radiographs may show evidence
of active or healed tuberculosis in 50% of patients.
The remainder have normal chest studies.
14. Changes of renal tuberculosis are unilateral in
75% of patients.
15. A tuberculoma usually starts as a localized
caseating lesion, most commonly in the upper pole
of the kidney, although it may arise anywhere.
16. With time, the nidus of infection enlarges and
ruptures into a neighboring calyx, discharging
necrotic caseous material and distorting the calyx.
At this stage, a variety of radiologic abnormalities
may be demonstrated, including smudged
papillae due to surface irregularity of the papillae,
a moth-eaten calyx (early sign), irregular tract
formation from the calyx to the papilla, and large
irregular cavities with extensive destruction
secondary to papillary necrosis. Changes may be
detected on intravenous urography, retrograde
pyelography, and on some CT and MRI scans.
17. The kidney enlarges initially but subsequently
may return to normal or become atrophic.
18. Once communication with a tuberculous cavity is
established, the involved calyx becomes an
ulcerocavernous lesion.
19. The finding of hydrocalyces with no pelvis dilatation
or an atrophic pelvis is highly suspicious for
tuberculosis. The cephalic retraction of the inferior
medial margin of the renal pelvis at the PUJ, or
“the hiked up renal pelvis,” is another suggestive
urographic/pyelographic change.
20. The infection spreads to the stem of the involved
calyx, which may develop a stricture, thus sealing
off the involved calyx (phantom calyx). This
change may be apparent as a mass lesion.
21. Dilated calyces often are associated with
infundibular strictures and may be demonstrated
radiologically. The lesions may be depicted better
on cross-sectional imaging.
22. If the ulcer or stricture extends to the renal pelvis
or the pelvic ureteral junction, urine outflow ob-
struction may occur. In this instance, intravenous
urogram may show delayed function, clubbed
calyces, or absence of function. At this stage, a “putty”
kidney may be depicted. Ultrasound, CT scan, and
MRI can better depict an outflow obstruction.
23. If tuberculous infection extends directly to the rest
of the kidney, the entire kidney becomes a bag of
caseous necrotic pus.
24. Plain radiographs may reveal dystrophic
calcification, but intravenous urography usually
shows absence of function, although a faint
nephrogram may be demonstrated if some function
remains.
25. Associated renal calculi are found in as many
as 20% of patients with renal tuberculosis.
26. The final outcome of renal tuberculosis is
autonephrectomy, which represents a small,
shrunken, scarred, nonfunctioning kidney and
is often associated with dystrophic calcification.
27. Renal calcification is present in as many as 50%
of patients and may appear as an amorphous
granular opacification associated with active
granulomatous infection and dense punctate
calcification, which is associated with healed
tuberculomas.

28. Shell-like/egg-shell calcification within the
renal collecting system and a thinned-out renal
cortex are more a feature of autonephrectomy.
29. Renal infection may extend into the perirenal or
pararenal spaces and/or the psoas sheath.
Findings in the ureters
1. Although ureteral involvement is usually unilateral,
bilateral changes are asymmetric when they occur.
The most common site of involvement is the lower
third of the ureter.
2. Mucosal granulomas may be demonstrated as
intraluminal filling defects on intravenous urogram or
retrograde pyelography.
3. Mucosal ulceration is difficult to depict radiologically
but rarely may show as irregularity in the contrast-
filled ureter.
4. The involved ureter may appear beaded or with a
corkscrew configuration as a result of alternating
dilatations and strictures.
5. Ultimately, the ureter may form a rigid, aperistaltic,
shortened tube.
6. TB of ureter produces mucosal and wall ulceration,
fibrosis, stricture and calcification.
Saw tooth ureter, beaded ureter, short, straight, rigid
and narrow ureter especially terminal segment.
Calcification is however rare in ureteral tuberculosis
and when occurs involves lower segment to.
Findings in the bladder
1. When tuberculosis involves the bladder, progressive
thickening of the bladder wall occurs with increasing
diminution of bladder volume.
2. Trabeculation may develop.
3. The vesicoureteric junction orifice may become fixed
and patulous, resulting in vesicoureteric reflux.
4. The vesicoureteric junction may be affected by
progressive narrowing, causing stenosis and resulting
in bilateral hydroureters and hydronephrosis.
5. Bladder wall calcification is rare.
6. Bladder tuberculosis may be complicated by fistulae
or sinus tract formation although these complications
are rare and are demonstrated better on CT and MRI
scans.
Renal Infections 115
7. Symmetrical small spastic, and thickened bladder or
small multilobular bladder (Thimble bladder). As
compared to tuberculosis of kidney, that of bladder
is rarely associated with calcification. Usually bladder
calcification in schistosomiasis is linear and continuous
and occurs chiefly at the bladder base going on to
encircle the bladder lumen.
Findings in the prostate
1. Prostatic tuberculous cavities or abscesses may
discharge into the surrounding tissues, forming sinuses
or fistulae to the perineum or rectum and eventually
resulting in a watering-can perineum. These changes
are demonstrated best on MRI scans.
2. Plain radiographs may show dense calcification within
the prostatic bed, which can also be demonstrated
on ultrasound and CT images.
3. Urethrography or a micturating cystourethrogram
typically demonstrates filling of variable dilated
prostatic ducts associated with destruction of the
prostatic parenchyma.
4. Sloughing and irregular cavitation of the prostate
eventually may result in a smooth-walled cavity that
replaces the prostate.
Findings in the seminal vesicles
1. Calcification is depicted on plain abdominal
radiographs in as many as 10% of patients with
tuberculosis of the seminal vesicles.
2. Calcification of the seminal vesicles is more common
in patients with diabetes mellitus.
Findings in the epididymis and vas deferens
1. Calcification of the epididymis and vas deferens may
be visualized on plain radiographs of the male pelvis
and must be differentiated from diabetes and schisto-
somiasis.
Findings in female genital tuberculosis
1. Tuberculosis can affect any part of the female
genital tract but more commonly involves the
fallopian tubes.
2. Hydrosalpinx and pyosalpinx are usually large and
may appear as soft tissue masses on plain abdominal
radiographs.
116 Uroradiology: Text and Atlas

3. The pyosalpinx may be calcified. awareness of sonographic changes associated with

4. Tuberculous tuboovarian abscesses may calcify, are tuberculous infection may improve diagnostic accuracy
observed on either side of the pelvis, and sometimes and help avoid clinical mismanagement and surgical
appear as well-defined homogeneous masses, explorations in patients with genital infections associated
occasionally with areas of increased density with wet-type tuberculosis (peritonitis).
presumably due to the granuloma. Serpiginous or
Findings: Sonography is not as sensitive as intravenous
linear calcification can occur in the tubes.
urogram or CT scanning because of problems with
5. HSG findings may suggest a diagnosis. HSG
identifying calyceal, pelvic, or ureteric abnormalities.
appearances vary as widely as the pathologic
The kidney may appear entirely normal in both early
changes observed in this condition.
later stages of renal tuberculosis; later, hypoechoic/cystic
6. Tubal involvement is almost always bilateral but the
masses communicating with the collecting system may
degree of involvement varies between the two sides.
be observed, representing “excluded” calyces without
7. HSG may demonstrate a flask-shaped dilatation of
dilatation of the renal pelvis.
the fallopian tubes due to obstruction at the fimbria.
Large abscesses may distort the renal contour and
Occasionally, the obstruction is at the uterine end
may mimic tumors or cysts.
of the tube; therefore, the tubes are not depicted.
Usually, renal tuberculomas appear as a solid mass
8. HSG may demonstrate sacculation with infiltration
with diminished through transmission; however, a diffuse
of contrast material resembling salpingitis isthmica
infiltrative type of renal tuberculosis has been described
nodosa. Infiltration around the tube, which creates
in which the kidney may appear normal on ultrasound
a cloudlike appearance of the delicate sinus tracts,
images.
has also been described.
Fibrosis and scarring may appear identical to chronic
9. A characteristic HSG feature suggestive of
pyelonephritis or multiple renal infarcts.
tuberculosis has been described in which irregular
Calcification is common in the late stages and varies
contrast distribution occurs resembling a cotton-
from punctate foci to dense calcification of the entire
wool plug. Focal irregularity and areas of
kidney, which is associated with hydronephrosis or
calcification may occur within the lumen of the
atrophy.
fallopian tubes.
Bacille Calmette-Guérin (BCG) delivered intravesi-
10. Obstruction of the fallopian tubes is not
cally in the treatment of superficial bladder cancer may
pathognomonic for tuberculosis and may occur with
be complicated by a renal granuloma, probably as a result
other pathology.
of vesicoureteric reflux. The granulomas have been
11. In end-stage disease, the tubes become rigid, lack
reported as small intrarenal hypoechoic masses.
peristalsis, and resemble pipelike conduits.
Bladder tuberculosis causes fibrosis and mucosal
12. Within the endometrial cavity, tuberculous endo-
thickening, leading to a thick-walled small-volume bladder
metritis findings include adhesions, which may vary
with vesicoureteric reflux.
from very thin to very thick synechiae. In end-stage
Tuberculosis is an unusual cause of chronic epididy-
disease, the uterine cavity may be obliterated
mitis and epididymoorchitis. In tuberculous epididymitis,
completely.
the epididymis may appear heterogeneous and hypo-
13. Within the pelvis calcified lymph nodes and ovaries
echoic, associated with concomitant hypoechoic lesions
may be observed.
in the testes and a discharging sinus. The most notable
USG finding is an enlarged and heterogeneous epididymis,
Sonographic findings in the appropriate clinical setting predominantly in the body and tail.
may help avoid orchidectomy for benign testicular Testicular involvement is shown as a diffusely
disease. In patients with female genital tract tuberculosis, hypoechoic testis or focal intratesticular areas.

Thickening of the scrotal wall and tunica albuginea and
moderate hydrocele may be observed occasionally.
Follow-up scans may reveal intratesticular abscesses. The
testes may become as hard as stone, which is associated
with extratesticular calcification.
Sonographic findings may suggest genitourinary
tuberculosis in the appropriate clinical setting and findings
may help eliminate the treatment choices using renal
surgery or orchidectomy for benign disease. In patients
with female genital tract tuberculosis, awareness of
sonographic changes associated with the infection may
improve diagnostic accuracy and avoid clinical mismana-
gement and surgical explorations in genital infections
associated with wet-type (peritonitis) tuberculosis.
CECT
CT scans may demonstrate dense prostatic calcification
in tuberculous prostatitis, sloughing, and irregular
cavitation of the prostate, eventually resulting in a smooth-
walled cavity that replaces the prostate.
Since the type and distribution of calcification features
may be suggestive of tuberculosis, CT scans (with the
ability to depict calcification) may show relatively specific
findings. While CT scans clearly demonstrate changes
of advanced disease, sensitivity in early disease may be
low because scans do not demonstrate the detailed
calyceal anatomy.
MRI
It is useful when fistulae or tuberculous tracts are formed.
Findings: MRI is good at depicting tuberculous cavities,
sinuses tracts, fistulous communications, and extrarenal
and extraprostatic spread. Multiplanar MRI allows
evaluation of the disease extent in the prostatic bed and
the presence of sinuses and fistulae. MRI contrast agents
facilitate evaluation. MRI is also useful in the evaluation
of peritonitis and adnexal masses.
MRI is an excellent modality at depicting extraorgan
spread and discharging sinuses and fistulae but
calcification is not readily demonstrated.
Limitations of all techniques in general:
1. All imaging findings may be normal in patients with
early genitourinary tuberculosis.
2. Genitourinary calcification may occur in patients with
diabetes mellitus and schistosomiasis.
Renal Infections 117
3. Brucellosis also may mimic tuberculosis.
4. The differential diagnosis of an adnexal mass is wide.
5. A congenital megacalyx and focal papillary necrosis
may mimic renal tuberculosis radiologically. Papillary
necrosis can result from tuberculosis.
6. A tuberculous testicular granuloma may mimic a
testicular neoplasm on ultrasound images.
7. Small areas of calcification are difficult to detect on
MRI scans although they are pivotal to the diagnosis
of tuberculosis.
8. HSG findings are also nonspecific; blockage of the
fallopian tubes is not pathognomonic for tuberculous
salpingitis and may occur as a result of other forms
of infective processes of the genital tract.
RNI
Isotope renography is the most sensitive imaging modality
available for the assessment of renal function.
Findings: The role of radionuclides in imaging patients
with renal tuberculosis is confined to assessment of relative
renal function by renography when surgery or nephrec-
tomy is contemplated. The agents used are technetium
99m
Tc diethylenetriamine pentaacetic acid (DTPA),
technetium 99mTc mercaptotriglycylglycine (MAG-3), or
iodine I 123 orthoiodohippurate (OIH).
Mortality/Morbidity
Untreated, the end result of renal tuberculosis is auto-
nephrectomy. The exact incidence of infertility in patients
with genital tuberculosis is unknown but in parts of the
world where tuberculosis is frequent, genital tuberculosis
is an important cause of infertility.
SCHISTOSOMIASIS (BILHARZIASIS)
Introduction
It is one of the most common parasitic infestations in
the world and is caused by the Schistosoma genus of
fluke. The form of schistosomiasis affecting the urinary
tract involves Schistosoma haematobium. The other
forms, Schistosoma japonicum, Schistosoma mansoni,
and Schistosoma mekongi affect the gastrointestinal tract.
The disease is endemic in the Middle East, India, Africa,
Central America, and South America, yet it is rare in the
United States.
118 Uroradiology: Text and Atlas
Pathophysiology
Schistosomiasis typically affects the urinary system,
especially the bladder, but ureteral involvement is found
in as many as 30% of patients. The eggs of Schistosoma
flukes are excreted into the urinary tract, causing an intense
granulomatous reaction and subsequent calcification.
The life cycle of the schistosome begins with the
passage of egg-containing urine into freshwater regions
where the intermediate host is a snail. When the eggs
are hatched, miracidia are produced. These penetrate
the snail and eventually form into cercariae. The cercariae
penetrate the skin of human hosts and are eventually
carried to the liver, lymphatic system, lungs, and venous
system, where the fluke matures. The flukes live and
copulate in the portal vein in most individuals, except
for S haematobium, which migrates to the perivesical
venous plexus through the hemorrhoidal plexus.
The fluke attaches to the walls of the venous plexus
by means of two suckers. The female fluke then deposits
eggs into the venules of the urinary bladder wall or distal
ureter. Some eggs penetrate the lumen of the bladder,
but most become encapsulated in the vesical tissues,
causing an inflammatory granulomatous reaction, fibrosis,
foreign body reaction, and calcification of the dead ova.
The eggs, not the flukes, cause tissue damage to the host.
The degree of calcification is roughly correlated with the
number of eggs deposited. The earliest calcification of
dead eggs occurs 50–120 days after deposition. The
female fluke can produce as many as 3500 eggs per day.
Frequency
Schistosomiasis is the most common cause of bladder
calcification worldwide, causing as many as 56% of
known calcifications in the bladder. It is endemic to the
Middle East and Africa.
Clinical Features
Sex: Schistosomiasis affects men more often than
women, with a ratio of approximately 9:1.
Age: Schistosomiasis usually occurs in individuals
younger than 30 years.
It typically causes a chronic low-grade infection with
flulike symptoms. Clinical symptoms may include fatigue,
headache, a stiff neck, a lack of energy, and neurologic
symptoms due to central nervous system (CNS) compli-
cations.
Urologic symptoms include either microscopic or gross
hematuria, dysuria, urinary frequency, and urinary
urgency.
Differential Diagnosis
1. Tuberculosis is the only real differential diagnosis. The
propagation of both entities is different because
schistosomiasis starts in the bladder and ascends,
whereas tuberculosis starts in the kidney and
progresses distally. In addition, the bladder is usually
distensible with schistosomiasis, but it is fibrotic and
limited in volume with tuberculosis.
2. Primary amyloidosis
3. Cytostatic medications
4. Alkaline incrustation cystitis.
Role of Radiology and Imaging
Ureter: Involvement of the ureters occurs in as many
as 65% of patients. The ureters commonly have persistent
filling in the lower segment; dilated ureters are another
finding. Ureteral strictures can be found, and, as the
disease progresses, beading of the lower ureteral segment
may be observed. Subsequent ureteral fibrosis leads to
calcifications of the distal ureter, which have a
characteristic pattern of linear or parallel calcifications
on plain radiographs. As many as 80% of the
strictures occur in the bladder wall near the
junction with the ureters. Dilatation of the ureter is
common. This is often caused by vesicoureteric reflux,
stenosis of the ureter, or an edematous ureteral wall that
causes deficient peristalsis.
Bladder: With regard to the bladder, indistinctness or
hazy changes are caused by submucosal edema and
pseudotubercles. The body forms an intense granuloma-
tous reaction to the ova, and fibrosis ensues. This fibrosis
traps the ova in the tunica propria of the bladder wall
where the ova die and become calcified. The calcification
is not in the fibrous tissue, but it is caused by calcified
ova. The calcification spreads around the bladder wall
and can completely encircle the bladder, appearing as
a curvilinear ring (curvilinear ring calcification of
bladder). A calcified area in the bladder has an estimated

500,000 to 1 million eggs per cubic centimeter. The
extent of the calcification is roughly correlated
with the number of eggs in the bladder lumen.
The bladder wall becomes fibrotic, but in contrast to
tuberculosis, it is still distensible and maintains a
normal capacity as schistosomiasis mainly involves the
submucosal layer, while in tuberculosis muscular layer
is primarily involved.
Plain radiographs: Conventional radiographs are not
useful until calcifications have developed in the bladder
or ureters Calcification in the wall of the bladder or distal
ureters can be identified on plain radiographs.
Intravenous urography (IVU), retrograde uretero-
graphy, or cystography
1. Mucosal irregularity,
2. Inflammatory pseudopolyps
3. Ureteritis cystica
4. Ureteral dilatation and stricture, and
5. Reduced bladder capacity.
With regard to IVU, most of the findings are in the
bladder and distal ureter because the kidneys remain
normal until late in the disease.
USG: Ultrasound may be normal in early or mild cases,
but often shows wall thickened up to 1 cm or more and
single or multiple polypoidal lesions, which may be sessile
or wave-like and may protrude in the lumen of ureter.
Changes are most marked in the bladder base and trigone.
CT: Compared with other techniques, CT better
delineates the extent of the calcifications related to schisto-
somiasis. Bladder calcifications are characteristically
Renal Infections 119
linear, coarse, or floccular in schistosomiasis. Usually, the
calcifications are first seen in the base of the bladder on
plain radiographs, but they more commonly appear in
the anterior wall of the bladder on CT scans. The thickness
of the ureteral wall is better evaluated with CT than with
any other modality. Later fibrosis and calcification
develops which may be seen as ‘egg-shell or linear’
calcification in the submucosa of the bladder and
the distal ureters.
Mortality/Morbidity
The most serious complication of urinary tract schisto-
somiasis is an increased incidence of squamous cell
carcinoma of the bladder. Additional complications
include urolithiasis, ascending urinary tract infection,
urethral and ureteral stricture with subsequent hydronep-
hrosis, and renal failure.
Treatment
It involves mainly two drugs: praziquantel and metr-
ifonate. Oxamniquine is another medication.
MALACOPLAKIA
It is a rare inflammatory disease usually associated with
chronic E. coli infection.
The histologic hallmark of the disorder is the presence
of basophilic inclusions, called Michaelis-Gutmann
bodies, within large eosinophilic macrophages.
It is usually unilateral. C findings are nonspecific, and
renal parenchymal malacoplakia may be indistinguishable
from a neoplasm.
120 Uroradiology: Text and Atlas
RENAL TRAUMA
INTRODUCTION
Renal trauma is the most common urologic trauma and
occurs in 8–10% of patients with significant blunt or
penetrating abdominal trauma. In most cases, major renal
injuries are associated with injuries to other major organs.
The goal in trauma care is to resuscitate the patient,
to diagnose injuries, and to implement appropriate
therapeutic measures as quickly as possible. Efficient
organization of trauma centers with optimal resuscitation
techniques and early imaging leading to accurate staging
are needed to determine appropriate clinical manage-
ment. Radiologists serve an integral role in the multidis-
ciplinary approach to achieve that goal, playing a large
part in the diagnosis and staging of injuries. Furthermore,
interventional radiologists help manage arterial injuries
using angiography with transcatheter embolization.
PATHOPHYSIOLOGY
Causes and Associated Features
Renal trauma can result from a variety of mechanisms.
In the United States, motor vehicle accidents are the most
common cause of blunt abdominal trauma leading to
renal trauma. Fall from a height and assault, including
penetrating injuries, are less common causes. In rare
cases, renal trauma occurs secondary to iatrogenic causes
and renal masses (e.g. angiomyolipoma) can manifest
with bleeding after a minor trauma.
Most renal injuries are associated with hematuria
(95%), which can be profused in more severe renal
trauma. However, in vascular pedicle injury or avulsion
of the pelviureteric junction (PUJ), hematuria may not
be present. Because the most contemporary trends in
trauma care, including renal trauma, call for less invasive
procedures, trauma imaging by a skilled radiologist is
increasingly important. By accurately distinguishing
patients that can be optimally managed conservatively
from those who need surgery, radiologists can improve
the long-term outcome of patients.
Grading
Renal injuries are graded by the American Association
for the Surgery of Trauma (AAST) on the basis of the
depth of injury and the involvement of vessels or the
collecting system as follows (Table 9.1):
Grade 1
Hematuria with normal imaging studies
Contusions:
Nonexpanding subcapsular hematomas
Grade 2
Nonexpanding perinephric hematomas confined to the
retroperitoneum

Superficial cortical lacerations less than 1 cm in depth
without collecting system injury.
Grade 3
Renal lacerations greater than 1 cm in depth that do not
involve the collecting system.
Grade 4
Renal lacerations extending through the kidney into the
collecting system.
Injuries involving the main renal artery or vein with
contained hemorrhage.
Segmental infarctions without associated lacerations.
Expanding subcapsular hematomas compressing the
kidney.
Grade 5
Shattered or devascularized kidney
Ureteropelvic avulsions
Complete laceration or thrombus of the main renal
artery or vein.
INCIDENCE
Renal trauma is the most frequent urologic trauma,
occurring in 8-10% of patients with considerable blunt
Table 9.1: Contrast-enhanced spiral CT grading of blunt renal injury
Injury Description or CT finding
grade
I. Superficial laceration(s) involving cortex
Renal contusion(s)
<1 cm subcapsular hematoma
Perinephric hematoma not filling Gerota’s space and no active
bleeding
II. Segmental renal infarction
Deeper renal laceration extending to
Medulla, with intact collecting system
>1 cm subcapsular hematoma with intact renal function
Perinephric hematoma limited to and not
Distending the perinephric space:
No active bleeding
III. Laceration extending into collecting system with
Urine extravasation limited to retroperitoneum
Perinephric hematoma distending perinephric space
Or extending into perineal spaces; no active bleeding
IV. Fragmentation (3 or more segments) of the kidney
(usually partially devitalized with large perinephric hematoma
Devascularization >50% of parenchyma
Main renal pedicle injury
Active bleeding by CT
Extravasation of urine into peritoneal
Cavity or extensive extravasation
Subcapsular hematoma compromising renal perfusion
Urorenal Trauma 121
or penetrating abdominal trauma. Blunt trauma is the
overwhelming cause of 80% of renal injuries.
CLINICAL FEATURES
Clinical findings that can exist in a patient with renal
trauma include hematuria, flank hematoma, lower rib
fractures, and vital sign instability, such as hypotension.
About 95% of significant renal injuries are associated with
hematuria; however, hematuria may be nonexistent,
especially with renal vascular injuries and UPJ avulsion
or ureteral injuries. Of 1000 blunt abdominal trauma
patients with only microscopic hematuria and without
hypotension, only approximately 1–5 have significant
injury of the urinary tract. Therefore, microhematuria
alone is not an absolute indication for imaging.
PREFERRED INVESTIGATIONS
Indications in General
Specific imaging of the genitourinary tract is indicated
for patients with gross hematuria, microscopic
hematuria, and hypotension or in patients with
injuries associated with renal trauma, such as the
lumbar spine, lower rib, or transverse process
fractures. CT is the current preferred imaging technique
used in these situations.
Radiography
The use of radiography for blunt abdominal trauma is
nearly nonexistent, despite being an important tool in
the primary evaluation of chest and skeletal trauma. In
general, abdominal radiography has been replaced by
CT because of its widespread accessibility and, to some
degree, ultrasonography. However, radiography still plays
a role in the assessment of penetrating trauma to the
abdomen.
Intravenous Urography (IVU)
Before the widespread use of CT, the traditional tools
used to search for genitourinary trauma were intravenous
urography (IVU), standard cystography, and retrograde
urethrography. Today, however, IVU has a more limited
role, as CT has replaced many of its applications.
Occasions that may still warrant the use of intravenous
urethrography include the imaging of hemodynamically
122 Uroradiology: Text and Atlas
unstable patients on their way to surgery or urologic
imaging of a patient already in the operating room. This
approach is used to confirm that two kidneys are present
if nephrectomy might be needed.
The traditional tools for assessing genitourinary injury
have been IVU, standard cystography, and retrograde
urethrography. The role of IVU, however, has become
more limited as CT has become more available. IVU may
still be used if CT is not readily available, for unstable
patients going to surgery or for urologic imaging of a
patient in the operating room. These studies are typically
performed as a one-shot IVU, which consists of the
acquisition of a scout radiograph, a radiograph taken
immediately after the injection of contrast material, and
a third radiograph obtained approximately 10 minutes
after the injection. Additional delayed radiographs may
be necessary to assess delayed excretion of contrast
material if present and to detect the presence of urinary
contrast extravasation (Figure 9.1).
Findings that may be revealed by IVU include the
loss of the renal outline or psoas shadow if there is
perinephric hemorrhage, diminished or absent excretion
or contrast extravasation. The ureters should also be
visualized to evaluate for ureteral injury or displacement,
and the presence of a contralateral functioning kidney
FIGURE 9.1: Contrast extravasation with improper visualization of
lower pole calyces on right due to trauma
should be confirmed in the event that significant unilateral
renal injury warrants nephrectomy. However, the findings
on IVU may not always accurately specify the cause or
extent of renal involvement, while minor vascular injury
or urinary extravasation may be missed. A non-visualized
kidney (nephrogram/pyelogram) does not necessarily
represent significant renal trauma.
Retrograde Pyelography
Retrograde pyelography is primarily useful when there
is a suggestion of ureteral, UPJ, or renal pelvic injury
and delayed images were not made or were not sufficient
to exclude these injuries on CT or IVU. However, this
is not routinely needed; drawbacks to retrograde
pyelography include its impracticality in the emergent
evaluation of a severely injured patient and the fact that
it does not characterize renal parenchymal injuries.
VCUG
If a trauma patient has blood at the urethral meatus, a
high-riding prostate, or an inability to void, urethral
trauma should be investigated by means of retrograde
urethrography. In almost all cases, this should be done
prior to the placement of a Foley catheter, unless the index
of suspicion is low. In this case, a pericatheter urethrogram
can be obtained later.
Ultrasonography
Has limited clinical usefulness in the evaluation of renal
trauma. The main application of this technique in the
trauma setting has been for the focused abdominal
sonography for trauma (FAST) scanning, with the
goal of detecting any free fluid in an unstable patient.
The primary advantage to this technique is that it can
be performed in a matter of minutes in the trauma bay
while a patient is being resuscitated. In many cases, the
presence of fluid is an indication for exploratory
laparotomy by surgeons.
Ultrasonography, however, is limited in the types of
injuries it can depict. First, although sonography can
depict-free fluid in the abdomen and pelvis, it lacks the
ability to distinguish the type of fluid or source of fluid.
Further, ultrasonography has not demonstrated significant
sensitivities and specificities to adequately search for solid

FIGURE 9.2: Subcapsular hematoma
organ injuries. In most cases, even if a solid organ injury
is found or if injury is clinically suggested but not found,
CT examination is still indicated if the patient’s condition
is stable.
Findings: The use of abdominal ultrasonography for
trauma patients remains controversial, particularly for
detecting renal and urologic injuries. Despite this, in the
United States, ultrasonography has achieved moderate
acceptance for evaluating a patient with blunt abdominal
trauma (Figure 9.2).
In the trauma setting, sonography is usually performed
as a FAST scan for the primary purpose of identifying
free fluid in the unstable patient. In most circumstances,
FAST scans can be executed in the few minutes during
patient resuscitation in a trauma bay. The examination
includes probing six locations for the existence of free
fluid: the right upper quadrant with the hepatorenal recess,
the left upper quadrant with the splenorenal recess, both
paracolic gutters, the pelvis and its various peritoneal
cavity recesses, and the pericardial space. If the
examination demonstrates the presence of fluid, surgeons
will generally perform an exploratory laparotomy.
In situations in which sonography has been used to
screen blunt abdominal trauma as part of a management
Urorenal Trauma 123
algorithm, there is some variability in the training of the
individual performing the examination. In some
institutions, radiologists or sonologists perform the study,
but in many centers, the trauma surgeon or emergency
physician do so. These specialists may have little training
in clinical sonography and virtually no training in its
technical aspects. Therefore, their ability to execute high-
quality examinations has been seriously questioned.
However, if the radiology staff is to perform trauma
sonography, the service must be readily available at all
times.
Although sonography can depict free fluid in the
abdomen and pelvis, it cannot be used to make the
clinically important distinction between extravasated
urine, blood, or other types of fluid. Moreover,
ultrasonography cannot depict the source of the bleeding.
Ultrasonography may demonstrate renal laceration, a
change in echogenicity of an injured kidney, or a decrease
in the usual perinephric echogenicity if perinephric fluid
or hemorrhage is present. However, if sonograms are
negative and if noteworthy hematuria is present, or if
the sonogram is positive, CT is still indicated for evaluation
of the injury if the patient is stable. For this reason, the
use of sonography is probably best reserved for the rapid
evaluation for intraperitoneal fluid in the unstable patient
who may require urgent surgery.
Computed Tomography
In general patients with blunt trauma and abdominal
symptoms, hypotension or an appreciably depressed level
of consciousness consistently undergo abdominal and
pelvic CT, which serves as the most comprehensive
diagnostic tool for evaluating such a patient. Other
imaging modalities, such as ultrasonography, answer
questions of limited scope and do not afford the broad
evaluation provided by CT. As such, CT is the primary
tool for staging all injuries to the abdomen.
If, during the CT examination, considerable
perinephric fluid is noted (particularly on the medial side
of the kidney), or if a deep laceration is noted, urinary
extravasation should be investigated by using delayed
CT images.
While investigating the genitourinary tract, examiners
should also thoroughly explore for active hemorrhaging,
124 Uroradiology: Text and Atlas
as urgent surgery or embolization is frequently needed
in such situations to prevent exsanguination.
If findings consistent with a bladder injury, such as
gross hematuria or pelvic ring fracture, are present,
conventional cystography or CT cystography should be
performed after initial CT. Compared with a standard
pelvic CT with intravenous contrast enhancement,
cystography has a higher sensitivity for detecting bladder
injuries. However, CT cystography is equal to or better
than conventional cystography, if adequate bladder
distension can be achieved with contrast material. CT
cystography also provides the ability to differentiate
between intraperitoneal, extraperitoneal, or combined
bladder rupture.
Limitations: CT is the overwhelming leader for
diagnosing and staging renal traumatic injuries. The main
drawback to CT, however, is the time to complete a CT
examination, especially if CT equipment is not available
near the trauma bay. For the most critically injured
patients, this time is extremely limited; therefore,
ultrasonography has found some clinical appeal as a quick
method for searching for critical injuries.
Findings: Across all imaging modalities, CT is the most
comprehensive diagnostic tool for assessing patients with
blunt abdominal trauma. CT can be used to evaluate
a large breadth of intra-abdominal injuries with accuracy,
and hence, it has a primary role in evaluating the trauma
patient. Further, the success of CT in staging abdominal
injuries has contributed to the growing trend toward
non-operative management of traumatic abdominal
injuries. As such, the CT scanner should be as close to
the trauma bay as possible to minimize patient transport
time.
CT technique: To best evaluate blunt abdominal
trauma, the technique with which a CT is obtained must
first be optimized. Conventional axial CT scanners can
provide sufficient scans; however, helical CT scanners
offer a considerable gain in speed and quality.
Multidetector-row CT (MDCT) scanners are even more
powerful than single-slice helical CT scanners because
their thin-section, high-quality images can be obtained
more quickly. As a result of shorter scanning times, less
opportunity is available for motion or breathing artifact
to appear. Furthermore, MDCT is advantageous because
of its improved ability to depict injuries such as active
arterial extravasation. Apart from faster scanning time
that MDCT provides, it also utilizes the tube-heat capacity
in a more efficient manner. This allows multiple,
successive CT examinations to be carried out without
the need to wait for the CT tube to cool.
Intravenous and oral contrast material: Intravenous
contrast enhancement is essential for abdominal CT.
Without intravenous contrast enhancement, solid-organ
injuries such as renal lacerations can often be impercep-
tible. In addition, active arterial extravasation is only
detectable with intravenous contrast material. Its usage
with helical CT and MDCT scanners has further increased
the frequency with which active arterial extravasation is
seen. For adults, the typical contrast dose is 100–150
mL, whereas for children, the dose is 1.5–2 mL/kg. The
desirable injection rate is at least 2 mL/s; however, rates
of 3-4 mL/s allow for optimal enhancement of the
vasculature and parenchyma. A low-osmolarity, non-ionic
contrast agent is standard.
Contrast material, when given orally, also has clinical
utility in aiding in the detection of bowel injuries.
Fortunately, oral contrast material is safe, even for
children. As soon as an abdominal CT scanning is
requested, 400–600 mL of a dilute solution, for example,
4% diatrizoate meglumine in tap water, is given by mouth
or by nasogastric tube. Images of trauma patients are
then obtained without delay. Thus, the stomach,
duodenum, and proximal jejunum are typically the only
structures opacified; fortunately, these are the most
common sites of bowel injury. Finally, some authors
suggest withdrawing the nasogastric tube into the distal
esophagus during the scan in an attempt to reduce upper
abdominal streak artifact.
For CT, an image thickness of 5 mm or less prevents
major volume-averaging artifacts, and a scanner pitch
of 1.5:1 for single-slice helical scanners optimizes speed
while preventing excessive section-profile broadening. For
an MDCT scanner, a pitch greater than one but less than
two hastens image acquisition yet usually results in
excellent image quality. Further, by scanning at speeds
less than the maximum table speed or with a detector
 Urorenal Trauma 125

configuration narrower than the image thickness usually

produced, thinner sections can be retrospectively
reconstructed. This is sometimes needed to evaluate
subtle injuries or associated spine or bony pelvic injuries.
Some institutions regularly scan through the kidneys
a second time during the urographic phase of
enhancement to aid in detection of subtle injuries of the
parenchyma and collecting system. At the author’s
institution, images of trauma patients are regularly
evaluated as they are obtained while the patient is still
in the CT scanner. If noteworthy perinephric or
periureteral fluid is found, urinary contrast extravasation
is investigated by taking images delayed at 5–15 minutes.
If clinical findings, such as gross hematuria or pelvic
ring fracture are present, and if bladder injury is a concern, FIGURE 9.3: Small right renal laceration involving cortex
cystography or CT cystography should be performed.
Standard CT with intravenous contrast enhancement has
a lower sensitivity for these injuries. CT cystography offers
a few advantages over conventional cystography. First,
the patient can be evaluated by CT cystography after
the initial scan without the need to move to another
location. CT cystography can also distinguish intraperi-
toneal, extraperitoneal, or combined bladder rupture.
When CT cystography is performed, the urinary
bladder is first drained by Foley catheter following the
abdominal CT scan. The CT cystogram is done with either
standard scans or scout imaging. The cystogram should
be performed before intravenous injection of contrast FIGURE 9.4: Deeper laceration extending to medulla
media. In the adult, a minimum of 300 mL of dilute but with intact PCS
contrast media is necessary. If this is normal, drainage
and wash out (bladder flushed with sterile fluid) may be
performed but is not routinely needed.
CT Interpretation (Figures 9.3 to 9.7): CT scans for
blunt abdominal trauma must be meticulously reviewed
for proper interpretation. On evaluation, urgent life-
threatening injuries, such as a large hemoperitoneum,
a large or tension pneumothorax, pneumoperitoneum,
signs of hypovolemic shock, or active arterial
extravasation, should be sought out first. This should be
followed by a thorough interrogation for injury of the
abdomen and pelvis: liver and right paracolic gutter;
spleen and left paracolic gutter; upper abdominal organs, FIGURE 9.5: Laceration extending to collecting system with
including the stomach, duodenum, pancreas, gallbladder perinephric hematoma
126 Uroradiology: Text and Atlas
FIGURE 9.6: Fragmented left kidney with hematoma
FIGURE 9.7: Devascularized left kidney
and biliary tree; retroperitoneum, including the adrenals,
kidneys, inferior vena cava, and aorta; small bowel, colon,
and mesentery; pelvis, including the urinary bladder;
muscles, including the abdominal wall, psoas, iliacus,
and gluteals; bones, including the spine and pelvis; and
thighs.
To perform a complete evaluation, the entire scan must
be scrutinized with three different window/level settings:
soft tissue, lung, and bone. The entire systemic review has
been called the “every-organ-on-every-slice”
approach. The authors believe that, with the modern
Picture Archiving and Communication System (PACs)
workstation, image review is best accomplished by rapidly
paging through the images multiple times, with special
attention to one organ at a time; hence, “every slice of
every organ”. With this method, renal injuries can be readily
identified and classified for proper treatment.
Grade 1 injuries
AAST grade 1 renal injuries include hematuria with
normal imaging, contusions, and nonexpanding
subcapsular hematomas; overall, this grade accounts for
80% of renal injuries. In CT images, contusions are
perceived as ill-defined or sometimes sharply marginated
areas of reduced enhancement and excretion. A
segmental infarction, which is an AAST grade 4 renal
injury, is differentiated from contusions by a lack of
enhancement altogether.
Subcapsular hematomas usually appear as a
hyperattenuating fluid collection between the renal
parenchyma and the renal capsule, at times deforming
the underlying kidney. These hematomas are less
common than perinephric hematomas in blunt abdominal
trauma. Small, subcapsular hematomas often take on a
crescent shape, whereas larger hematomas may appear
elliptical and compress the renal parenchyma. On rare
occasions, the hematoma may progressively enlarge and
compress the kidney enough to lower renal perfusion.
This may result in reactive hypertension (Page kidney).
Grade 2 and 3 injuries
Renal injuries that are classified as grade two include
nonexpanding perinephric hematomas contained by the
retroperitoneum and superficial cortical lacerations less
than 1 cm in depth without injury to the collecting system.
On CT, a perinephric hematoma often appears as an
ill-defined, hyperattenuating fluid collection located
between the Gerota fascia and the renal parenchyma.
More often than not, such a hematoma is associated with
underlying injury, though they can occur in isolation.
Thus, when a perinephric hematoma is discovered, a
thorough investigation of the kidney should be
undertaken to look for associated renal injury. Unlike a
subcapsular hematoma, even a large perinephric
hematoma does not traditionally deform the kidney.
Renal lacerations are seen on CT as jagged or linear
parenchymal disruptions that can contain fresh or clotted
blood. The laceration may thus show attenuation higher
than that of water, but this would occur without the
contrast enhancement present in the renal parenchyma.

By definition, grade two renal lacerations are less than
1 cm in depth, while grade three lacerations are greater
than 1 cm in depth. Both grade two and grade three
renal lacerations, however, do not involve the collecting
system. As such, there would be no evidence of urinary
contrast extravasation on delayed CT.
The treatment of most grade one, two, or three renal
injuries is usually conservative, except when a vigorous
active hemorrhage is present. In such cases, the active
hemorrhage may be treated successfully with selective
catheter embolization in an otherwise stable patient.
Occasionally, continued bleeding or extravasation can
lead to complications and higher morbidity if not identified
and managed appropriately. Follow-up CT is useful for
restaging the renal trauma and helps in identifying the
patients with progressive worsening on conservative
management. Appropriate intervention in these patients
can help prevent complications.
Grade 4 injuries
Grade 4 renal injuries include renal lacerations that extend
into the collecting system, injuries to the main renal artery
or vein with contained hemorrhage, and segmental
infarctions without associated lacerations. The first of
these, renal lacerations with collecting system involve-
ment, frequently produce extravasation of urine or
contrast agent. Extravasation such as this should be
thoroughly sought any time a laceration extends through
the kidney or substantial perinephric fluid is seen on CT,
especially if that fluid is around the renal hilum. Delayed
images allow contrast material to filter into the collecting
system, providing adequate views of any urinary
extravasation.
Under many circumstances, the healing of even large
urinary extravasations can occur with conservative
treatment; however, stenting is sometimes necessary to
facilitate the process. Surgical debridement or repair is
usually necessary only when the laceration is
accompanied by significant devitalized renal tissue,
particularly when concomitant intraperitoneal injuries are
also present. The main purpose of such a procedure is
to prevent the development of urinoma, infection, or
abscess. In the absence of such repair, a nephrectomy
may be needed later to prevent sepsis.
Urorenal Trauma 127
On CT, renal segmental infarctions appear as well-
delineated, linear or wedge-shaped, often multifocal
and nonenhancing areas that extend through the
parenchyma in a radial or segmental orientation.
Thrombosis, dissection, and laceration of segmental renal
arteries are primary causes of segmental infarctions, and
such infarctions are frequently associated with other renal
injuries. These injuries are treated conservatively, as they
often resolve spontaneously or result in relatively minor
renal scaring. In 6–20% of patients, hypertension may
develop as a delayed complication; however, this often
resolves or can be medically managed.
Grade 5 injuries
Grade 5 renal injuries include a shattered or
devascularized kidney, UPJ avulsions, and complete
laceration or thrombosis of the main renal artery or vein.
The first of these, a shattered kidney, essentially describes
the extreme of multiple renal lacerations, often with
devitalized areas due to infarction, and urinary
extravasation resulting from injuries to the collecting
system.
A different type of grade five renal injury, the UPJ
injury, characteristically involves a medial or circumrenal
urinoma on CT. Such injuries are caused by a shearing
force on the renal pelvis. Complete avulsion or partial
tear of the UPJ occurs when rapid deceleration of the
kidney pulls on the relatively fixed ureter and renal blood
supply. Imaging can distinguish a partial tear from a
complete avulsion by the presence of contrast agent in
the distal ureter. In many cases, hematuria is absent or
minimal. Treatment for complete UPJ tears is surgical
repair, but some partial tears can be managed with
stenting and/or observation. When a UPJ injury is
undiagnosed and when the proximal collecting system
is not drained, an urinoma can develop. This may lead
eventually to a nephrectomy.
With CT imaging, a devascularized kidney appears
nonenhancing. Often, little hematoma or other sign of
injury is depicted. In some cases, CT angiography shows
a blind-ending renal artery. Retrograde opacification of
the renal vein from IV contrast indicates an acute injury
indicating the need for immediate emergency surgery to
reestablish blood flow. In late evaluation, the renal vein
128 Uroradiology: Text and Atlas
is thrombosed, and this reverse flow is not seen. The
cortical rim sign may be apparent, but not early. This
usually indicates a dead kidney with rare recovery of renal
function (if it ever occurs). In the absence of other
associated injuries, hematuria is many times nonexistent.
The most common cause of a devascularized kidney
is an incomplete renal artery tear with thrombosis; a
complete tear of the renal artery with an extensive
hematoma or active bleeding is less common. When they
occur, these injuries are often present with other renal
injuries. This association contributes to the poor renal
outcome after attempted repair; therefore, the care of
stable patients is usually expectant. For patients with active
bleeding or major parenchymal disruption, treatment is
usually nephrectomy except in the case where there is
injury to or absence of the contralateral kidney. A potential
complication of these injuries is hypertension; it can
develop weeks to months after the initial injury in as many
as 40–50% of patients. This often resolves or can be
medically managed, but nephrectomy is sometimes
necessary.
Another less frequent form of vascular pedicle injury
is damage to the main renal vein. One type of such an
injury is laceration of the renal vein. On CT, this usually
presents with medial or circumrenal subcapsular or
perinephric hematoma. Thrombosis is a second type of
renal vein injury that is depicted on CT as a filling defect
or as nonenhancement of the vein. A delayed or persistent
nephrogram may be present when thrombosis results in
complete occlusion. This may be lethal in the adult.
Vascular extravasation of contrast material
Contained or active hemorrhage is indicated by bright
enhancement with attenuation similar to that of nearby
arteries within a laceration or around an injured kidney
during the early phases of CT scanning. Active
hemorrhage appears as an ill-defined, flame-shaped, or
waterfall-shaped area on CT, with an associated fresh
hematoma. The hematoma often demonstrates
circumferential or dependent layering of older and fresher
hemorrhage. On the contrary, contained hemorrhage or
pseudoaneurysm is somewhat bound and contained
within the renal parenchyma or laceration. If active
extravasation of arterial contrast material from the main
renal artery or lacerated kidney appears present,
immediate transcatheter embolization or surgery may be
needed to prevent exsanguination.
Delayed bleeding or rare cases of hypertension
occasionally result from persistent pseudoaneurysms.
Renal lacerations from blunt or penetrating trauma can
also produce arteriovenous fistulas. Initially, these may
be difficult to detect, but they can enlarge over time. The
results of this may be delayed bleeding, hypertension,
or high-output cardiac failure.
MRI
Findings: For stable patients with a strong contraindication
for iodinated contrast material, MRI with a gadolinium-
based contrast agent can be helpful in assessing a renal
injury; however, for the acutely injured patient, MRI is
usually not practical because of motion artifacts and the
examination time.
RNI
It may be used to evaluate renal function after injury
or to directly evaluate the patient for urinary injury,
especially those with an extravasation of urine.
Scintigraphy is generally not useful in the acute trauma
setting because of its low specificity and inability to
evaluate for injuries outside the urinary tract.
Angiography
Angiography has played in the initial diagnosis of trauma
to the renal vasculature has diminished with the advent
of faster CT scanners. Despite this development, use of
angiography in the management of vascular and
exsanguinating solid-organ injuries has continued to
increase, with the trend toward nonoperative manage-
ment of trauma. Furthermore, angiography with
transcatheter embolization is becoming the standard of
care for treating stable patients with vascular injuries, such
as traumatic pseudoaneurysms and active arterial
bleeding.
Findings: Prior to the common availability of CT,
angiography was often used to initially diagnose renal
arterial or parenchymal aberrations found on IVU. Today,
however, faster CT scanners and the increased detection

of active arterial extravasation have limited the use of
angiography for the initial diagnosis of traumatic injuries.
Moreover, CT can also depict many injuries not seen on
angiography.
On the other hand, the role of angiography in the
management of vascular and exsanguinating solid-organ
injuries continues to rise in parallel with the increasing
emphasis on nonoperative management of trauma.
Angiography with transcatheter embolization is becoming
the standard of care for patients with many vascular
injuries, such as pseudoaneurysms and active arterial
bleeding resulting from renal trauma.
RADIOLOGIC INTERVENTION
Radiologic interventions in the setting of acute renal
trauma are mainly limited to those of a vascular nature.
Examples include embolization of bleeding vessels and
arteriovenous fistulas.
MANAGEMENT OF RENAL INJURY
Treatment options must be weighed against related
mortalities and morbidities. In the evaluation for treatment
options, the AAST injury grade is correlated with the
apparent need for surgery to repair or remove the injured
kidney.
Non-operative management may be successful or
even preferred in stable patients with high-grade injuries.
The preservation of long-term renal function is often better
when renal injuries are treated non-operatively. Thus,
unless there is extensive devitalized tissue, active
hemorrhage, a large injury to the collecting system with
progressive renal compression on follow-up or with
ureteral disruption, conservative management is often
chosen for renal injuries. Overall, with modern manage-
ment techniques, renal salvage rates approach 85–90%.
MORTALITY/MORBIDITY
Mortality and morbidity rates for renal injuries vary with
the severity of renal injury, the degree of injury to other
organs, and the treatment plan utilized. Thus, treatment
options must be weighed against related mortalities and
morbidities. In the evaluation for treatment options, the
AAST injury grade is correlated with the apparent need
for surgery to repair or remove the injured kidney.
Urorenal Trauma 129
SUMMARY
Blunt trauma, usually deceleration injury from motor
vehicle accidents, may result in shearing injury to the
renal arteries, resulting in hematoma formation, dissection
or disruption. A hematoma may form between the renal
cortex and the kidney fibrous capsule. These subcapsular
hematomas accumulating in a closed space, may create
increased tissue pressure and reduced tissue prefusion.
As renal perfusion decreases, the kidney reacts to
increase perfusion by secreting renin. In turn, this causes
sytemic hypertention. This entity is referred to as Page
kidney. This physiologic entity may also result from other
processes, including renal cystic disease or any renal mass.
URINARY BLADDER TRAUMA
INTRODUCTION
Trauma continues to be a major cause of morbidity and
mortality in all areas of the world. Many immediately
life-threatening insults are to the vital organs or their blood
supplies, and many diagnostic skills and studies are meant
to rapidly reveal these complications. However, other life-
threatening conditions must be addressed in a timely
manner to avoid morbidity and occasionally mortality.
Ideally, these conditions are diagnosed simultaneously,
rather than individually, and the search for a universally
applicable study is underway. Immediate surgery or other
approach is commonly the diagnostic and therapeutic
procedure of choice if the patient is exsanguinating or
if his or her condition is deemed otherwise unstable by
the trauma physicians. One semi-emergent condition is
trauma to the bladder, especially trauma that results in
uroperitoneum. Sepsis can develop within 24 hours in
these injuries if surgery with repair is not performed.
MECHANISM OF INJURY
Bladder trauma can occur in a number of settings. They
are usually considered in the context of whether blunt
or penetrating trauma were the inciting events. Blunt
trauma is responsible for a rather large number of severe
associated injuries, such as pelvic, splenic, renal, aortic,
bowel, and hepatic insults. Injury is not necessarily
localized to areas obviously traumatized.
130 Uroradiology: Text and Atlas
Penetrating injury is often secondary to missiles,
impaling objects, and knives. These injuries are of varying
severity and often, but not always, result in damage to
more focal areas. Some missile injuries have a vaguely
estimable trajectory when one considers the entrance and
exit wound, and many knife wounds still have the
impaling blade in place at the time of presentation.
CLASSIFICATION OF INJURY
Any discussion of bladder trauma must include the
classification of injury and associated injury patterns. In
bladder trauma, five grades of insults are recognized.
Type I injuries are partial tears of the mucosa. This is
the most common injury pattern of multisystem trauma
patients and associated with blunt trauma for obvious
reasons. These patients present with hematuria and
suprapubic pain, but no rupture is present, and findings
on cystography, conventional CT, and CT cystography
are normal, unless an intraluminal hematoma is present.
This pattern is generally only mentioned to recognize that
it is not a major bladder injury.
Type II, or intraperitoneal bladder ruptures, account for
approximately 10-20% of all major bladder injuries. Most
commonly, this is the result of a direct blow to the
distended organ. The bladder is weakest at its dome where
reinforcing tissue is absent, thus intraperitoneal rupture
usually occurs as a result of a rift in the bladder dome.
Intraperitoneal fluid is observed bathing loops of bowel
and presents in the paracolic gutters and mesenteric folds.
Type III, or interstitial pattern, is described as intramural
or partial-thickness laceration of the intact serosa. Only
CT cystography is commonly diagnostic and
demonstrates intramural contrast within the bladder wall.
This condition is most often secondary to blunt trauma.
However, laceration by pelvic fragments or a penetrating
object, with minimal serosal damage, can present with
a primarily interstitial pattern with minimal extracystic
urine demonstrated.
Type IV bladder injury is extraperitoneal. It is the most
common bladder rupture. In blunt trauma, one theoretic
cause for laceration of the lower bladder is from secondary
injury from pelvis fragments. Simple extraperitoneal
ruptures involve urine buildup in the perivesicular space.
More complex patterns of urine tracking involve different
fascial planes. Urine or contrast material can be seen in
the thigh or scrotum with disruption of the inferior fascia
of the urogenital diaphragm (perineal membrane). Urine
also may breach the Scarpa or Camper fascia, and it
may be observed in the rectus sheath or even under the
skin.
Type V, or combined rupture, consists of both intra-
peritoneal and extraperitoneal urine. It occurs in only
5-12% of bladder ruptures and results from penetrating
and blunt trauma.
CLINICAL FEATURES
Sex: No significant difference.
Age: Bladder trauma does not appear to be age specific.
Trauma to the bladder is associated with significant
trauma to the pelvis and intra-abdominal organs. Thus,
patients present in a wide variety of ways with large
differences in the stability of their condition. Commonly,
they have few symptoms secondary to their bladder injury
or even rupture. The literature suggests that they have
no strong propensity to develop peritonitis initially, even
with a large amount of uroperitoneum.
Physical examination findings suggestive of bladder
trauma include vague peritoneal signs or abdominal
tenderness. However, more suggestive findings include
isolated suprapubic tenderness, pelvic instability, or lap-
belt ecchymosis. One study revealed that approximately
4% of children with lap-belt ecchymosis suffered bladder
rupture.
Unlike upper renal trauma, bladder injury is essentially
ruled out when no RBCs are observed in the urine.
Urogenital injury is suggested when microhematuria is
present (defined as >25,000–35,000 RBCs per high-
powered field). Gross hematuria is highly suggestive and
certainly warrants full investigation. Gross hematuria is
present in 95% of patients, and the remaining patients
have microscopic hematuria.
A problem can arise when bladder trauma is presumed
to be the cause of hematuria because this finding is not
specific and can stem from more ominous sources such
as renal fracture. Collect urine from the first few hundred
milliliters of the initial sample to prevent errors in
interpretation. Furthermore, always rule out urethral
trauma before placing a Foley catheter, especially when

gross hematuria is present. Suggestive findings include
blood at the meatus, a high-riding prostate, the patient’s
inability to void, perineal hematoma or scrotal swelling,
and pelvic fracture.
Bladder injury is strongly associated with pelvic
fracture. Of bladder ruptures associated with pelvic
fracture, 80% are extraperitoneal. Pelvic fracture is
associated with bladder injury in 80% of patients, but
the reverse is not true: Only 10% of pelvic fractures are
associated with major bladder trauma. When a pubic rami
fracture is present or if pubic symphysis diastasis is present,
maintain a higher index of suspicion. A great deal of effort
has been made to determine which pelvic fractures are
associated with bladder injury. Patients with disruption
of the pubic symphysis, pubic rami, and vertically unstable
pelvic fractures have high degrees of concomitant bladder
trauma, whereas those with isolated acetabulum, femur,
and ileac crest fractures have a low incidence of bladder
injury or rupture.
ANATOMICAL BASIS
The bladder is located within the bony pelvis and in adults
is considered to be a mostly extraperitoneal organ. There,
the bladder, prostate, and proximal urethra are protected
by one of the most secure bony enclosures in the body.
It has a tetrahedral form when empty and has four primary
surfaces. A superior, posterior, and two inferolateral
surfaces define the shape. The superior portion is
triangular and lined completely by the visceral
peritoneum. This portion extends into the abdomen when
distended and has little support from other structures.
It is considered to be a dome when distended and contacts
the uterus in the female and the sigmoid colon in addition
to loops of bowel in the male.
The posterior surface or fundus of the bladder is
anterior to the rectum but remains mostly retroperitoneal.
A male bladder has the seminal vesicles coursing between
the posterior bladder wall and the rectum. The posterior
base of the bladder is supported by the rectum and
secured by the rectovesicular ligaments. In females, the
posterior and superior surface is loosely fixed to the upper
vaginal wall and uterus.
The pelvic floor musculature and overlying loose areolar
tissue support the inferolateral margins of the bladder.
Urorenal Trauma 131
The pubovesicular, medial, and paired lateral umbilical
ligaments strengthen the association with the anterior
body wall. The space of Retzius exists anterior to the
bladder. This area is loose connective tissue that allows
easy mobilization of the bladder from other surrounding
structures. There is little preventing motion of the bladder,
in that the only rigidly fixed point is the bladder neck.
This is the primary adaptation allowing distention during
filling.
PREFERRED INVESTIGATIONS
Radiologic examination is of paramount importance and
should be performed to identify and classify the injury
and to plan surgical repair, but it should not hinder patient
treatment and stabilization. Several radiologic evaluations
are appropriate, ranging from CT cystography to basic
retrograde cystography. All have been moderately well
studied and require different equipment, locations,
protocols, and operator expertise. Always consider the
stability of the patient’s condition with regard to airway
patency and circulation during transfer and radiologic
evaluation of the patient.
The amount and type of radiologic evaluation required
depends on the patient’s condition and on the size of
the area that may be affected. Many patients in stable
condition require extensive screening, thus diagnostic
procedures should ideally provide views of large area with
quick and common preparation. For many patients in
unstable condition or those with penetrating abdominal
injuries who are immediately treated in the operating
theater (at the discretion of the surgeon) intraoperative
radiologic evaluation is needed.
Retrograde Cystography
Retrograde cystography performed after urethrography,
was considered the criterion standard for evaluation of
bladder trauma. However, in recent years, support has
grown for using CT cystography in proper diagnosis. Initial
studies were not indicative of the reliability of CT when
retrograde contrast enhancement was not used. However,
contemporary studies have overwhelmingly
demonstrated that the technique is both sensitive and
accurate, provided that adequate bladder distention with
at least 300-400 mL of contrast material is achieved before
132 Uroradiology: Text and Atlas
the study is performed. In diagnosing bladder rupture,
CT cystography, performed with 400 mL of contrast
material administered in a retrograde fashion, is as
accurate as plain radiography with retrograde
cystography.
Ultrasonography
Ultrasonography is not sensitive or specific enough to
be useful for evaluation of bladder rupture.
However, blood clots and at times site of tear in
bladder wall can be depicted (Figure 9.8).
Retrograde cystograms have long been used for
detecting bladder rupture. They are nearly 100% sensitive
for detecting rupture, provided adequate distention is
accomplished and postvoiding images are obtained.
However, they are time consuming, the examinations are
costly when one considers value relative to the benefit,
and they require extra radiography that does not occur
in addition to necessary trauma evaluation. Furthermore,
they are not useful in thoroughly evaluating other
structures present in the abdomen and pelvis.
CT Retrograde Cystograms
CT retrograde cystograms are completed in the radiology
suite when routine spiral scans of the head, neck, chest,
and abdomen and pelvis are performed. The same
retrograde introduction of contrast agent is generally
performed as with retrograde cystography. However,
multiple images, including postvoiding and oblique views,
are not necessary as in plain radiography. Thus, this
FIGURE 9.8: Large clot in bladder with tear in its posterior wall
procedure is less time consuming and, some would argue,
less costly. At 1 hospital cited in the literature, the cost
of CT cystography was $500 or more, a marginal increase
over a plain radiographic examination. Costs should be
specifically evaluated at each institution.
A final step is the washout study. After the full-bladder
findings are recorded (on radiographs or CT scans), the
bladder is drained. If no residual contrast enhancement
is present, the examination is completed, and the results
are negative. If residual contrast enhancement is present
in the bladder area, fluid (e.g. sterile water) is used to
lavage the bladder. If no residual contrast enhancement
is noted after drainage, the examination is completed,
and the results are negative. If contrast enhancement
remains, a bladder wall injury is present.
CT Cystography
CT cystography may be used somewhat less often in
patients not undergoing CT for another reason. In a study
of 157 patients with hematuria, an absence of free fluid
on abdominopelvic CT was a strong negative predictor
of bladder rupture. In these patients, not performing
cystography may be reasonable.
Further study is warranted regarding this matter.
Perhaps one of the greatest advantages of retrograde CT
cystography with prior abdominopelvic CT is the ability
to detect renal parenchymal injury. In these patients,
intravenous urography is not necessary, as it commonly
is with traditional retrograde cystography.
A few studies have focused on delayed evaluation
of the bladder. For example, the use of contrast material
for chest and abdominal CT (for which a large amount
is routinely required) has been studied. In these
examinations, the contrast agent was allowed to distend
the bladder in an anterograde fashion. However, this
distension occurs at the expense of valuable time, because
the Foley catheter should be clamped for at least
20–30 minutes to have any opportunity to achieve
accurate results. Furthermore, if preexisting renal
insufficiency or renal pedicle injury is present, this method
may be inadequate.
The author does not recommend this diagnostic
strategy for the reasons mentioned. Because results of

recent studies have also cast doubt on the consistent
accuracy of this method in the evaluation of blunt trauma,
its use is discouraged.
Limitations of Techniques
Cystography generally has served to greatly decrease
trauma morbidity and mortality by helping in successfully
screening for bladder rupture. Little doubt exists
concerning the accuracy of plain-film cystography, as long
as a bladder hematoma does not occlude a rift in the
bladder wall and prevent dye from flowing out into the
surrounding spaces. The primary concern is that the
examination often does not occur in parallel with other
radiologic examinations of patients with trauma who
require CT scanning.
A caveat should be noted: A normal cystogram finding
does not exclude bladder rupture. At surgery,
intraperitoneal or extraperitoneal extravasation may be
found. The consideration in this scenario is the spasm
of the detrusor muscle, which is possibly secondary to
the irritation effect of the contrast medium that causes
a leak to become sealed. With general anesthesia, the
detrusor relaxes; this is associated with the eventual
intraoperative leak.
CT cystography is faster than plain radiographic
studies; it has no labor-intensive requirements for
completion; and it can be used to diagnose large
hematomas of the bladder, which potentially could overlie
an occult breech in the bladder wall. Furthermore,
classification of bladder injury patterns requires CT
scanning because cystography addresses perforations but
not more-subtle findings.
Consider the cost in each prospective hospital,
because the monetary costs, which favor classic
cystography, may not reflect actual benefits. For instance,
because X-ray technologists currently are in short supply,
increasing their use adds to the expense. Furthermore,
time is valuable in the trauma setting, especially because
patients in seemingly stable conditions can deteriorate
quickly, and a more-rapid evaluation can facilitate their
transfer to the trauma intensive care unit or operating
theater. In general, the author believes that evaluation
with CT cystography is the study of choice when patients
already require transfer to the radiology suite for
Urorenal Trauma 133
CT evaluation. This is true especially when microhema-
turia is present and a possibility of renal trauma exists.
MORTALITY/MORBIDITY
Morbidity and mortality is most commonly infectious in
nature. Therefore, complications are usually associated
with bladder rupture. Bladder disruption occurs in
5-10% of patients with pelvic fractures, and the type of
perforation, with respect to classification, is important to
prognosis. Broadly classified, approximately 50-85% of
ruptures are extraperitoneal (many of which have
associated pelvic fractures), 15-45% are intraperitoneal,
and only 1-10% of disruptions are both.
In the event of intraperitoneal rupture, morbidity and
mortality are greatly influenced by preexisting urinary tract
infection. Thus, sepsis can ensue within 24 hours in
certain circumstances. Treated properly with operative
repair and urologic consultation, nearly all patients with
intraperitoneal bladder ruptures have few or no long-term
complications.
URETHRAL TRAUMA
INTRODUCTION
Trauma to the urethra can be attributed to guns, knives,
surgical or urologic instruments, blunt trauma, straddle
injuries, or penile fracture. Most male posterior urethral
injuries, however, are the result of blunt pelvic trauma
most often associated with a vehicular accident or a fall
from a height. Most cases of anterior urethral trauma result
from straddle injuries.
The male posterior urethra is entirely encased within
the rigid pelvis, a protective structure that must be
disrupted before the posterior urethra can be damaged
by blunt external trauma. The potential for urethral
trauma is thus influenced by the extent of the pelvic injury,
and this potential has been classified as no risk, low risk,
and high risk). Examples of no risk injuries include isolated
fractures of the acetabulum, ilium, or sacrum; low-risk
injuries include single ischiopubic ramus or ipsilateral rami
fractures; and high-risk injuries include straddle fractures
or Malgaigne fractures. Overall, disruption of both the
anterior and posterior sides of the pelvic ring introduces
greater risk of urethral trauma.
134 Uroradiology: Text and Atlas
Damage of the posterior urethra is thought to
occur as its support mechanism becomes disrupted. As
soft tissue becomes compressed, the puboprostatic
ligament ruptures, disconnecting the prostate from the
anterior pubic arch. This mobilizes the prostate and
bladder. In many cases, a hematoma develops inferior
to the prostate from sheared periprostatic vessels. The
prostate is then driven cephalad by the growing
hematoma. The posterior urethra, however, is firmly
attached to the pubic arch by the perineal membrane.
The resultant shearing force stretches or ruptures the
urethra in varying locations as described by radiographic
findings).
Anterior urethral injuries are seen in a small
minority of patients because of the mobility of the anterior
urethra compared with the posterior urethra. Most cases
are the result of straddle incidents, in which the patient
falls on the crossbar of a bike or the top of a fence. Force
from the structure on the perineum compresses the
corpora spongiosum and bulbous urethra against the
pubic symphysis, disrupting the urethra. In some mild
cases, the resulting injury will go untreated; however, a
stricture develops over time. The patient presents at
this time with an inability to void. In some cases, the
patient is unaware of the relationship to the past straddle
injury.
If the Buck fascia remains intact, the injury will be
limited to the space between the fascia and the tunica
albuginea. If, however, the Buck fascia is also disrupted,
a hematoma may spread within the confines of the Colles
fascia. Thus, blood or contrast material extravasation may
extend to the scrotum, perineum, or anterior abdominal
wall. Contrast would not extend into the thigh because
of the insertion of the Colles fascia into the fascia lata
of the thigh.
Penile fracture results only when the penis is erect,
and the injury results in disruption of the corpora and
tunica albuginea.
Among women, the most common types of urethral
injuries described are longitudinal tears and avulsion-
distraction injuries, with the later attributed to more severe
lateral compressive pelvic trauma.
INCIDENCE
Most posterior urethral trauma cases in males result from
pelvic injury. Among male pelvic traumas, the reported
frequency of urethral injury varies widely from 1-25%
with an average of approximately 10%. Urethral
injury in women with pelvic trauma is considered a less
common event; however, some studies have reported
incidences as high as 4-6%. Anterior urethral trauma
is thought to occur less frequently due to its higher
mobility, but the frequency of occurrence has not been
established.
ANATOMICAL BASIS
Historically, the male urethra has been divided into
anterior and posterior parts, which are demarcated at
the urogenital diaphragm. The proximal posterior urethra
begins at the interface with the bladder, the internal
urethral orifice, and the prostatic urethra. The prostatic
urethra is entirely contained within the prostate and is
continuous with the membranous urethra at the prostatic
apex inferiorly. A principal support structure, the
puboprostatic ligament, firmly attaches the prostate to
the anterior pubic arch. This anatomy is important for
locking the posterior urethra and prostate into their relative
positions within the extraperitoneal pelvis.
The membranous urethra is located within the anterior
tip of the urogenital diaphragm and becomes the proximal
portion of the anterior urethra after passing through the
perineal membrane. The principal mechanism of
continence, the external urethral sphincter, is located
within the urogenital diaphragm around the membranous
urethra. The Cowper glands are also located within the
urogenital diaphragm adjacent to the urethra.
The bulbous urethra, a swelling in the proximal
anterior section, travels within the proximal corpus
spongiosum and is continuous with the penile urethra.
The ducts to the Cowper glands drain into the bulbous
urethra. The penile or pendulous urethra extends the
length of the penis where it ends as the fossa navicularis
and urethral meatus.
CLINICAL DETAILS
Sex: Urethral traumas are more frequent in the male
population than in the female population among women,

the most common types of urethral injuries described are
longitudinal tears and avulsion-distraction injuries, with
the later attributed to more severe lateral compressive
pelvic trauma.
Age: An age-linked risk of urethral injury associated
with pelvic fracture has been shown for children younger
than 15 years. The suggested cause for this pattern is
the difference in pelvic fracture severity seen between
children and adults. For pelvic fractures in children,
approximately 56% of cases are at high risk for urethral
injury. Among adults, only 24% are at high risk for urethral
injury.
A diagnosis of urethral trauma should be investigated
in the presence of pelvic fracture, straddle injury,
penetrating trauma in the vicinity of the urethra, or penile
fracture. While there are no findings specific for urethral
trauma, there are many that suggest its presence. Findings
can include blood at the urethral meatus, gross hematuria,
an inability to spontaneously void, and a high riding
prostate on rectal examination.
For many patients with urethral injury, extravasation
of blood contained within different fascial planes is also
present.
ROLE OF RADIOLOGY AND IMAGING
Retrograde Urethrography
The possibility of urethral trauma should be properly
investigated by retrograde urethrography. This should
always be done prior to the insertion of a urethral catheter.
If, however, a urethral catheter is properly in place prior
to evaluation for urethral trauma, it should not be
removed in order to perform urethrography. In such a
case, a pericatheter urethrogram may be obtained.
After a diagnosis of urethral trauma has been made,
management and repair can be planned with the possible
aid of other imaging modalities, such as MRI and
ultrasonography. MRI has some utility in planning surgical
approach for posterior urethral disruptions, and ultraso-
nography has been used at times to aid in the repair of
urethral trauma.
Limitations: While RUG provides clinically valuable
information on the presence, location, and severity of
Urorenal Trauma 135
urethral extravasation, it provides limited information
about the details of surrounding soft tissue damage.
Furthermore, imaging of the proximal urethra can
occasionally be inadequate. This is usually caused by
subpar contrast-agent filling of the proximal urethra or
by gross extravasation of contrast blocking visualization
of the proximal urethra.
Technique: The standard imaging method used to
diagnose urethral trauma is RUG. While various
techniques have been described to implement RUG, the
most common utilizes a Foley catheter. With this method,
the patient is ideally positioned for imaging in an
approximate 45° oblique angle with the penis stretched
so that the meatus points cephalad. This produces a C
configuration from the bladder level to meatus tip. If the
penile shaft points caudad, the femur may obscure the
opacified urethra. For some patients with multiple injuries,
this position is unobtainable. In this case, the patient
should be supine with the penis stretched perpendicular
to the leg. When the image is obtained in this antero-
posterior projection, however, the urethra can appear
foreshortened, allowing for possible errors in inter-
pretation of extravasation.
The Foley catheter is then placed inside the urethra
with the balloon inflated in the fossa navicularis.
Approximately 20-30 mL of 30% contrast material is
injected into the urethra, with the exposure being made
during the active injection of the last few mL of contrast.
Obtaining the image during the injection allows for
maximum filling of the deeper bulbar, membranous, and
prostatic urethral sections. In the most ideal conditions,
the entire procedure should be performed under fluoro-
scopic control; however, in the emergent environment
this is often impossible.
Classification of Retrograde Urethrography Findings
The most accepted and unified classification of RUG
findings for urethral injuries is the Goldman classification,
with its foundation in the earlier system developed by
Colapinto and McCallum (Table 9.2).
The Goldman classification of urethral trauma is
defined entirely on the anatomical findings of the injury
and not on its mechanism.
136 Uroradiology: Text and Atlas
Table 9.2: Classification of urethral injuries
Colapinto and McCallum
Grade I Posterior urethra stretched,
But intact
Grade II Posterior urethral tear above
Intact urogenital diaphragm
(UGD)
Grade III Posterior urethral tear with
Extravasation through torn
UGD
Grade IV — Bladder neck injury with
Grade IVa __
Grade V __
This system defines five major types of urethral injuries
as seen in RUG.
Type I urethral injury results when the puboprostatic
ligament is ruptured, and the prostate is allowed to move
superiorly. The urethra remains intact however, and is
only severely stretched by the movement of the prostate.
No extravasation of contrast material is seen with radio-
graphy, and continuity is maintained with the bladder.
True cases of Type I urethral injury are uncommon.
Type II urethral trauma is the classically described
posterior urethral injury in which the urethra is torn
superior to the urogenital diaphragm. In such an injury,
contrast-agent extravasation is seen within the
extraperitoneal pelvis, but contrast material is not present
within the perineum. Here, the urogenital diaphragm is
intact, preventing the spread of contrast material inferiorly.
This type exists in approximately 15% of urethral trauma
cases resulting from pelvic crush injuries.
Type III urethral injury: The most common type of
urethral trauma has proven to be type III urethral injury.
Type III urethral injury, like type II, shows disruption above
the urogenital diaphragm. Unlike type II, though, this
injury extends through the urogenital diaphragm and
includes the proximal bulbous urethra. In this injury,
extravasation can be found within the extraperitoneal
pelvis and within the perineum. The amount of contrast
material found above or below the urogenital diaphragm
Goldman and Sandler
Posterior urethra stretched
but intact
Partial or complete
Posterior urethral tear above
intact urogenital diaphragm
Partial or complete
tear of combined
anterior and posterior
Urethra with torn UGD
Extension to the urethra
Injury to bladder base with
Extravasation simulating type
IV (pseudo grade IV)
Isolated anterior urethral injury
depends upon the exact location of the injury and the
degree of disruption to the perineal membrane.
Type II or III urethral injury can be further classified
as a partial or complete urethral tear (Goldman, 1997).
With RUG, partial tears are diagnosed when extravasation
of contrast material occurs with the presence of contrast
material in the bladder. Complete tears are diagnosed
when extravasation is present and no contrast agent is
present in the bladder or in the proximal torn end of the
urethra. The relative frequency of partial tears versus
complete tears is highly variable in the literature, and
no reason for this variance has been agreed upon.
Type IV urethral trauma is a tear to the bladder neck
that extends into the proximal urethra. Contrast-agent
extravasation is seen in the extraperitoneal pelvis around
the proximal urethra. Such injuries can damage the
internal urethral sphincter, resulting in incontinence.
Proper diagnosis is therefore essential to ensure adequate
patient care.
A related injury, as described in the Goldman
classification, is type IVA. This is not a urethral injury;
however, it can easily be mistaken for a proximal urethral
tear. In this case, the base of the bladder is disrupted,
with periurethral extravasation of contrast agent. The
resulting radiographs can easily mimic those of a true
type IV urethral trauma. Distinguishing the two conditions
is important because type IV injury is typically treated
surgically and type IVA injury is not. Dynamic RUG under
fluoroscopic control facilitates the differentiation.

Type V urethral trauma describes all cases that are
isolated to the anterior urethra. Such an injury occurs
distal to the urogenital diaphragm and is more associated
with perineal crush or straddle injuries. The resulting
urethral injury is usually a partial tear of the bulbous
urethra, though complete tears can also occur. In this
case, contrast-agent extravasation occurs inferior to the
urogenital diaphragm. If the Buck fascia remains intact,
the extravasation is limited to its confines, ie, the penile
shaft. If the Buck fascia is disrupted, the contrast material
contained within the limits of the Colles fascia. In this
case, contrast agent might be found in the lower abdomen
and in the scrotum.
Ultrasonography
Like MRI and CT, ultrasonography alone has not yet
proven adequate and is not typically used for the primary
diagnosis of urethral trauma. However, a few reports
suggest that ultrasonography can be used for defining
the extent of urethral damage in certain cases and for
preparing for surgical repair.
High-frequency probes used in sonourethrography
provide a high spatial resolution; therefore, details of
urethral anatomy can be studied after the injection of
a saline solution. This saline solution technique uses a
Foley catheter in a similar manner as described for RUG
to promote distension of the urethra. The presence of saline
in the urethra produces high contrast relative to the urethral
mucosa. Thus, this technique allows accurate visualization
of the urethral wall as well as the urethral lumen.
Only a limited number of reports exist in the literature
regarding the usage of sonourethrography. Such cases
include the use sonography for the diagnosis of urethral
trauma associated with penile fracture and in evaluating
anterior urethral trauma prior to delayed urethroplasty.
Sonourethrography has been shown to accurately depict
trauma to soft tissues surrounding the urethra, such as
the tunica albuginea. Other investigators have shown that
sonourethrography can more accurately measure stricture
length than RUG. This information could prove useful
for planning surgical repair for specific cases.
CT
Despite the prevalent use of CT as the initial screening
modality for general acute trauma, the literature has
Urorenal Trauma 137
historically described few applications of CT in diagnosing
urethral injuries.
A distance of 2 cm between the prostatic apex and
urogenital diaphragm was specific for type I urethral
injuries. The CT findings specific for type II and type III
urethral trauma were contrast-agent extravasation above
the urogenital diaphragm and extravasation below the
urogenital diaphragm, respectively. CT findings associated
with but not specific for urethral trauma were distortion
or obscuration of the urogenital fat plane, hematoma of
the ischiocavernosus muscle, distortion or obscuration
of the prostatic contour, distortion or obscuration of the
bulbocavernosus muscle, and hematoma of the obturator
internus muscle.
Because many patients with generalized trauma
undergo CT before a specific evaluation for urethral
trauma, CT might serve as an initial screening exami-
nation for such injuries. Presently, no test supersedes RUG
for the confirmation of urethral trauma. CT might help
exclude unnecessary RUG.
Because few studies have been conducted to evaluate
the accuracy of CT in identifying urethral trauma, further
investigation is necessary for a well-defined degree of
confidence (Figures 9.9 and 9.10).
All specific findings are found only in patients with
urethral trauma. Among associated findings, distortion
and obscuration of the urogenital fat plane was found
in 88% of those with urethral trauma and in 3% without
urethral trauma. Hematoma of the ischiocavernosus
muscle was found in 88% with urethral trauma and in
17% without urethral trauma. Distortion or obscuration
of the prostatic contour was present in 59% with urethral
FIGURE 9.9: Posterior urethral rupture with contrast extravasation
138 Uroradiology: Text and Atlas
FIGURE 9.10: Extraperitoneal bladder rupture
trauma and in 7% without urethral trauma. Distortion
or obscuration of the bulbocavernosus muscle was present
in 47% with urethral trauma and in 10% s without urethral
trauma. Hematoma of the obturator internus muscle was
found in 53% of patients with urethral trauma and in
13% without urethral trauma.
MRI
Traditionally, MRI has not been used as an initial
diagnostic tool for urethral traumatic injuries; nevertheless,
some researchers have demonstrated the advantage of
using MRI as a preparatory tool when planning surgical
repair of urethral disruption.
One of the most common methods of treatment for
urethral injury is delayed reconstruction after 3–4 months
of suprapubic cystotomy. After the initial delay, the surgical
reconstruction is usually done with a transperineal or
combined transperineal and transpubic approach with
pubectomy. The approach chosen is dependent on the
length of the urethral disruption, the degree of prostatic
dislocation, and the amount of scar tissue present.
MRI has shown positive results in evaluating the
anterior-posterior, superior-inferior, and lateral
displacement of the prostate; the degree of scar tissue
around a urethral defect; and the precise length of a
posterior urethral defect. In one study, the results of MRI
preoperative evaluations changed the surgical repair
approach in 26% of the patients studied. Because of its
superiority in defining local disruption to adjacent tissues,
MRI can be an important tool in combination with RUG
in evaluating urethral trauma for management.
MRI has proven clinical utility in its ability to define
damage to soft-tissue neighboring the urethral trauma.
Alone, however, MRI should not be used to investigate
urethral extravasation or to define urethral trauma as
partial or complete.
INTERVENTION
Interventional radiology has played only a small role in
the treatment of urethral injuries. In a few situations,
delayed realignment of the urethra following suprapubic
diversion has been accomplished under radiological
guidance.
Fluoroscopic guidance for percutaneous suprapubic
cystotomy has also been suggested for clinical use when
the bladder is distorted by a retroperitoneal hematoma
or when the bladder has been displaced superiorly.
Treatment techniques for urethral tears include
suprapubic cystotomy with delayed repair, immediate
realignment, and immediate suturing. For suprapubic
cystotomy with delayed repair, the incidence of stricture
is 97%, the incidence of incontinence is 4%, and the
incidence of impotence is 19%. With immediate
realignment, the incidence of stricture is 53%, the
incidence of incontinence is 5%, and incidence of
impotence is 36%. For immediate suturing, the incidence
of stricture is 49%, the incidence of incontinence is 21%,
and the incidence of impotence is 56%.
MORTALITY/MORBIDITY
The three most common morbidities associated with
urethral trauma are stricture, incontinence, and
impotence.
The incidence of these morbidities is dependent on
the severity of the injury and the method of management
and repair.
SUMMARY
Urethral trauma primarily affects males, because of the
short length of the female urethra. The male urethra is
divided into posterior (membranous and prostatic) and
anterior (bulbous and pendulous) portions, at the
urogential diaphragm. Urethral injuries are associated with
high rates of stricture, impotence and incontinence.
Anterior urethral injuries usually result from a low velocity,
compressive injury of the perineum –e.g. a straddle injury.

Again, blood at the urethral meatus, perineal hematoma,
hematuria and difficulty in voiding are often present. RUG
demonstrates contrast extravasation below the urogenital
diaphragm.
Primary repair of urethral injuries is associated with
severe stricture formation, incontinence, and impotence.
Initial treatment may consist of endoscopic realignment.
Catheter drainage for several weeks is then undertaken
allow healing. Subsequent treatment of short segments
of scarring is frequently necessary.
In the evaluation of urethral strictures, the RUG is
again the initial examination. Voiding cytourethography
is complementary, as it allows better distension of proximal
urethral segments. Both techniques can underestimate
bulbar strictures because of the oblique angle of this
portion of the urethra to the beam. Sonography of the
urethra is helpful in these cases to provide a more
accurate measurement of the length of the bulbar stricture,
which has a major impact on operative planning.
Ultrasound is also useful in the assessment of penile
Urorenal Trauma 139
scarring, or spongiofibrosis. Scanning is performed during
retrograde injection of saline. Nodularity of the urethral
margins, acoustic shadowing, and narrowing of the urethra
all are indicative of spongiofibrosis.
Posterior urethral injuries are associated with high
velocity blunt force injury, pelvic fractures, and multi-
organ trauma. The spleen, liver, bowel and bladder are
often also injured. A spectrum of injuries occurs, from
stretching and elongation of the urethra, to laceration,
to transection.
Exam findings include a high riding, boggy prostate,
blood at the urethral meatus, and perineal hematoma.
Hematuria and difficulty in voiding are also often present.
Retrograde urethrogram (RUG) is the initial study of
choice, and demonstrates abnormal urethral contour.
Extravasation of contrast occurs in cases of laceration
or transection. If the urogenital diaphragm is intact,
contrast will collect in the pelvic extraperitoneal space.
If the UGD has ruptured, contrast will be present in the
perineum.
140 Uroradiology: Text and Atlas

RENAL NEOPLASMS (PEDIATRIC AND ADULT) Table 10.1: Most common age at presentation for solid renal
malignancies
CLASSIFICATION OF RENAL NEOPLASMS (TABLE 10.1) Renal neoplasm Age range Peak age
1. Wilms’ tumor Wilms’ tumor
2. Nephroblastomatosis Unilateral form 1–11 yr 3½ yr
Bilateral form 2 mo–2 yr 15 mo
3. Mesoblastic nephroma Nephroblastomatosis Any age 6–18 mo
4. Ossifying renal tumor of infancy Renal cell carcinoma 6 mo–60 yr 10–20 yr*
5. Multilocular cystic partially differentiated nephro- Mesoblastic nephroma 0–1 yr 1–3 mo
blastoma Multilocular cystic renal tumor
Cystic nephroma Adult female Adult female
6. Clear cell sarcoma Cystic partially differentiated
7. Rhabdoid tumor of kidney nephroblastoma 3 mo–4 yr 1–2 yr
Clear cell sarcoma 1–4 yr 2 yr
8. RCC (Gravitz tumor/Hypernephroma)
Rhabdoid tumor 6 mo–9 yr 6–12 mo
9. Multilocular cystic nephroma Angiomyolipoma 6–41 yr 10 yrt
10. Renal medullary carcinoma Renal medullary carcinoma 10–39 yr 20 yr
11. Oncocytoma Ossifying renal tumor of infancy 6 d–14 mo 1–3 mo
12. Angiomyolipoma Metanephric adenoma 15 mo–83 yr None
Lymphoma
13. Metanephric adenoma Hodgkin >10 yr Late teens
14. Lymphoma (Hodgkin and Non-Hodgkin lymp- Non-Hodgkin Any age child < 10 yr
homa) * von Hippel-Lindau syndrome
15. Metastasis.
t
Tuberous sclerosis, neurofibromatosis, von Hippel-Lindau syndrome

is the most common solid abdominal mass and by far

WILMS’ TUMOR/ NEPHROBLASTOMA
INTRODUCTION
It is a malignant, embryonic neoplasm containing
epithelial, blastemal, and stromal elements. It has almost
the same overall incidence as neuroblastoma, accounts
for approximately 8% of all childhood malignant tumors,
the most common renal pediatric malignancy.
INCIDENCE
Incidence is around three years of age; approximately
80% of all cases are detected between 1 and 5 years
of age. An asymptomatic mass is the most common

clinical presentation. Uncommonly, it may present as
abdominal pain, anorexia, hematuria and hypertension.
GENETICS
Although most Wilms’ tumors are sporadic, 1% demon-
strate autosomal dominance with variable penetrance.
A child with a sibling or parent with bilateral Wilms’ tumor
has a 30% risk for development of the tumor.
ASSOCIATIONS
Wilms’ tumor is associated with (Acronym: WHAGR)
• Hemihypertrophy (overgrowth disorders)
• Aniridia (Sporadic)
• Genital and renal malformations.
In congenital hemihypertrophy and Beckwith-
Wiedemann syndrome (macroglossia, hepatomegaly,
gigantism, omphalocele, Wilms’ tumor), the mean age
of diagnosis of Wilms’ tumor is similar to that of the
general Wilms’ population. However, Wilms’ tumor
occurs at an earlier age when associated with aniridia
and Drash syndrome (pseudohermaphroditism, renal
failure). Weakly associated with Wilms’ tumor are Soto
syndrome (cerebral gigantism), neurofibromatosis and
Klippel-Trenaunay-Weber syndrome.
PATHOPHYSIOLOGY
Wilms’ tumor is usually bulky and replaces most of the
involved kidney. The renal capsule is usually intact; rarely,
the tumor breaks through this capsule and extends into
the extrarenal spaces. Wilms’ tumor may invade the renal
vein and inferior vena cava. Venous extension of Wilms’
tumor follows the “rule of 10’s”: 10% extend into the
renal vein; 10% of that group extends into the IVC; 10%
of the latter further extend into the right atrium. Distal
metastases most commonly involve the lungs; the liver
is next most common.
MORTALITY AND MORBIDITY
The most important prognostic factor in Wilms’ tumor
is histology. Approximately 10% of all Wilms’ tumors
have unfavorable histology with anaplasia. Wilms’
tumor is bilateral in approximately 5% of cases.
Synchronous tumors (bilateral tumors at initial
presentation) have a 87% survival while metachronous
Urorenal Neoplasms 141
tumors (multiple separate primary tumors separated in
time) have a survival rate of only 40%.
STAGING OF WILMS’ TUMOR
Staging of Wilms’ depends on the involvement as
determined by imaging, surgery, and pathology. Anatomic
staging of Wilms’ tumor is as follows:
• Stage I, tumor limited to the kidney and completely
resected;
• Stage II, tumor extending beyond the kidney but
completely resected;
• Stage III, residual tumor confined to the abdomen
without distant metastasis;
• Stage IV, hematogeneous metastases to lung, liver,
bone, brain;
• Stage V, bilateral renal involvement appearing initially
or during the course of treatment.
ROLE OF RADIOLOGY AND IMAGING
Imaging of Wilms’ tumor should define the size and
location of the primary tumor, any local spread, and any
distant metastases. Imaging is also used for surveillance
of individuals at risk for primary or recurrent Wilms’ tumor.
Plain Radiography
Usually shows a soft-tissue mass that displaces bowel.
The dystrophic calcification which occurs in 5% of Wilm’s
tumors is curvilinear or amorphous is distinguished from
the stippled or flaky calcifications that occur in 55% of
neuroblastomas (Figure 10.1).
FIGURE 10.1: Two well circumscribed nodules in right upper zone:
Metastases from Wilms’ tumor with, haziness of mass on right side
of abdomen without calcifications
142 Uroradiology: Text and Atlas

IVU structures, identifies nodal involvement, and evaluates

See Figure 10.2. for liver metastases, and images the contralateral kidney.
The tumor mass is usually rounded, low attenuation and
heterogeneously enhancing. The vessels are displaced,
not encased as in neuroblastoma. Abdominal CT also
evaluates the renal vessels, IVC, lymph nodes, liver and
contralateral kidney. Chest CT is also performed,
as pulmonary metastases are present in up to 20% of
patients at the time of diagnosis. CT is also excellent for
surveillance after resection (Figures 10.4 to 10.6).

FIGURE 10.2: Displaced, stretched and distorted calyces due to

mass involving right kidney at mid and lower pole

Ultrasound
It is usually the first imaging modality for a child with
FIGURE 10.4: CECT-Axial section: well-defined, rounded low
a palpable abdominal mass. Wilms’ tumor is seen as a attenuation mass in the right side of abdomen showing heterogenous
large, sharply marginated, echogenic mass. Hypoechoic but bright enhancement
areas may represent hemorrhage, necrosis or dilated
calyces. Venous extension is diagnosed when intra-
vascular echogenic focus is identified (Figure 10.3).

FIGURE 10.3: Large, sharply marginated, isotohyperechoic mass

involving mid and lower pole of right kidney

Computed Tomography
CT confirms the presence of an intrarenal mass, deter- FIGURE 10.5: Coronal reconstruction image of same patient,
mines the extent of the Wilms’ tumor, visualized vascular showing lung metastases and the Wilms’ tumor, together
 Urorenal Neoplasms 143

of the interaction of the advancing and bifurcating ureteric

bud which branch and form the collecting system of the
kidney and the metanephric blastema which give rise to
form epithelial and stromal elements of the kidney.
Metanephric blastema lies peripherally in the subcapsular
and interlobular spaces. Nephrons and associated
supporting structures arise from the metanephric
blastema. Nephrogenesis is complete in the normal fetus
at 34–36 weeks of gestation.
Nephroblastomatosis is defined as the persistence of
metanephric blastema, also known as nephrogenic rests,
into infancy and childhood.
Beckwith classified nephrogenic rests as:
1. Dormant (nascent),
2. Sclerosing (obsolescent) or
FIGURE 10.6: Coronal reconstruction of thorax showing 3. Hyperplastic/neoplastic.
lung metastasis
Thus, nephrogenic rests may regress, sclerose or
Magnetic Resonance Imaging become hyperplastic/mitotically active or give rise to larger
and frankly neoplastic rests such as Wilms’ tumor.
MRI is becoming the preferred imaging modality because
the multiplanar imaging capability and excellent contrast ROLE OF RADIOLOGY AND IMAGING
between vessels and adjacent soft tissues. In general,
Nephroblastomatosis can be differentiated from Wilms’
Wilms’ tumors are T1 dark and T2 bright.
tumor by its gross and microscopic appearance and
Differences between Wilms’ tumor and neuroblastoma
imaging characteristics. Nephroblastomatosis is usually
are important (Table 10.2)
diffuse, involves the entire subcapsular portion, has no
Table 10.2: Differentiating features of Wilms’ tumor and renal capsule, has a lobulated margin separating it from
Neuroblastoma
underlying uninvolved kidney and has a uniform pink-
Finding Wilms’ tumor Neuroblastoma
flesh appearance and firm consistency. On the other hand,
1. Location and epicenter Intrarenal Extrarenal
2. Shape Round or oval Irregular Wilms’ tumors are usually a bulky, spherical mass,
3. Hemorrhage and Common Rare occupies one portion of the kidney with areas of necrosis,
necrosis
4. Calcifications Rare Common hemorrhage and macroscopic cysts. On ultrasound,
5. Vasculature Invades Encases and nephroblastomatosis may show enlarged kidneys and
displaces
6. Crosses midline Uncommon Common hypoechoic foci in a diffuse or mutifocal pattern or normal
7. Distorts calyces Most Rare appearing enlarged kidneys. On CT, nephroblastomatosis
8. Retroperitoneal lymph Uncommon Common
nodes or contiguous may appear as a multifocal or diffuse subcapsular layer
extension
of abnormal hypodense tissue. Nephrogenic rests may
not demonstrate enhancement with IV contrast material.
NEPHROBLASTOMATOSIS Normal enhancing renal tissue is typically seen in the
INTRODUCTION central portion of the kidney (Figure 10.7).
It is a complex abnormality of nephrogenesis. Normal
developmental anatomy of the kidney occurs when the TREATMENT
ureteric bud contacts aggregates of primitive nephroblasts Treatment options for patients with nephroblastomatosis
(metanephric blastema) in the paraspinal region of the include follow-up with ultrasound or CT every 2–6 months.
developing embryo. Renal development occurs as a result Chemotherapy in nephroblastomatosis is controversial.
144 Uroradiology: Text and Atlas

Imaging Findings
General features
• Best imaging clue
– CECT: Multilocular cystic mass herniating into
renal hilum
• Plain film
– Soft tissue mass (particularly if large and displaces
adjacent structures)
– Curvilinear/amorphous calcification CT Findings.
NECT
– Large/well-defined/encapsulated/multiloculated
cystic mass
– CT HU equal to water/higher than water (gela-
FIGURE 10.7: Right sided nephroblastomatosis tinous fluid)
– Solid component (CT depict very small cysts as
solid component)
Beckwith recommends use of chemotherapy in stage 1
– Curvilinear/amorphous calcification
WT and histologically proven nephroblastomatosis to
• CECT (Figures 10.8A and B)
decrease the size of the lesion. Although potential for
– Septa: Moderate enhancement (regular and thick)
malignant transformation is low, the mass effect of
– Capsule: Enhancement
growing nephrogenic rests may mechanically injure the
– Cystic component: No enhancement (Figures
kidney. These benefits may be outweighed against the
10.8A and B)
potential long-term side effects and unproven efficacy
(A) Cystic mass wit
of chemotherapy.
– Distortion of colli MR Findings
• T1 WI: Multiloculated I.
MULTILOCULAR CYSTIC NEPHROMA
Mass consisting of multiple noncommunicating cysts
herniates into the renal pelvis.

Key Facts
• Synonym(s): Multilocular cystic renal tumor/benign
cystic nephroma
• Definition: Multiple noncommunicating cysts within
a well-defined capsule. Other key facts
• Rare nonhereditary benign renal neoplasm
• Usually solitary but rarely multiple
• Location: Typically unilateral (usually lower pole)
• Usually symptomatic in adults/asymptomatic
palpable mass in children 0 tumor may grow slowly
over years or rapidly within months
• Males: Approximately 90% of tumors occur in first
2 years of life
• Females: Equally divided between < 5 years and FIGURE 10.8A: Schematic representation of multicolor cystic
between 40 and 60 years. nephroma (For color version see Plate 3)
 Urorenal Neoplasms 145

Ultrasound Findings
• Large/well-defined multiloculated cystic mass
• Innumerable anechoic cysts+hyperechoic septa
• Thick hyperechoic fibrous capsule
• Hyperechoic areas within cystic tumor mimicking a
solid component (due to numerous tiny cysts causing
acoustic interfaces)
Angiography Findings
• Hypovascular mass (rarely avascular/hypervascular)
Imaging Recommendations
• NE+CECT; MR+CEMR; US.

Differential Diagnosis
• Multilocular cystic renal cell carcinoma (RCc)
FIGURE 10.8B: Axial CECT section of abdomen: Large, well defined,
• Usually has mural nodularity/solid component
encapsulated, multiloculated low-attenuation cystic mass in left side • May be indistinguishable from multilocular cystic
of abdomen with moderate enhancement of septae nephroma.
Cystic Wilms’ Tumor
• T2WI: Multiloculated / CET1WI: Enhanced excertory • Grows entirely by expansion of large cystic spaces
urography film. within stroma
• Depending on size and I. • Septa: Numerous and thick.
– Obstructed collect 0 : Tumor herniates/p Multicystic Dysplasia
tumor of collecting • Usually involves entire kidney
Differential Diagnosis • Segmental multicystic dysplasia: Associated with
ureteral duplication.
1. Multilocular Cystic Renal Cell
2. Cystic Wilms’ Tumor Pathology
3. Multicystic Dysplasia
4. Renal neoplasm General
(A) Cystic mass with thick septa and wall. • Embryology–Anatomy
– Tumor arises from metanephric blastema
(B) Mass herniates into renal hilum.
• Etiology–Pathogenesis
• Distortion of collecting system/herniation of mass into
– Unknown
renal hilum MR.
– Theories of pathogenesis: Dysplasia/hamartoma/
Findings neoplasia
• TlWI: Multiloculated hypointense mass (fluid intensity) • Epidemiology
• T2WI: Multiloculated hyperintense mass – Rare tumor
• CET1WI: Enhancement of thick septa. Gross Pathologic–Surgical Features
• “Honeycombed” cystic areas of varied sizes/thick
Excretory Urography Findings
fibrous capsule. Non-communicating locules
• Depending on size and location of mass
separated by thick fibrous septa
– Obstructed collecting system/pyelocaliectasis
• Mostly intraparenchymal tumors.
– Tumor herniates/protrudes into renal pelvis
(mimicking a primary tumor of collecting system) Microscopic Features
• Tomogram of nephrographic phase: May show • Locules: Lined by flattened/cuboidal epithelium
septations. • Septa contains fibrous tissue + tubular elements
146 Uroradiology: Text and Atlas
• Cystic poorly differentiated nephroblastoma
– Septa contain blastemal cells I other embryonal
elements
• Cystic nephroma: Septa have no undifferentiated
elements.
Clinical Issues
Presentation
• Adults: Abdominal pain/I palpable mass/hematuria/
urinary tract (UT) infection
• Children: Nonpainful palpable abdominal mass I
hematuria UT infection . Age: Biphasic age + sex
distribution
• Predominantly boys in childhood and women in
adulthood
• Size: Few cm to > 30 cm (average size 10 cm)
• Lab: U/A may show RBC/WBC
• Complications: Local recurrence/obstructive uropathy/
rarely malignancy.
Treatment
• Surgical: Nephrectomy (complete/partial)
Prognosis
• Good: After nephrectomy
• Few cases: Local recurrence.
RENAL CELL CARCINOMA (RCC)
INTRODUCTION
It is the most common primary renal malignant neoplasm
in the adult. It accounts for approximately 85% of renal
tumors and 2% of all adult malignancies. RCC is more
common in men than in women (ratio, 2:1), and it most
often occurs in patients aged 50–70 years. One-fourth
to one-third of patients have metastatic disease at the
time of presentation. In only approximately 2% of
sporadic cases are bilateral tumors seen at presentation,
especially in von Hippel-Lindau syndrome.
RISK FACTORS
• Increased age
• Male sex, smoking
• Cadmium, benzene, trichloroethylene and asbestos
exposure
• Excessive weight
• Chronic dialysis use
• Several genetic syndromes (familial RCC, hereditary
papillary RCC, von Hippel-Lindau syndrome, and
tuberous sclerosis).
PATHOPHYSIOLOGY
RCCs arise from the tubular epithelium and are usually
based in the renal cortex. Several pathologic subtypes
have been described, including the clear cell, papillary,
granular cell, chromophobe cell, sarcomatoid, and
collecting duct subtypes. These tumors vary from being
nearly completely cystic to being completely solid. The
imaging features reflect this heterogeneity. Bilateral RCCs
are common in von Hippel-Lindau syndrome, tuberous
sclerosis, and chronic dialysis; however, bilateral RCCs
occur in only approximately 2% of sporadic cases of RCC.
RCCs are multicentric in as many as 25% of patients.
Spread by means of direct local invasion of adjacent
structures, such as the adrenal glands, liver, spleen, colon
or pancreas, can occur. Local regional lymph node
metastases are also common. RCCs have a propensity
to extend into the renal vein and, subsequently, into the
inferior vena cava. The lungs are the most common sites
of distant metastases. Liver, bone, adrenal gland, and
kidney metastases may also occur. Typically, skeletal
metastases are purely lytic and expansile.
STAGING
RCCs can be staged by using the American Joint
Committee on Cancer TNM classification, as follows:
• Stage 1: RCCs are 7 cm or smaller and confined to
the kidney.
• Stage 2: RCCs are larger than 7 cm but still organ
confined.
• Stage 3: tumors extend into the renal vein or vena
cava, involve the ipsilateral adrenal gland and/or
perinephric fat, or have spread to one local lymph
node.
• Stage 4: tumors extend beyond the Gerota fascia, to
more than one local node or have distant metastases.
Recent literature has questioned whether the cutoff
in size for stage 1 and 2 tumors should be 5 cm instead
of 7 cm.
 Urorenal Neoplasms 147

Staging of RCC (Robson vcrsus TNM staging) (Figures ANATOMICAL BASIS

10.9 to 10.13B).
The kidney is a retroperitoneal structure surrounded by
Robson Disease extent a fibrous capsule and enclosed in the perirenal space
I Tumor confined to kidney with the adrenal gland and fat. In the general population,
Small < 2.5 cm 70–80% of individuals have single renal arteries to each
Large > 2.5 cm kidney, and the remainders have multiple arteries.
II Tumor spread to perinephric fat Multiple renal veins are rarer, occurring in approximately
IIIA Tumor spread to renal vein or inferior vena 10% of patients. The vascular anatomy becomes
cava important whenever minimally invasive surgery or
IIIB Tumor spread to local lymph nodes
IIIC Tumor spread to local vessels and nodes
IVA Tumor spread to adjacent organs, outside
Gerota’s fascia
IVB Distant metastasis.

INCIDENCE

Approximately 2% of adult malignancies.

FIGURE 10.9: Schematic: Stage 1 RCC-limited to capsule FIGURES 10.10A AND B: Stage 2 RCC-Perinephric spread been
(For color version see Plate 4) (For color version for figure 10.10A see Plate 4)
148 Uroradiology: Text and Atlas
A
B B
FIGURES 10.11A AND B: RCC with thrombus in renal vein
(For color version for figure 10,11A see Plate 5)
nephron-sparing surgery is considered because control
of potentially bleeding vessels is paramount.
CLINICAL DETAILS
Sex: RCC is more common in men than in women, with
a male-to-female ratio of approximately 2:1.
Age: The incidence peaks in patients aged 50–70 years,
but the age distribution is broad. RCC rarely occurs in
young children.
Clinically, patients present with hematuria, flank
A
FIGURES 10.12A AND B: RCC with thrombus up to IVC
(For color version for figure 10.12A see Plate 5)
pain, or (less frequently than in the past) a flank mass.
Currently, nearly half of RCCs are discovered incidentally
during imaging for indications other than the assessment
of RCC. In one series, 0.3% of all CT scans demonstrated
incidental RCC. Incidental detection has also increased
on ultrasound. Occasionally, patients present with
systemic symptoms such as fever, nausea, anorexia, and
weight loss. Rarely, patients have symptoms related to
humoral factors such as parathormone, prolactin,
erythropoietin, or renin.

FIGURE 10.13A: Left RCC with RV thrombosis
FIGURE 10.13B: RCC with right renal vein thrombosis
PREFERRED INVESTIGATIONS
Plain Radiography
Plain radiographic findings are often unrevealing in
patients with RCC unless the mass contains detectable
calcification or is large enough to distort the normal renal
contour. Plain radiography has no role in the primary
search for RCC or in the follow-up observation of patients
with RCC because of its limited sensitivity and specificity
(Figure 10.14).
Intravenous Urography
IVU is also limited in depicting RCCs. Large lesions, which
can distort the renal contour or the collecting system, may
be detected. If RCC is suggested, further imaging with
CT or MRI is necessary to confirm a solid mass and to
Urorenal Neoplasms 149
FIGURE 10.14: Plain radiography in case of RCC
stage the disease. If the lesion appears to be a cyst, USG
is the next best test in the patient’s work-up.
Findings of RCC are nonspecific and include mass
effect on the collecting system, distortion of the renal
contour, enlargement of a portion of the kidney, and
calcifications. If good nephrotomograms are obtained at
peak renal enhancement, most RCCs are less attenuating
than surrounding renal parenchyma. Renal vein invasion
may be inferred if contrast material excretion by the
affected kidney is poor or absent. Alternatively, this finding
may result from extensive involvement of the kidney or
ureteral obstruction caused by mass effect.
USG
The primary limitations of USG include problems related
to incomplete staging (bones, lungs, regional nodes)
and to the detection of small non-contour deforming
masses. In addition, large patients are not good
candidates for USG. For the work-up in RCC, USG is
used primarily to differentiate solid masses from simple
cysts and to visualize the internal architecture of lesions
more effectively than can be accomplished by using CT
or MRI.
150 Uroradiology: Text and Atlas

Findings: On sonograms, RCC can be isoechoic,

hypoechoic, or hyperechoic relative to the remainder of
the renal parenchyma. Smaller lesions with less necrosis
are more likely to be hyperechoic and may be confused
with AMLs. Isoechoic tumors are detected only by
distortion of the renal contour, focal enlargement of a
portion of the kidney, or distortion of the central sinus
fat.
A prominent column of Bertin or fetal lobulation may
mimic a solid renal mass and can be resolved with
dedicated CT or MR.

CECT
FIGURE 10.15: Well circumscribed left RCC with central necrosis
Although a variety of modalities can be used in the
workup of patients with suspected RCC, the preferred
method of imaging these patients is dedicated renal CT.
In most cases, this single examination can be used to
detect and stage RCC and to provide information for
surgical planning without additional imaging.
Protocol: The dedicated renal CT examination consists
of thin-section (2.5–5 mm) helical imaging of the kidneys
before the intravenous administration of contrast agent,
followed by imaging after 60-70 seconds and after
3–5 minutes. The imaging parameters (kV, mA, field of
view, section thickness) should be kept constant for all
phases of imaging to enable comparison of the
attenuation measurements. The addition of an arterial
phase CT (either with bolus tracking or after a 20–25
second delay) with thin slices (1–2 mm) may be helpful FIGURE 10.16: IVC thrombus upto right atrium
to evaluate arterial anatomy, especially if partial resection
is contemplated or renal parenchymal or vascular
anomalies are suspected.
Findings: On nonenhanced CT scans, RCCs may appear
as isoattenuation, hypoattenuation, or hyperattenuation
relative to the remainder of the kidney. Calcifications may
be present and are usually amorphous and internal,
although rim-like calcifications can also be present.
On contrast-enhanced CT scans, RCC is usually solid,
and evidence of necrosis is often present. Sometimes RCC
is a predominantly cystic mass, with thick septa and wall
nodularity.
RCC may also appear as a completely solid and highly
enhancing mass (Figures 10.15 to 10.18). FIGURE 10.17: Right RCC with extension into IVC and RRV

FIGURE 10.18: Right RCC with multiple dilated vascular channels
supplying it–hypervascular mass
FIGURE 10.19: Right RCC on T2 MRI
Staging of RCC, which can be performed by using
CT or MRI, includes the assessment of ipsilateral or
contralateral adrenal involvement, direct extension into
adjacent organs, enlargement of retroperitoneal lymph
nodes, invasion of the ipsilateral renal vein (with or
without extension into the inferior vena cava), and distant
metastatic disease (liver, bone, lungs). Retrocrural,
subcarinal, or mediastinal lymph nodes can also be
enlarged.
Limitations: The primary limitation of CT is in the
characterization of hypoattenuation in masses of smaller
Urorenal Neoplasms 151
than 8–10 mm in which pseudoenhancement may be
a problem. In these cases, USG may be of some use in
characterizing the lesions as cysts.
In addition, spread to regional lymph nodes in the
absence of lymph node enlargement can be missed.
If contrast material cannot be intravenously
administered, CT is a poor choice and MRI should be
performed instead.
MRI
Findings: MRI findings are similar to those of CT, with
masses ranging from predominantly cystic with septa or
nodularity to solid with enhancement. The numeric
criteria for enhancement are not defined for MRI as they
are for CT, but MRI signal intensity changes can be
measured.
On nonenhanced T1 eighted images, RCCs usually
appear isointense or hypointense relative to the remainder
of the kidney. With chemical shift imaging, some clear
cell carcinomas show focal or diffuse loss of signal
intensity. On T2 weighted images, RCCs are usually
hyperintense. Most often, they are heterogeneous.
The presence of necrosis or hemorrhage may alter
these signal intensity characteristics. MRI may be
especially helpful in imaging the superior or inferior poles
of the kidneys, in direct coronal or sagittal imaging, and
in determining invasion of venous structures (Figure
10.19).
MRI is limited by patient cooperation because MRI
is more sensitive to motion artifact than CT. In addition,
MRI is more expensive and less readily available than
CT. Furthermore, patients with pacemakers, those with
certain types of medical implants, and those with severe
claustrophobia are excluded from undergoing MRI.
MRI has no advantage compared with contrast-
enhanced CT for the diagnosis of RCC, but MRI is
superior to nonenhanced CT.
RNI
Findings: In a patient with a suspected renal mass, nuclear
medicine studies help in differentiating the mass from
a pseudomass (e.g. column of Bertin, dromedary hump,
fetal lobulation). Scintigraphy with technetium dimethyl-
succinic acid demonstrates normal uptake in the region
152 Uroradiology: Text and Atlas
of a pseudomass, whereas a real mass causes a focal
photopenic defect.
Bone scanning with technetium methylene diphos-
phonate is indicated to confirm bony metastatic disease
in a patient with RCC and symptoms referable to the
skeleton.
Angiography
Noninvasive cross-sectional imaging (CT, MRI, US) has
replaced angiography in the work-up of patients with
known or suspected RCC. Advances in CT angiography
and magnetic resonance angiography have diminished
the need for preoperative conventional angiographic
mapping of the renal vasculature prior to nephron-sparing
or minimally invasive surgery. Angiography is still
occasionally used if the origin of a tumor (e.g., renal vs
adrenal) is not certain. In these patients, selective injection
of the renal and adrenal arteries, as well as additional
vessels, may be necessary.
INTERVENTION
Because RCCs are usually resistant to chemotherapy and
radiation therapy, surgical resection offers the best
likelihood of cure. Unresectable RCCs have a 5-year
survival rate of less than 20%.
When a solitary mass is noted in a patient with
suspected RCC, image-guided biopsy is generally
unnecessary. In one series, fine-needle aspiration of
solitary proven RCC had a yield of 40% definitely
malignant, 36% questionably malignant, and 24%
negative tumors. In a patient with a prior malignancy,
lymphoma, or multiple masses, fine-needle aspiration or
core biopsy guided with CT or US may prove helpful
in treatment planning. In one series, 31 of 54 biopsies
performed for a new renal mass in a patient with a known
malignancy proved to be RCC.
Image-guided radiofrequency or cryogenic ablation
has been used to treat patients with RCC, especially
patients with a high surgical risk, aversion to surgery,
or bilateral lesions. Recent studies have reported short-
term success rates of up to 97% with 1 or 2 ablation
sessions, with size (<3 cm) being a significant
determinant of tumor eradication in a single session.
Complication rates are low. Radiofrequency ablation can
also be considered in patients with local recurrence. In
patients considered for ablation, preprocedure biopsy
may be important because, in one series, nearly 10
(nearly 40%) of 27 patients referred for ablation had
a benign diagnosis.
DIFFERENTIAL DIAGNOSIS
Oncocytomas cannot be reliably differentiated from
RCC without pathologic analysis. Macroscopic areas
of fat in the tumor mass are reported in RCC, but they
are extremely rare. Almost all renal tumors with
measurable areas of fat are angiomyolipomas (AMLs),
but some AMLs do not contain visible fat and may be
mistaken for RCCs. In one series, homogeneous and
prolonged enhancement were valuable predictors for
differentiation of AML with minimal fat from RCC. High
attenuation on nonenhanced CT scans and the degree
of enhancement were helpful but less valuable.
MORTALITY/MORBIDITY
The prognosis of patients with RCC depends on its stage
at diagnosis.
The prognosis is worst for patients with metastatic
disease at presentation and best for patients with small
masses confined to the kidney.
The size of the primary lesion also affects the prognosis
because larger lesions tend to be higher grade and also
metastasize more frequently. Poorly marginated or
necrotic lesions also tend to be of higher grade.
Unresectable RCCs are associated with a 5-year
survival rate of less than 20%.
LYMPHOMA OF THE KIDNEYS
INTRODUCTION
It is discovered at the time of autopsy in almost one half
of cases. It rarely is discovered with conventional urologic
studies, such as intravenous pyelography. However, in
patients with known lymphoma who often undergo cross-
sectional imaging, such as CT scanning for staging
purposes, renal involvement with lymphoma is commonly
diagnosed.

PATHOPHYSIOLOGY
Familiarity with tumoral growth and the mechanism of
lymphoma spread is crucial to understanding the resultant
imaging patterns of organ involvement. Renal lymphoma
is often a secondary process that is discovered in patients
with known lymphoma.
Hematogenous involvement of the kidneys usually
results in a bilateral distribution of the tumor foci within
the renal cortex. Tumor proliferation begins in the inters-
titium and the underlying nephrons; however, collecting
systems and blood vessels provide a framework for tumor
growth. Infiltrative growth results in preservation of the
parenchymal structures and renal contour. Consequently,
detection is often difficult, and renal involvement can easily
be missed. As lymphomatous tumors enlarge, the
surrounding renal parenchyma is compressed and
destroyed, and continuous tumor infiltration results in the
formation of expansile renal masses. Nonuniform growth
can result in single or conglomerate masses that extend
beyond the renal contour and displace the collecting system
and thereby resemble primary renal neoplasms.
Primary renal lymphoma is controversial and a rare
disease.
INCIDENCE
Incidence of renal involvement in patients with lymphoma
is 34–62% in several autopsy series. Renal involvement
occurs more commonly in non–Hodgkin lymphoma than
in Hodgkin lymphoma.
ANATOMICAL BASIS
The kidneys are bean-shaped structures located in the
Gerota fascia in the retroperitoneal region. The lateral
edge of the kidneys is convex, whereas the medial border
is concave with a marked depression or notch termed the
hilus. In adults, each kidney is approximately 11 cm long,
2.5 cm thick and 5 cm wide; it weighs 120-170 g.
Usually, the left kidney is approximately 1.5 cm higher
than the right. When the patient is lying in the supine
position, the superior pole of the left kidney is at the level
of the 12th thoracic vertebra, while the inferior pole is
at the level of the 3rd lumbar vertebra. In the erect position
or during deep inspiration, both kidneys may descend
near the iliac crest or lower.
Urorenal Neoplasms 153
As a result of the proximity of the kidneys to the psoas
muscles, the oblique course of these muscles causes slight
lateral displacement of the lower pole of each kidney.
Between the two kidneys are the aorta and inferior vena
cava, as well as the celiac plexus and the ganglia of the
autonomic nervous system. The renal artery and vein
anterior to the renal pelvis run medially and anteriorly
from the hilus of each kidney. Although the left renal vein
normally courses anterior to the aorta to drain into the
vena cava, it can occasionally run behind (retroaortic
renal vein) and anterior or posterior (circumaortic) to the
aorta.
The renal parenchyma is enclosed in a thin, fibrous,
glistening membrane that represents a true capsule.
CLINICAL FEATURES
Race: Renal lymphoma demonstrates no racial
predilection.
Sex: Renal lymphoma demonstrates no sex predilection.
Age: Renal lymphoma occurs in all age groups.
Patients with renal lymphoma may not be sympto-
matic; however, the renal function panel occasionally
reveals elevated blood urea nitrogen (BUN) and creatinine
levels, which may suggest an obstruction. Therefore, the
patient may need to undergo radiologic evaluation.
Occasionally, symptoms of back pain are attributed
to the patient’s known underlying lymphoma. Sometimes,
patients present with nonspecific signs and symptoms,
including flank pain, weight loss, hematuria, or a palpable
mass. The nature of lymphomatous infiltration around
the renal pedicle is such that it may not cause vascular
compromise; however, the tumor usually surrounds the
renal vascular pedicle. The tumor mass can obstruct urine
flow, resulting in hydronephrosis.
PREFERRED INVESTIGATION
IVU
It provides information regarding involvement of the
collecting system, the functional status of the kidneys,
and the severity of hydronephrosis.
Intravenous urography may show distortion of the
collecting system resulting from single or multiple renal
masses. This finding cannot be differentiated from findings
154 Uroradiology: Text and Atlas
in simple cysts or renal cystic disease. However, intra-
venous urograms of renal lymphoma can demonstrate
normal or near-normal findings.
Limitations: Intravenous urography can depict only the
renal collecting system and suggestive large masses that
have caused calyceal distortion. Small parenchymal
masses and tumors around the kidney and in the
retroperitoneum are often not demonstrated with this
diagnostic examination.
Ultrasonography
It is a good screening modality, particularly for the
assessment and follow-up of patients with hydronephrosis.
On sonograms, the masses are often hypoechoic,
reflecting tissue homogeneity, and they can be
misidentified as renal cysts.
Although gallium-67 citrate is an isotope that often
accumulates in lymphomatous tissue, it can be taken up
by inflammatory masses.
Nonenhanced CT or MRI can cause masses to be
missed, particularly when they are small.
Findings: Sonography often demonstrates single or
multiple renal masses that have low-level echoes.
Occasionally, the ultrasonographic findings may appear
normal because of the small size of the renal nodules.
In addition, varying degrees of hydronephrosis may be
seen because of compression of the renal hilum caused
by lymph nodes or obstruction of the ureters.
On sonograms, a perirenal hypoechoic halo is
characteristic of perirenal lymphoma.
CT
Numerous diagnostic studies are available for the
evaluation of renal involvement by lymphoma; but CT
remains the most sensitive, efficient, and comprehensive
examination. CT scanning is the diagnostic modality of
choice in patients with suspected renal masses. CT depicts
renal involvement in most patients with lymphoma. CT
often helps in defining the extent of disease within and
outside of the kidneys, and it provides information for
staging of the patient’s underlying malignancy. In
addition, the result of treatment can be assessed on follow-
up CT scans.
CT scans demonstrate a wide variety of appearances
in renal lymphoma. CT patterns depend on the technique
of CT scanning. Helical CT is universally accepted as
the technique of choice in patients with renal involvement,
and it has a high degree of sensitivity in the detection
of renal lymphoma.
Breath-hold images can be quickly obtained during
the multiple phases of renal enhancement after the
intravenous injection of contrast medium. These images
are essentially free of motion artifact and respiratory
misregistration. This approach helps in accurately
detecting and characterizing most renal masses, including
smaller lesions that may involve the renal parenchyma
in lymphoma. In addition, the vascular phase of contrast
enhancement enables characterization of the renal
vasculature, which may be involved in renal cell
carcinoma but uncommonly so in renal lymphoma.
Without intravenously administered contrast material,
infiltrative forms of renal lymphoma can be entirely missed
on CT studies. Also, CT scanning should not be limited
to the cortical medullary phase of contrast enhancement
because the lesions can be missed in this phase.
Lymphoma typically involves the kidney in one of
several recognizable patterns. These patterns include
multiple renal masses, a solitary mass, renal invasion from
contiguous retroperitoneal disease, perirenal disease, and
diffuse renal infiltration.
Multiple renal masses are most common in patients
with lymphomas –The masses are typically bilateral, but
they may also be unilateral. Multiple masses are seen
in approximately 60% of patients, and they reflect
advanced disease in patients presenting for staging
evaluation. Depending on the size and expansile nature
of individual neoplastic deposits, little mass effect on the
renal contour may be seen. Therefore, although renal
involvement may be extensive, findings can be subtle,
and intravenous contrast enhancement is essential. The
masses range in size from a few millimeters to several
centimeters and are seen as areas of low attenuation.
Though the masses are often homogeneous on CT scans,
they can be heterogeneous or cystic as well; this is typically
a sign of tumor necrosis in patients undergoing
chemotherapy. In approximately 50% of patients,
associated retroperitoneal adenopathy is noted.

Solitary masses are reported in approximately
10–20% of patients. The mass can be as large as 15 cm,
and it can cause significant distortion of the renal contour.
Solitary lesions resemble other renal neoplasms that grow
primarily by expansion, including renal cell carcinoma
or isolated metastasis.
Continuous retroperitoneal extension into the kidney
is a common pattern of renal involvement in lymphoma
and is seen in approximately 30% of patients. Continuous
extension typically results in a large, bulky retroperitoneal
mass that envelopes the renal vasculature and invades
the renal hilum. In most patients, the renal vascular pedicle
is patent and engulfed by the retroperitoneal mass.
Continuous extension of retroperitoneal involvement in
the renal collecting system can often cause obstruction,
and patients commonly present with hydronephrosis.
Rarely, perirenal disease is seen in an isolated form
without involvement of the renal parenchyma or
retroperitoneal nodes. Occasionally, this feature is seen
without compression of the renal parenchyma or
functional impairment. This finding is rare and is virtually
pathognomonic. A variety of CT manifestations of
perirenal lymphoma, including renal sinus infiltration,
thickening of the Gerota fascia, and perirenal masses,
have been described. The normal renal parenchyma
cannot be differentiated from the perirenal abnormality
if intravenous contrast enhancement is not used in CT
scanning.
Infiltrative disease is associated with lymphomatous
proliferation within the interstitium of the kidney, which
is manifested as nephromegaly with preservation of renal
contour. Diffuse infiltration often is bilateral and is seen
in approximately 20% of patients. The diagnosis is often
subtle and depends on the finding of global renal
enlargement. Usually, kidneys infiltrated by lymphoma
have poor function, but the disease is often clinically silent.
Atypical manifestations of renal lymphomatous mass,
such as spontaneous hemorrhage, necrosis,
heterogeneous attenuation, cystic transformation, and
calcifications, are occasionally depicted on CT scans.
Often, these findings are the result of prior treatment.
More commonly, the findings of renal lymphoma regress
after chemotherapy, and the kidneys regain a normal CT
appearance.
Urorenal Neoplasms 155
In patients who are immunocompromised, the
prevalence of lymphoma is increased. Lymphoma
typically occurs in patients with human immunodeficiency
virus (HIV) infection or in secondarily immunosuppressed
recipients of organ transplants. Lymphoma is particularly
common in patients who have undergone cyclosporine
therapy. Typically, lymphoma in patients who are
immunocompromised is of small noncleaved cell or
immunoblastic origin and has a B-cell phenotype. It often
has an extranodal origin, and the most common sites
include the central nervous system, bone marrow,
gastrointestinal tract, lungs, heart, and liver. Renal
involvement also occurs in these patients, but it is
uncommon.
MRI
It provides information for characterizing the lesion, and
it also is helpful in assessing the renal vascular pedicle.
Findings: MRI findings in lymphoma are similar to those
seen on CT scans, and they are diagnostic to the same
degree. Usually, lymphoma displays low signal intensity
on T1 weighted images, and it is either isointense or
moderately hyperintense on T2 weighted images.
Lymphomatous tissue may be minimally enhancing, but
it does not enhance as much as normal renal parenchyma;
therefore, it remains hypointense relative to the kidney
on contrast-enhanced T1 weighted MRIs.
RNI
RNI particularly that using gallium-67 citrate, have a
higher degree of specificity in the detection of lympho-
matous infiltration of the kidneys.
Findings: Gallium-67 citrate has been used for diagnosing
and staging lymphoma. This radioisotope concentrates
in lymphoma. Gallium is taken up by lymphomatous
tissue in the kidneys, and it is also concentrated in
inflammatory masses of the kidney; therefore, obtaining
the clinical history of patients is important.
The use of a newer agent, technetium- 99mTc–labeled
antibody (LL2), has been advocated in imaging and
staging lymphomas.
Angiography
Findings: Usually, lymphoma is a hypovascular neoplasm;
therefore, angiography cannot help in the diagnosis or
156 Uroradiology: Text and Atlas
staging of these tumors. As indicated, with contrast-
enhanced CT, the lesions remain hypovascular compared
with the renal parenchyma when contrast material is
delivered to the kidney, via either intravenous injection
for CT scanning or direct arterial injection for angiography.
Therefore, the degree of confidence with angiography
is low, and the degree of false-negative findings is
high.
INTERVENTION
Patients with renal lymphoma are treated with
chemotherapy, and surgical intervention is not indicated.
The lesions are treated with systemic chemotherapy, and
the response is usually favorable. The tumors often
completely respond to such treatment without residual
disease in the kidneys.
Occasionally, when a single mass is noted in a kidney,
biopsy may be attempted to differentiate renal lymphoma
from a primary renal cell carcinoma. Primarily, biopsy
is performed because the treatments for the two
neoplasms completely differ. In addition, in patients with
another known primary malignancy, biopsy is needed
to differentiate metastasis to the kidney from renal
infiltration by lymphoma.
MORTALITY/MORBIDITY
Because involvement of the kidneys usually indicates
disseminated disease, the prognosis is poor if the patient
does not receive proper treatment.
With treatment, renal lesions may completely regress,
often with minimal scarring of the renal parenchyma.
RENAL ANGIOMYOLIPOMA (AML)
INTRODUCTION
It is a benign renal neoplasm composed of fat, vascular,
and smooth muscle elements. It has an incidence of about
0.3–3%. Two types are described: isolated AML and AML
associated with tuberous sclerosis.
PATHOPHYSIOLOGY
AML is a benign tumor. The majority of AMLs are small
and single, although they vary in size from a few
millimeters to larger than 20 cm. At gross pathologic
examination, they are round or lobulated and yellow to
gray on cut sections because of their fat content. They
are composed of fat and vascular and smooth muscle
elements. AML is not a hamartoma by definition, because
fat and smooth muscles are not normal constituents of
renal parenchyma. AML is a choristoma; that is, as the
name implies, it is composed of variable amounts of
vascular, muscular, and fatty tissues.
The blood vessels in these tumors frequently have
an angiomatous arrangement. These vessels are tortuous
and thick walled. They do not have elastic tissue, but
they do have a disorganized adventitial cuff of smooth
muscle. AMLs do not have a capsule, but they often are
well marginated. The majority (88%) extend through the
renal capsule into the perinephric space. The tumor is
slow growing. It is truly space occupying; it displaces the
renal parenchyma and distorts the collecting system, and
sometimes causes renal destruction. The characteristic
absence of elastic tissue in the tumor vessels predisposes
the patient to aneurysm formation and spontaneous
hemorrhage. The amounts of fat, smooth muscle, and
blood vessels in the tumor vary. In 5% of the tumors,
fatty elements can be detected only at microscopy; this
limitation makes accurate characterization on the basis
of radiologic findings alone impossible.
INCIDENCE
The frequency is 0.3–3%. Approximately 80% of cases
occur in patients with tuberous sclerosis.
CLINICAL FEATURES
Sex: The male-to-female for isolated AML is 1:4 to 1:8.
The male-to-female ratio for AML associated with
tuberculous sclerosis is 1:1 to 1:2.
Age: With isolated AML, most patients are aged 27–72
years, with a mean age of 43 years. With AML associated
with tuberous sclerosis, the mean age of patients 1–17
years.
Isolated AML, which occurs sporadically, often is
solitary and accounts for 80% of the tumors. The mean
patient age at presentation is 43 years, and isolated AML
is about four times more common in women than in men.
Interestingly, 80% of the cases involve the right kidney.
AML associated with tuberous sclerosis accounts for
20% of the tumors; these lesions are typically larger than

isolated AMLs, and they are often bilateral and multiple.
AML occurs in 80% patients with tuberous sclerosis. The
sex distribution of AML in patients with tuberous sclerosis
is closer to being equal, but women still outnumber men
in terms of prevalence. AML also occurs young women
with lymphangiomyomatosis without other stigmata of
tuberous sclerosis. AML and lymphangiomyomatosis are
sometimes considered the forme fruste of tuberous
sclerosis. AML is considered benign, but rare cases of
extension into the renal vein and/or inferior vena cava
(IVC) and of deposits in the regional lymph nodes are
reported. This involvement possibly is related to
multicentric disease.
Most small lesions are asymptomatic and incidental
findings on images. As many as 40% are symptomatic;
these can cause a palpable abdominal mass, hematuria,
or flank pain. The solitary sporadic tumors may cause
acute abdomen and shock as a result of spontaneous
hemorrhage in the tumor. The demonstration of fatty
attenuation in renal tumor is virtually diagnostic of AML.
PREFERRED INVESTIGATIONS
• Plain abdominal radiography
• Ultrasonography
• Computed tomography
• Intravenous urography
• Magnetic resonance imaging
• Angiography
• Isotope renography and dimercaptosuccinic acid
(DMSA) scanning
• Percutaneous renal biopsy
• Renal arterial embolization.
FINDINGS
The majority (60%) of AMLs are asymptomatic. In one
series, which included patients with tuberous sclerosis,
82% of patients with a tumor 4 cm or larger were
symptomatic, whereas only 23% of patients with tumors
smaller than 4 cm were symptomatic. The development
of abdominal ultrasonography, CT, and MRI in recent
years has increased the incidental detection of
asymptomatic AMLs. Recent imaging experience shows
that AML is more common than previously reported.
Urorenal Neoplasms 157
When AMLs are symptomatic, the main presenting
symptoms are related to intratumoral or retroperitoneal
hemorrhage. Symptoms related to hemorrhagic
complications occur in 87% of patients, and hematuria
is reported in 40%. A palpable abdominal mass is present
in 47% of symptomatic patients. Shock due to massive
retroperitoneal hemorrhage most commonly occurs in
white females with a sporadic unilateral tumor and aged
40–50 years. In younger patients with AML and in those
with associated tuberous sclerosis, tumor size and
symptoms are significantly correlated.
Other symptoms reported in patients with associated
tuberous sclerosis are flank or abdominal pain, weight
loss, hypertension, fever, and nausea. In almost half of
these cases, the tumors are bilateral. This observation
illustrates the importance of follow-up in this group of
patients.
LIMITATIONS OF VARIOUS MODALITIES USED FOR
DIAGNOSIS AND EVALUATION
The most characteristic sonographic feature of an AML
is its echogenicity. Also, AML may cause acoustic
shadowing. The echogenic appearance is thought to be
related to its fat content and the presence of multiple tissue
interfaces within it. However, this appearance in a mass
is not pathognomonic for AML, and it is described in
renal cell carcinoma. In one series with pathologically
proven renal cell carcinomas, 32% of tumors with a
diameter smaller than 3 cm were echogenic. Not all AMLs
are hyperechoic because the tumor constituents vary, and
the fat content may be low. Hemorrhage, necrosis, and
dilated calyces also may alter the echogenicity of the
tumor.
In a sonographically typical mass, fatty attenuation
on plain abdominal radiographs, planar tomograms, and
CT scans is virtually diagnostic of AML. However, AML
is not the only renal tumor that can contain fat. Rarely,
but most importantly, fat can be found in a renal cell
carcinoma because of the invasion of perinephric fat or
metaplasia in the tumor. Intratumoral fat also has been
found in renal lipomas, liposarcomas, Wilms tumors,
teratomas, xanthogranulomatous pyelonephritis, and
oncocytomas (engulfing of renal sinus fat).
158 Uroradiology: Text and Atlas
If fat cannot be demonstrated within a renal mass in
a patient with tuberous sclerosis, a diagnosis of renal cell
carcinoma must be considered. Rapidly enlarging lesions
or dystrophic calcification within a mass may suggest the
diagnosis. Although the natural history of renal cell
carcinoma in tuberous sclerosis is not well known, the
risk of metastases likely increases with the size of the
tumor, and the risk probably is very low in tumors smaller
than 3 cm in diameter. Therefore, the consideration of
nephron-sparing surgery may be reasonable in patients
with tuberous sclerosis and lesions without demonstrable
fat that are enlarging and close to or larger than 3 cm
in diameter.
Although routine follow-up seems reasonable in all
patients with tuberous sclerosis, more intensive follow-
up is necessary to establish the need for diagnostic
resection in patients with tuberous sclerosis who have
small masses (<3 cm in diameter) that are radiologically
atypical for AML. Apart from this group with tuberous
sclerosis, follow-up may be reasonably restricted to
patients with sporadic tumors larger than 4 cm in diameter
who have a higher incidence of hemorrhagic
complications.
TREATMENT
With advances in cross-sectional imaging, the diagnosis
of renal AML can usually be established without surgery.
Most tumors can be managed conservatively, particularly
if they are asymptomatic. In suitable patients in whom
the diagnosis is not established with imaging findings,
partial nephrectomy enables pathologic diagnosis with
a minimal loss of function. Nephron conservation is of
even greater importance in tuberous sclerosis, in which
tumors are often bilateral. In cases with recurrent episodes
of hemorrhage or massive bleeding, the tumor can be
resected. In the acute severe presentation in which more
conservative methods fail, radical nephrectomy may be
the only option.
Partial nephrectomy is ideal for masses with a diameter
smaller than 3 cm, and partial nephrectomy may be
possible in masses with a diameter smaller than 5 cm
that do not abut the hilum. Partial nephrectomy may be
more suitable for the removal of indeterminate masses,
rather than symptomatic masses, for diagnosis because
the symptomatic masses are often larger. Renal arterial
embolization can be used to control hemorrhage.
FOLLOW-UP
No universal agreement exists regarding the follow up
of AML. Because the risk of hemorrhage is greater in
masses with a diameter of more than 4 cm in, the
restriction of follow-up to patients with multiple AMLs
(i.e. tuberous sclerosis) or those with tumors larger than
4 cm may be reasonable. Small (<4 cm in diameter)
solitary AML masses are the most common. They have
little growth (<5% per year), are less likely to be
complicated, and do not require follow-up unless the
diagnosis is in doubt.
MORTALITY/MORBIDITY
Most tumors have a benign course. If the diagnosis is
certain, patients can usually be treated conservatively and
followed-up with sonography. However, one subset of
patients who present with severe hemorrhage as the first
sign may have life-threatening condition. In cases with
recurrent episodes of hemorrhage or massive bleeding,
the tumor can be resected. Surgery, whether planned or
performed emergently, has a certain risk of morbidity
and mortality. Renal arterial embolization may also be
used to control hemorrhage.
ONCOCYTOMA
INTRODUCTION
It is the most common benign solid renal tumor.
First described by Zippel in 1942, this tumor represents
a distinct pathologic entity. Later, Klein and Vaensi
published case series of patients with oncocytoma and
highlighted the benign course of the disease and its
discrete pathologic features.
PATHOPHYSIOLOGY
Oncocytomas originate from the intercalated cells of the
collecting duct. On gross pathologic examination, the
tumors appear spherical and are large (average size,
7 cm), with a pseudocapsule. On cut sections, they appear
homogeneous with a mahogany color in contrast to
yellow renal cell carcinomas. A fleshy central scar, a
 Urorenal Neoplasms 159

characteristic finding of oncocytoma, may be observed
in 33–54% of tumors. Necrosis, hemorrhage and
calcification are rare findings.
On histologic examination, oncocytomas are
composed of oncocytes, which are large cells with granular
eosinophilic cytoplasm that shows abundant mito-
chondria on electron microscopy.
Each kidney is supplied by main renal artery arising
directly from the aorta. Multiple renal arteries are common
and important in nephron-sparing surgeries (partial
nephrectomy). A single renal vein drains each kidney.
Multiple renal veins are uncommon. Lymphatics from the
kidney drain into the lymph nodes in the renal hilum,
which in turn drain into nodes in the para-aortic region.

FREQUENCY PREFERRED INVESTIGATION (TABLE 10.3)

This tumor accounts for approximately 3–7% of all renal
neoplasms. About 2–12% are multifocal, and 4–14% are
bilateral.
CLINICAL FEATURES
Approximately 56–91% of the tumors are incidentally
detected on imaging studies performed for another
indication. However, 17–21% of patients present with
symptoms such as hematuria, flank pain, and an
abdominal mass. In patients presenting with symptoms,
hematuria is more common than mass-like findings.
Sex: These tumors are more common in males than
females, with a male-to-female ratio of 2–3:1, which is
similar to the ratio for RCC.
Age: Can occur at any age. But, the mean patient age
is 62–68 years at the time of resection.
ANATOMICAL BASIS
The kidneys are retroperitoneal organs enclosed in a
fibrous capsule. The kidneys are surrounded by perirenal
fat. The anterior pararenal fascia separates the kidneys
from the pancreas, and the posterior pararenal fascia
demarcates the paraspinal muscles from the kidneys. The
adrenal glands are located superomedially.
KUB Radiograph
Plain radiographic findings are nonspecific, and images
may demonstrate a large, soft-tissue mass in the renal
area with displacement of the fat planes. Calcification
is rare. Excretory urography shows a large mass with a
renal-contour abnormality and compression of the
collecting system.
USG
Oncocytomas appear as well-defined, homogeneous,
hypoechoic to isoechoic masses. The central scar cannot
be confidently identified on sonograms. However, when
it is seen, especially in large lesions, the scar may appear
echogenic. Color Doppler sonography may show central
radiating vessels.
CECT
CT scanning of the abdomen with the intravenous
administration of iodinated contrast medium is the
examination of choice. CT is the best modality for
the evaluation of a solid renal mass. It assists in
the detection and localization of the tumor, and it may
help in its characterization, especially if fat-containing
lesions (e.g., angiomyolipomas) are present. Additionally,

Table 10.3: Differential diagnosis of transitional cell carcinoma

Uric acid calculi Diagnose with ultrasound or CT
Vascular Impression Linear extrinsic impression
Use compression
Oblique or prone films
Crossed calcies
Tuberculosis Narrowed infundibulum
Irregular calices
Pyeloureteritis cystica Bullous edema due to stones/infection
Papillary necrosis Irregular calices ± sloughed papillae
Renal cell carcinoma May invade pelvicaliceal system
Cholesteatoma Squamous metaplasia related to infected stone
Leukoplakia 10–20% associated with carcinoma
Fungus balls Diabetes
160 Uroradiology: Text and Atlas
staging of the tumor can be performed to classify the
extent of the lesion, regional lymphadenopathy, vascular
involvement, and metastases. CT also helps in detecting
calcifications and in differentiating a complex cyst from
a solid neoplasm.
On nonenhanced CT scans, oncocytomas appear
isoattenuating or slightly hyperattenuating relative to
kidney parenchyma. On contrast-enhanced CT scans
obtained during nephrographic phase, the mass appears
less attenuating than the renal parenchyma.
Oncocytomas are well encapsulated and have
distinct margins, a smooth contour, and a homogenous
appearance. The tumors may range from 3 to 10 cm,
and in symptomatic patients, they are most often larger
than 5 cm.
A central hypoattenuating scar may be observed
in 33% of cases, but this scar cannot be differentiated
from the central necrosis commonly found in RCC. With
the advent of multisection CT, high-resolution, thin
sections through the kidneys may improve detection of
the central scar.
Calcification, necrosis, and hemorrhage are rare.
Typically, features of a malignant tumor, such as invasion
or infiltration into the perinephric fat, collecting system,
or vessels, are absent. Likewise, regional lymphadeno-
pathy and metastases are not encountered in patients
with oncocytoma. Occasionally, multifocal or bilateral
tumors may be found.
With the advent of CT, routine angiography is not
performed to diagnose renal masses. However, the
classical angiographic findings include a spoke-wheel
arrangement of tumoral vessels, homogeneous tumoral
contrast during the capillary phase, sharp demarcation
from the kidney and surrounding areas, and a peritumoral
halo (lucent-rim sign). The bizarre neoplastic vessels
are conspicuously absent, in contrast to RCC.
MRI
Findings: On nonenhanced T1weighted images,
oncocytomas are well-defined, homogeneous masses.
They may appear isointense to hypointense relative to
the renal cortex. On T2 weighted images, the tumors are
typically isointense to slightly hypointense. However, slight
T2 hyperintensity is also reported.
When present, the scar may be seen as a hypointense,
stellate area in the center of the lesion on T1 and
T2weighted images. On the contrary, tumor necrosis, a
common feature of malignant masses, appears
hypointense on T1 weighted images and hyperintense
on T2 weighted images. Rarely, the central scar may
appear bright on T2 weighted images.
After the intravenous administration of gadolinium
dimeglumine contrast material, oncocytomas show
homogeneous enhancement, with a nonenhancing
central scar. As discussed in the CT section above, features
of an invasive tumor are absent.
Angiography
Typical “Spoke wheel” pattern of blood vessels supplying
it are seen.
RNI
Scintigraphy is not routinely performed in the evaluation
of renal tumors.
Findings: On DMSA scans, the lesion appears as
photopenic area displacing the cortex and collecting system.
PET Scan
On fluorodeoxyglucose (FDG) positron emission
tomography (PET), oncocytomas usually have less FDG
uptake than RCCs. The amount of uptake is usually
isointense to renal parenchyma. However, oncocytomas
can occasionally have uptake in the range of RCC uptake.
Limitations of Techniques
The presence of a central scar on CT scans or MRIs and
a spoke-wheel pattern of vessels on angiograms are often
suggestive of oncocytoma but not entirely specific.
INTERVENTION
Percutaneous renal biopsy, fine-needle aspiration
cytology, and frozen-section biopsy have been used
with variable success for the differentiation of
oncocytoma from RCC. Because of these limitations
in preoperative pathologic evaluation, the consensus
is to treat a solid renal mass with partial or total
nephrectomy.
MORTALITY/MORBIDITY
Oncocytomas are benign tumors, and the prognosis after
total or partial nephrectomy is excellent.
 Medical Renal Disease 161

CAUSES OF UNILATERAL SMALL KIDNEY 4. Acute cortical necrosis

1. Reflux nephropathy 5. Arterial infarction
2. Ischemia 6. Proliferative necrotizing disorders
3. Post-obstructive atrophy 7. Multiple Myeloma
4. Radiation nephritis 8. GN (Glomerulonephritis)
5. Hypoplasia 9. Multisystem disease especially collagen vascular
6. Infarction and post-inflammatory atrophy diseases.
10. Bilateral hydronephrosis
CAUSES OF BILATERAL SMALL KIDNEYS (FIGURE 11.1) 11. Hormonal-Acromegaly, DM, hyperalimentation,
A. Vascular cirrhosis
Generalized arteriosclerosis 12. Developmental bilateral renal duplication,
Atheroembolic disease Horseshoe Kidney, PCKD
Benign and malignant nephrosclerosis 13. Glycogen storage disease
B. Renal 14. Hemophilia
1. Hereditary nephropathies 15. Sickle cell disease
a. Medullary cystic disease, i.e. Nephrophthisis 16. Fabry disease
b. Hereditary chronic nephritis (Alport syndrome) 17. Acute urate nephropathy
2. Chronic glomerulonephritis 18. Physiologic response to contrast material and
3. Amyloidosis (Late-Stage) diuretics.
a. Post-renal (papillary necrosis)
b. Cause of unilateral small kidney occurring INTRODUCTION
bilaterally. The kidneys are considered to have increased echoge-
nicity if the pyramids are unusually hypoechoic relative
CAUSES OF BILATERAL LARGE KIDNEYS
to the cortex. Echogenicity is considered increased if the
1. Amyloidosis echogenicity is greater than the liver or greater than or
2. ATN (Acute tubular necrosis) equal to the spleen. There is loose correlation with the
3. Acute RVT degree of echogenicity and the severity of disease.
162 Uroradiology: Text and Atlas
Increased echogenicity is a nonspecific finding and biopsy
is required for a diagnosis. Small, echogenic kidneys
usually indicates a chronic disease process with end-stage
changes.
FIGURE 11.1: Bilateral small kidneys, left more than right, in a
patient with chronic renal disease
DIFFERENTIAL DIAGNOSIS OF MEDICAL
RENAL DISEASE (TABLE 11.1)
1. Glomerulonephritis from: SLE, PAN, Wegener’s,
Good-pastures, hemolytic uremic syndrome
2. Acute tubular necrosis (Deposition of cellular debris
in the collecting tubules) from: Hypotension, Drugs,
heavy metals, solvent exposure
3. HIV nephropathy
4. Hypertensive glomerulosclerosis
5. Acute interstitial nephritis (Acute hypersensitivity
reaction) from Penicillin, Methicillin, Rifampin, Sulfa
drugs, NSAIDs, Cimetidine, Furosemide and Thiazides.
6. Diabetes mellitus.
7. Amyloidosis, primary and secondary (Secondary
causes include multiple myeloma, rheumatoid
arthritis, TB, renal cell carcinoma, Hodgkin disease).
Table 11.1: Differential diagnosis of chronic renal
parenchymal disease
No papillary/caliceal abnormality, diffuse parenchymal loss
A. Bilateral
1. Chronic glomerulonephritis, diffuse small-vessel disease,
Hereditary nephropathies
2. Focal parenchymal loss
3. Infarct previous trauma
Contd...
Contd...
B. Unilateral
1. Renal artery stenosis, Postirradiation
2. Hypoplastic kidney, Postobstructive atrophy
3. Papillary caliceal abnormality, Diffuse parenchymal loss
Obstructive nephropathy Generalized reflux nephropathy
No parenchymal loss papillary necrosis
1. TB
2. Medullary sponge kidney, Megacalices, Pelvicaliceal cyst
Focal parenchymal loss
1. Focal reflux nephropathy (chronic atrophic pyelonephritis)
2. TB
3. Calculus disease
ROLE OF RADIOLOGY AND IMAGING
USG
When imaging adult patients for evidence of the presence
parenchymal disease the essential features are:
1. Renal calcification or calculi
2. Abnormality of kidney size or shape; generalized
thinning focal loss of renal substance; asymmetry
3. Abnormality of the collecting system, especially
deformity the papillae/calices
4. Occasionally, abnormality of the nephrographic
pattern
The most valuable observations for differential
diagnosis, the presence or absence of:
1. Papillary/caliceal abnormality
2. Focal cortical loss
3. Differentiation in size between the two kidneys.
The term ‘papillary/caliceal abnormality’ is used here
to emphasize that deformity of the caliceal cups seen is
radiologically important deformity of the papillae. This
may arise primarily from the resubstance, as in papillary
necrosis and reflux nephropathy, from the collecting
system, as in obstructive nephropathy. 1 presence or
absence of papillary/caliceal abnormality and of cortical
loss can be used to divide the radiological appearances
renal parenchymal disease into four groups.
MRI
The differential diagnosis of low signal intensity of renal
parenchyma on magnetic resonance imaging can be
divided into three categories: hemolysis, infection and
vascular disease.

First category includes paroxysmal nocturnal hemo-
globinuria (PNH), hemosiderin deposition in the renal
cortex from mechanical hemolysis, and sickle cell disease.
Second category includes hemorrhagic fever with renal
syndrome (HFRS). Third category includes acute renal
vein thrombosis, renal cortical necrosis, renal arterial
infarction, rejection of a transplanted kidney, and acute
nonmyoglobinuric renal failure with sever loin pain and
patchy renal vasoconstriction. PNH, hemosiderin
deposition from mechanical hemolysis, and sickle cell
disease involve the entire cortex including the columns
of Bertin. HFRS involves the medulla, especially the outer
medulla, whereas cortical necrosis involves the inner
cortex including the columns of Bertin. Renal vein
thrombosis demonstrates low-signal intensity lesions
involving the outer medulla, resembling HFRS. Wedge
shaped low signal intensity regions involving both cortex
and medulla are seen in arterial infarction.
RENAL PAPILLARY NECROSIS
INTRODUCTION
It refers to ischemic necrobiosis of the papilla in the
medulla of the kidneys.
It can be:
• Localized or diffuse
• Unilateral or bilateral.
Earlier in the disease, renal size and function are
preserved.
Function may deteriorate with eventual renal failure
in the later stages of the disease.
PATHOPHYSIOLOGY
Renal papillary necrosis occurs in following conditions:
1. Prolonged hypotension
2. Pediatric gastroenteritis (infants)
3. Obstructive disease of kidney (Urinary tract
obstruction)
4. Sickle cell disease (Hemoglobinopathies)
5. TB (Urinary tract infection)
6. Trauma
7. Congestive heart failure
8. Cirrhosis
9. Christmas disease, Hemophilia
Medical Renal Disease 163
10. Acidosis and respiratory distress
11. Analgesics
12. Renal vein thrombosis
13. Diabetes mellitus with infection (no increase occurs
with uncomplicated DM)
14. Dehydration (Severe)
15. Severe neonatal jaundice.
CLINICAL FEATURES
Sex: Analgesic-induced renal papillary necrosis is often
observed in middle-aged and elderly women.
Age: Renal papillary necrosis resulting from analgesic
use is observed more often in middle-aged and elderly
women. Gastroenteritis and dehydration that are
associated with papillary necrosis are observed in infants
and children.
Clinical presentation may be related to symptoms of
urinary tract infection, such as recurrent fever, malaise,
dysuria, flank pain, proteinuria, hematuria, and
leukocytosis. Passage of sloughed papillae can cause renal
colic, ureteric obstruction and, rarely, urinoma. Rarely,
renal papillary necrosis can present as acute oliguric renal
failure. In the advanced stage, renal function may be
impaired and anemia and uremia may be noted.
ANATOMICAL BASIS
The renal cortex is subcapsular and arches around the
renal medulla. The renal medulla comprises triangular-
shaped, pale, striated, conical renal pyramids; their apices
converge to the renal sinus. The base of the renal pyramid
is capped by renal cortical tissue to form a renal lobe.
The conical renal pyramids project into calices as papillae.
Each minor calyx receives 1-3 of these papillae.
The minor calices unite with their neighbors to form
larger major calices, which in turn fuse with each other
to form the renal pelvis. The papilla is the site of drainage
of the papillary ducts, which are a continuation of the
terminal uriniferous ducts. The numerous openings of
the papillary ducts at the papillary summit give rise to
area cribrosa. Beside the papillary ducts, the renal papilla
has a rich blood supply comprising the vasa recta, part
of the loop of Henle, and meshes of capillary network.
Medullary ischemia is the central finding in experimental
164 Uroradiology: Text and Atlas

analgesic nephropathy. Necrobiosis of the loops of Henle

and the vasa recta is found as an early abnormality.

PREFERRED EXAMINATION
Plain radiographs demonstrate calcification in a
sloughed papilla, which is characteristically ring shaped
and may be the only abnormal radiologic finding in
necrosis in situ. Calcification is common in patients with
analgesic-induced papillary necrosis but has not been
reported in renal papillary necrosis associated with
hemoglobinopathy.
On plain radiographs, necrotic papillae can occa-
sionally demonstrate a ring of calcification.

Findings
Plain radiograph findings: Kidneys are normal in size and
contour except in the late stage in which they shrink and
demonstrate a wavy contour due to the prominence of
the septal cortex around the atrophied centrilobular
cortex.
Sloughed papillae may calcify and can be observed
as curvilinear or ringlike calcification up to 5-6 mm in
diameter. The appearance of calcification infers a change
in urine bacteriology to proteus organisms.
Tiny calcifications may be observed in the region of
the liver, spleen, adrenal glands, and lymph nodes in
patients with abdominal tuberculosis.
Calcification in a sloughed papilla is characteristically
ring shaped and may be the only abnormal radiologic
finding in necrosis in situ. Calcification is common in
patients with analgesic-induced papillary necrosis and has
not been reported in patients who have papillary necrosis
associated with hemoglobinopathy.
On excretory urography, persistent streaking of
contrast from the fornix at the upper and lower poles
is almost diagnostic of renal papillary necrosis. Necrosis
in situ is difficult to diagnose because the necrotic tissue
does not slough.
On excretory urography, the ulcerated papillae can
be observed. Sloughed papillae can cause filling defects
within the calyx, pelvocalyceal system, or ureter.
Findings of medullary calcification (nephrocalcinosis)
are nonspecific and can occur in patients with hyper-
parathyroidism, renal tubular acidosis, and medullary
FIGURE 11.2: Configurations in papillary necrosis
sponge kidney and in conditions associated with hyper-
calcemia. The presence of ringlike calcifications of up to
5–6 mm in diameter is characteristic of sloughed papillae
and calcification may be the only abnormal radiologic
finding in papillary necrosis in situ.
In the early stage when papillary swelling may be the
only abnormal radiologic finding, swelling is difficult to
differentiate from normal findings. Necrosis in situ cannot
be diagnosed unless calcification has occurred.
Pyelosinus extravasation, which can occur with
forceful injection of a large volume of contrast, can mimic
contrast tracking from the fornix in papillary necrosis.
Inadvertent injection of air bubbles can produce filling
defects but the defects are seen as smooth and rounded
and can be differentiated from the irregular filling defects
found in sloughed papillae.
Urographic findings depend on the stage of the disease
(Figure 11.2).
Kidneys are normal in size and the contour is smooth
until the late stage in which the kidneys shrink and
demonstrate a wavy contour.
In the early stage, papillary swelling may be the only
abnormal finding and papillary necrosis may be difficult
to diagnose.

Later, necrosis of the papillae with disruption of the
urothelial lining causes tracking of contrast from the fornix
parallel to the long axis of the papillae. This can produce
the lobster claw sign. Then cavitation of renal papillae
occurs, which can be incompleted (medullary) or
complete (papillary) and can be either central or eccentric.
Shrinkage and sloughing of the necrotic papillae cause
forniceal widening and calyceal clubbing.
Sloughed papillae cause a filling defect in the
pelvocalyceal system and in the ureter.
Persistent streaking of contrast from the polar fornix
is almost diagnostic of renal papillary necrosis. Necrosis
in situ is difficult to diagnose because necrotic tissue does
not slough. Filling defects within the pelvocalyceal system
and the ureter are nonspecific findings and opacification
of the collecting system is poor when renal function is
impaired.
Retrograde pyeloureterography is sensitive,
especially in the presence of renal impairment or when
urographic findings are inconclusive. Retrograde
pyelography can be helpful when the renal collecting
system opacifies poorly or when renal insufficiency is
present.
Findings are similar to those of excretory urography.
Minor abnormal papillary findings can be demon-
strated readily when urographic findings are indeter-
minate. Retrograde pyelography is sensitive, especially
in the presence of renal impairment or in patients in whom
urographic findings are inconclusive. The procedure
cannot help assess renal function or the renal
parenchyma.
Ultrasound is a noninvasive technique that is
frequently used to assess the urinary tract. Findings are
nonspecific for papillary necrosis. On ultrasound,
sloughed papillae can be revealed as echogenic material
within the collecting system, which is a nonspecific finding.
Correlation with clinical and laboratory findings help to
distinguish renal papillary necrosis from other renal
abnormalities with similar ultrasound features such as
other causes of increased echogenicity (e.g., nephro-
calcinosis).
Findings: Sonographically, areas of cavitation in the
papillae can be observed as multiple rounded or triangular
cystic spaces in the medulla arranged around a renal sinus
echo-demonstrating a garland pattern.
Medical Renal Disease 165
Occasionally, bright echoes produced by arcuate
arteries can be visualized at the periphery of the cystic
space. Sloughed papillae can appear echogenic and cast
shadows when calcified.
The collecting system may be dilated when obstructed
by sloughed papillae. Sonographic findings are
nonspecific. A hyperechoic medulla can be observed in
patients with hyperparathyroidism and medullary sponge
kidney and in patients with conditions that cause
hypokalemia or hypercalcemia.
CT findings are not diagnostic but may be useful in
assessing urinary tract obstruction, hemoglobinopathies,
and cirrhosis, which are recognized causes of papillary
necrosis.
No major role exists for CT and MRI in the evaluation
of renal papillary necrosis. The usefulness of reformatted
multislice spiral CT has yet to be determined. CT findings
are not diagnostic but can be useful in patients with poor
renal function in whom intravenous urogram radiographs
provide poor resolution. Medullary cavity and calcification
are nonspecific findings.
Findings: CT does not offer much help in the diagnosis
of renal papillary necrosis. Reformatted multidetector
images may change the role of CT.
CT is sensitive in detecting calcifications.
CT can demonstrate multiple bilateral ring shadows
in the medulla, some of which are triangular.
Contrast can be detected filling the clefts in the renal
parenchyma.
CT can be helpful in evaluating the nature of the
material (sloughed papillae) that causes the filling defect
within the collecting system.
CT findings are not diagnostic but the scans can be
useful in patients with poor renal function in whom
intravenous pyelogram findings are not helpful. However,
use iodinated contrast agents cautiously in patients with
compromised renal function.
MRI findings are nonspecific in papillary necrosis,
although MRI may be useful in patients who are allergic
to iodinated contrast medium because gadolinium may
provide a useful alternative. Gadolinium-enhanced MRI
is a useful alternative in patients with renal failure. MRI
is an expensive tool but may be useful in patients with
poor renal function and in those with hypersensitivity to
iodinated contrast media.
166 Uroradiology: Text and Atlas
Findings: MRI has no specific role in the management
of papillary necrosis; however, it may provide a useful
alternative to iodinated contrast in patients with depressed
renal function and in those who are allergic to iodinated
contrast medium.
Sufficient experience is not available with the use of
MRI in the diagnosis of papillary necrosis.
Radioisotope scan findings provide a sensitive
index of renal function. Radioisotope studies play a
significant role in evaluating renal function but provide
little anatomic information on the location of lesions. No
role exists for isotope studies in the diagnosis of renal
papillary necrosis; however, they are useful in evaluating
renal function.
MORTALITY/MORBIDITY
Progression of renal papillary necrosis can result in
eventual renal failure, anemia, and uremia. Transitional
cell carcinoma appears to be more common in patients
with analgesic nephropathy.
GENITOURINARY MANIFESTATIONS
OF DIABETES
DIABETIC NEPHROPATHY (KIMMELSTIEL-WILSON
DISEASE; DIABETIC GLOMERULOSCLEROSIS;
DIABETIC KIDNEY DISEASE)
Definition
Diabetic nephropathy is a complication of diabetes. If
you have this condition, your kidney loses its ability to
function properly. The condition is characterized by high
protein levels in the urine.
Causes, Incidence, and Risk Factors
Each kidney is made of more than a million units called
nephrons. Each nephron has a tuft of blood vessels called
a glomerulus. The glomerulus filters blood and forms urine,
which drains down into collecting ducts to the ureter.
The earliest detectable change in the course of diabetic
nephropathy is a thickening in the glomerulus. At this
stage, the kidney may start allowing more albumin
(protein) than normal in the urine, and this can be
detected by sensitive tests for albumin. This stage is called
“microalbuminuria” (micro refers to the small amounts
of albumin).
As diabetic nephropathy progresses, increasing
numbers of glomeruli are destroyed. Now the amounts
of albumin being excreted in the urine increases, and
may be detected by ordinary urinalysis techniques. At
this stage, a kidney biopsy clearly shows diabetic
nephropathy.
Protein may appear in the urine for 5 to 10 years
before other symptoms develop. High blood pressure
often accompanies diabetic nephropathy. Over time, the
kidney’s ability to function starts to decline. Diabetic
nephropathy may eventually lead to chronic kidney
failure. The disorder continues to progress toward end-
stage kidney disease, usually within 2 to 6 years after
the appearance of high protein in the urine (proteinuria).
Diabetic nephropathy is the most common cause of
chronic kidney failure and end-stage kidney disease in
the United States. People with both type 1 and type 2
diabetes are at risk. The risk is higher if blood-glucose
levels are poorly controlled. However, once nephropathy
develops, the greatest rate of progression is seen in
patients with poor control of their blood pressure.
Diabetic nephropathy is generally accompanied by
other diabetes complications including hypertension,
retinopathy, and vascular (blood vessel) changes,
although these may not be obvious during the early stages
of nephropathy. Nephropathy may be present for many
years before high protein in the urine or chronic kidney
failure develop.
Role of Investigations
The first laboratory abnormality is a positive micro-
albuminuria test. This means you are very likely to
develop diabetic nephropathy.
Most often, the diagnosis is suspected when a routine
urinalysis of a person with diabetes shows too much
protein in the urine (proteinuria). The urinalysis may also
show glucose in the urine, especially if blood glucose is
poorly controlled.
There may or may not be signs of other diabetic
complications. High blood pressure may be present or
develop rapidly and may be difficult to control. Serum
creatinine and BUN may increase as kidney damage
progresses.
A kidney biopsy confirms the diagnosis. Most
nephrologists do not need to perform the biopsy if the
case is straightforward, with a documented progression
 Medical Renal Disease 167

of proteinuria over time and presence of diabetic USG: Hypoechoic collection with air pockets and
retinopathy on examination of the retina of the eyes. moving internal echoes.
Should there be any doubt in the diagnosis, a biopsy
Emphysematous Pyelonephritis/cystitis.
may be performed to confirm the diagnosis and to study
KUB: Air lucency in renal region
the extent of the disease.
Air in PC system.
This disease may also alter the results of the following
Air in bladder.
tests:
USG: Hyperechoic (air) foci in renal parenchyma,
• protein electrophoresis—urine
P-C system and bladder
• creatinine—urine
CT: Hypodense foci CT density equal to air in KUB
• 24-hour urine protein.
region.
Imaging
Xathogranulomatous pyelonephritis (due to
Plain radiography: Proteus mirabilis)
Following things are to be seen: KUB: Enlarged kidneys
1. Calcification of aorta and great vessels Nephrolithiasis–Staghorn calculus usually
2. Pancreatic calcification associated.
3. Seminal vesicle calcification USG: Enlarged kidneys.
4. Emphysematous cholecystitis Diffuse/focal decreased echogenicity
5. Emphysematous pyelonephritis Calculi (+)
6. Emphysematous cystitis IVU: focal defect or complete nonfunctioning.
7. AVN of femoral capital epiphysis. CT: Enlarged kidney with fat density and calculus.
IVU:(Patient should be well hydrated) delayed
functioning with enlarged kidneys. Reproductive System
USG: Following findings may be noted in a patient of DM:
1. Enlarged kidneys • Vas deferens calcification.
2. Later progressive decrease in size due to nephro- • Genital infections; Fournier gangrene is the dreaded
sclerosis. one.
3. Diffuse cortical hyperechogenicity with Gradual loss • Postmenopausal tuboovarian abscess.
of CM • Increased risk of Ca endometrium.
4. Differentiation
Fournier gangrene is potentially lethal necrotizing
5. Resistive index in renal artery is > 0.7.
fascitis of the scrotum. Air pockets are noted in scrotal
Nephrocalcinosis wall and perineum with scrotal wall thickening in the
KUB: Triangular calcific lesion with central lucency. presence of normal testes.
USG: Hyperechoic foci s/o calcification noted at
papillac. Complications
Cystopathy (Neurogenic Bladder) Possible complications include:
MCU: Increased capacity due to decreased bladder • Hypoglycemia (from decreased excretion of insulin)
sensation. • Rapidly progressing chronic kidney failure
USG: Increase in post void residue. • End-stage kidney disease
Cystitis • Hyperkalemia
MCU: Irregularity and thickening of bladder wall with • Severe hypertension
trabeculations. • Complications of dialysis
Decrease capacity • Complications of kidney transplant
Renal and peri-renal abscesses • Coexistence of other diabetes complications
KUB: Increase in renal contour with effaced • Peritonitis (if peritoneal dialysis used)
perinephric fat planes. • Increased infections.
168 Uroradiology: Text and Atlas
RENOVASCULAR HYPERTENSION (RVHT)/
RENAL ARTERY STENOSIS (RAS)
INTRODUCTION
It denotes nonessential hypertension in which a causal
relationship exists between anatomically evident arterial
occlusive disease and elevated blood pressure. RVHT is
the clinical consequence of renin-angiotensin-aldosterone
activation as a result of renal ischemia.
Renal artery stenosis (RAS) is a major cause of RVHT.
Apart from the casual relationship of occlusive renal
artery disease and hypertension, RAS is also being
increasingly recognized as an important cause of chronic
renal failure. In older patients, atherosclerosis is
the most common cause of RAS. RAS due to
atherosclerosis is generally a progressive disease with
increasing luminal narrowing, which may eventually com-
promise renal blood flow and renal function and structure.
Arterial dysplasias (AD) are uncommon angiopathy
associated with heterogeneous histologic changes that
may affect the carotid circulation and the visceral and
peripheral arteries. Medial fibroplasia (MFP), as a
cause of RAS usually affects young to middle-aged
adults, mostly women, but it can also affect
children. It is an important cause of RVHT in children.
The average age range of patients with MFP is 30–40
years.
Although MFP is a pathologic diagnosis, characteristic
change is seen at vascular imaging. The most common
finding is the ‘string-of-beads’ appearance caused by
areas of relative stenoses or webs alternating with small
fusiform or saccular aneurysms of the artery. Approxi-
mately 10–30% of patients with RAS have MFP.
Diagnostic imaging plays an essential role in the
diagnosis and treatment of RVHT. Although primary
screening tool for RAS is radionuclide renography, CTA
and MRA have much higher sensitivity and specificity.
PATHOPHYSIOLOGY
Development of RVHT
A physiologically significant reduction in blood flow to
a region of the kidney causes decreased perfusion pressure
to the juxtaglomerular apparatus, leading to an increased
release of renin. Renin converts angiontensinogen
to angiotensin I. Angiotensin I is then converted to
angiotensin II by angiotensin converting enzyme
(ACE). Angiotensin II causes constriction of the efferent
arteriole, thus maintaining the glomerular filtration rate.
However, angiotensin II also causes an increase in
systemic pressure. ACE inhibitors give rise to a decrease
in glomerular filtration rate (in addition to a decrease in
systemic pressure).

RVHT is the clinical consequence of renin-angiotensin-
aldosterone activation. Since Goldblatt’s work in 1934,
RVHT has become increasingly recognized as a cause
of clinically difficult-to-control hypertension and chronic
renal insufficiency. Goldblatt demonstrated that occlusion
of the renal artery causes ischemia, which then causes
an elevation of blood pressure by triggering the release
of renin. Increased renin levels help in the conversion
of angiotensin I to angiotensin II, causing severe
vasoconstriction, aldosterone release. The ultimate
cascade of events depends on the presence of a
functioning contralateral kidney.
The development of RVHT involves the activation
of both limbs of the renin-angiotensin-aldosterone system
and depends on the presence or absence of a contralateral
kidney. Unilateral renal ischemia initiates an increased
secretion of renin, which accelerates the conversion of
angiotensin I to angiotensin II and which enhances the
adrenal release of aldosterone. Aldosterone-mediated
sodium and water retention is efficiently handled by the
noncompromised kidney, precluding the volume from
contributing to the angiotensin II–mediated hypertension.
Atherosclerotic disease is usually diffuse and may
involve both kidneys, leaving a solitary ischemic kidney
that has little reserve capacity for sodium and water
excretion; hence, volume plays an additive role in the
hypertension. An ischemic solitary kidney is unable to
perform the pressure diuresis required to handle the
aldosterone-induced sodium and water retention. Thus,
the resultant volume load further contributes to the
hypertension and also suppresses the production of renin
by the stenotic kidney.
Angiotensin II causes vasoconstriction of both afferent
and efferent arterioles, with a preferential affect on the
efferent side. Under physiologic conditions, efferent tone
is essential to the maintenance of intraglomerular
pressure. Angiotensin blockade increases efferent renal
arterial blood flow, resulting in an increased intraglo-
merular pressure and optimized glomerular filtration rate
(GFR).
In a kidney rendered ischemic by RAS with a reduced
afferent blood flow, the intraglomerular pressure and
glomerular filtration are maintained by angiotensin II–
mediated efferent vasoconstriction. Removal of the
Renal Vascular Diseases 169
efferent vasoconstriction effect by using angiotensin
blockade in the ischemic kidney may reduce the GFR.
Angiotensin blockade can be achieved by the use of
angiotensin-converting enzyme (ACE) inhibitors.
The use of ACE inhibitors causes a deterioration of
renal function in some patients with renovascular disease;
this effect is particularly pronounced in patients with in
bilateral RAS. Because angiotensin predominantly affects
the efferent renal arteriole, the decrease in renal blood
flow caused by afferent vasoconstriction is less than the
decrease in the GFR caused by efferent vasoconstriction.
The net result is a decrease in the filtration fraction. By
blockading angiotensin, ACE inhibitors eliminate efferent
vasoconstriction and cause a decrease in the
intraglomerular pressure and the GFR.
Normally, the perfusion of the kidney is increased by
as much as five times, as compared with that of other
organs, because it drives glomerular capillary filtration.
Both glomerular capillary hydrostatic pressure and renal
blood flow are essential components of the GFR.
In patients with RAS, chronic ischemia produces
adaptive changes in the kidney that are more pronounced
in the tubular tissue. These changes include tubular cell
atrophy, atrophy of the glomerular tuft, patchy
inflammation and fibrosis of tubular cells, tubular sclerosis,
thickening and duplication of the Bowman capsule, and
intrarenal arterial medial thickening. In RAS, the GFR
is dependent on angiotensin II and other modulators that
maintain the balance between the afferent and efferent
arteries. However, when perfusion pressure decreases
below 70–85 mm Hg, maintaining an adequate GFR may
no longer be possible. Significant functional impairment
of autoregulation, leading to a decrease in the GFR, is
not likely to be observed until arterial luminal narrowing
exceeds 50%.
In adults, renovascular disease tends to appear at
different times, and it affects the sexes differently.
Atherosclerotic disease affects mainly the proximal third
of the main renal artery, and it is most common among
older men. Fibromuscular dysplasia (FMD) involves the
distal two thirds and branches of the renal arteries, and
it is most common among younger women.
Other conditions that may be associated with RVHT
include cholesterol embolic disease, acute arterial
170 Uroradiology: Text and Atlas
thrombosis or embolism, aortic dissection, neurofibro-
matosis, renal arterial trauma, arterial aneurysm,
arteriovenous malformation of the renal artery, and
polyarteritis nodosa and other vasculitides.
Evolution of RVHT
The evolution of RVHT has been described as having
three stages.
1. In the first stage, the immediate elevation of blood
pressure is a direct result of increased levels of renin.
Over days to weeks, the blood pressure remains
elevated, but the course and presence of elevated renin
levels depends on the presence and function of the
contralateral kidney. The mechanism by which
hypertension is produced in patients with renovascular
disease thus changes over time and varies with the
sodium balance. With a normally functioning
contralateral kidney, volume expansion is avoided,
and renin levels remain high. The t kidneys function
out of synch: The ischemic stenotic kidney produces
excessive renin and retains sodium, whereas the
comparatively normal kidney continues to excrete
sodium and water to maintain normal volume levels.
The end result is systemic hypertension that is renin
and angiotensin mediated.
2. In the second phase, in the setting of an ischemic
solitary kidney, sodium and water retention, together
with the vasopressor effects of angiotensin II, act to
maintain renal perfusion pressure. The stimulus to
produce renin is impaired, and renin levels thus
decrease. In these circumstances, angiotensin II no
longer drives the hypertensive state, but the high blood
pressure instead results from volume expansion. Thus,
perfusion pressure tends to be maintained at the
expense of systemic hypertension and volume
retention. Renal perfusion may return to normal if
blood flow is normalized during the first two phases,
and the blood pressure soon returns to a normal level.
3. In the third phase, hypertension persists, even after
patency of the renal artery is restored. Once phase
3 is reached, restoration of renal blood flow may not
normalize the blood pressure, presumably because
of secondary irreversible vascular or renal paren-
chymal disease.
Atherosclerosis
How the initial arterial epithelial injury occurs in patients
with atherosclerosis is not clear. Nevertheless, lipid
abnormalities, hypertension, cigarette smoking, diabetes
mellitus, viral infection, immune injury, and increased
homocysteine levels have all been implicated in
contributing to the endothelial injury. At the site of the
endothelial atheromatous lesion, permeability to plasma
macromolecules (e.g., low-density lipoproteins) is
increased, with a subsequent increased turnover of
endothelial cells, smooth muscle cells, and intimal
macrophages. When atherogenic lipoproteins exceed a
certain critical mass, the mechanical forces may enhance
lipoprotein infiltration in these regions, leading to early
atheromatous lesions.
Atherosclerotic RAS may progress in as many as one-
third of patients, and ongoing ischemic renal parenchymal
damage is of concern. Furthermore, despite adequate
blood pressure control, this condition is associated with
reduced renal perfusion pressures, and renal function may
deteriorate.
Studies about the natural history of atheromatous RAS
obtained by means of sequential abdominal aortography
or duplex sonography in patients with documented and
medially treated RAS have shown that progressive arterial
obstruction occurs in 42–53% of patients within the first
two years of follow-up. In patients with a high-degree
RAS, the rate of progression to complete renal artery
occlusion in these studies is 9–16%.
Arterial Dysplasia
In 1967, McCormack et al classified AD on the basis of
the primary site of involvement of arterial wall, as
determined histologically.
Their classification of fibrosing lesions of renal arteries
included the categories of:
1. Intimal fibroplasia,
2. Medial fibroplasia with microaneurysms,
3. Subadventitial fibroplasia and
4. Fibromuscular hyperplasia.
They first coined the term chain of beads to describe
radiographic changes in MFP of the renal artery. The
term has subsequently been modified to string of beads.

MFP is the most common variety of AD and
represents 85% of the cases. The string-of-beads sign
is classically seen in MFP on angiography.
A similar radiographic appearance can be caused by
subadventitial fibroplasia, but in this variant, the size of
the aneurysms does not exceed the diameter of the renal
artery. MFP may appear as a single stenosis of a visceral
artery, but it is more often seen as multiple stenoses with
intervening outpouchings forming a chain. Radiogra-
phically, this is depicted as a string-of-beads sign.
Neurofibromatosis
Neurofibromatosis is a rare cause of RAS and usually
secondary to a direct effect of fibrous proliferation of the
intima or media. Less commonly, neurofibromatous tissue
may affect the adventitia, producing periarterial fibrosis
indistinguishable from other causes of RAS. These lesions
are usually at the origin of the artery, and they may be
bilateral.
Congenital Stenosis
Congenital stenosis (coarctation of renal artery) is
extremely rare and assumed congenital because of its
discovery in early life. This type of stenosis is generally
confined to the main renal artery, and it may be associated
with aortic coarctation. Some cases may eventually
involve changes related to arteritis, FMD, or neurofibro-
matosis.
Transplant RAS
Transplant RAS is seen in about 10% of patients after
renal transplantation, and it is the most important cause
of treatable hypertension. In renal transplantation
patients, RAS may occur as a complication of surgery,
as transplant rejection, or as intrinsic vascular disease;
this RAS usually occurs in the first year after surgery and
rarely after the third year. The presentation is usually with
hypertension and, occasionally, an elevated serum
creatinine level.
The extent to which the RAS stenosis contributes to
the hypertension is difficult to determine because rejection
is frequent cause of vascular disease, and systemic
hypertension often accompanies rejection. Of the 20%
Renal Vascular Diseases 171
of patients with normal blood pressure and renal failure,
50% become hypertensive after renal transplantation.
With this complex background and the ever-present
complication of graft rejection and acute tubular necrosis,
one may loose sight of RAS as a treatable cause of
hypertension.
INCIDENCE
RVHT is the most common type of secondary hyper-
tension, accounting for less than 1% of cases in unselected
populations and as many as 30% of cases in selected
populations.
CLINICAL FEATURES
Age: The age of onset depends on the cause of the
damage to the renal blood vessels. The average age range
is 30–40 years. RVHT tends to occur in patients younger
than 30 years or older than 50 years. The youngest patient
with FMD of the renal artery was reportedly six months
old.
RVHT often occurs in men older than 45 years with
atherosclerosis and in women younger than 45 years with
AD.
Sex: All types of AD, except intimal fibroplasia, more
commonly affect women than men. For intimal fibro-
plasias, the male-female distribution is equal. For FMD,
the male-to-female ratio is 1:3-5.
RVHT is most common in younger women and older
men. In younger women, RVHT most commonly
develops as a result of FMD affecting the distal two thirds
of the renal arteries and their branches. In older men,
RVHT most often develops as a result of atherosclerotic
disease that affects the proximal third of the main renal
artery.
Although the incidence of atherosclerotic RVHT is
independent of sex, Crowley et al showed that female
sex is an independent predictor of renovascular disease
progression. Other such predictors are older age, elevated
serum creatinine level, coronary artery disease, peripheral
vascular disease, hypertension, and cerebrovascular
disease.
172 Uroradiology: Text and Atlas
ROLE OF RADIOLOGY AND IMAGING
Hypertensive Urography
Hypertensive urography is of historical interest and no
longer used as a screening technique for RAS. CO2
angiography is also obsolete with MRA and gadolinium
imaging. CT angiography (CTA) with maximum intensity
projection (MIP) and the quantitative measurement of
stenosis is an accurate noninvasive technique in the
diagnosis of visceral artery stenosis; this is fast becoming
the diagnostic tool of choice with angiography reserved
in cases in which vascular intervention is planned.
RNI
Radionuclide renography technetium-mercaptoacetyltri-
glycine (MAG3)-captopril has a high sensitivity and
specificity, and it adds a physiologic element to the
diagnosis of RAS.
The acceptance of radionuclide renography as a
primary screening tool for RAS has been hindered by
the lack of standardized protocols.
Standard renography with iodine-131–labeled ortho-
iodohippurate (OIH) is of historical interest and no longer
performed in the investigation of RAS.
The Captopril Scan
The renal captopril scan is used to assist in the diagnosis
of renovascular hypertension. Although protocols vary,
one protocol is as follows:
Captopril (an ACE inhibitor) is given orally, followed
by IV MAG3 (a radiopharmaceutical) and IV Lasix
approximately 60 to 90 minutes later. Dynamic,
sequential scintigraphic images are then acquired for 30
minutes. If the scan is normal, further imaging is not
required. If the scan is abnormal, however, a “baseline”
scan is performed for comparison, again with IV MAG3
and Lasix, but without pre-medication with captopril.
Scan results: Perfusion of the kidneys should be relatively
symmetric (generally considered 50% ± 5%), rapid
(seconds), and demonstrate normal renal shapes. Time
to peak absorption should be approximately 2 to 3
minutes, with 5 minutes at the upper limits of normal;
followed by transit and washout of the MAG3 such that
in a kidney with normal function and absence of
significant pelvic or calyceal retention, the normal
20-min-to-maximum ratio (using background-subtracted
renogram curves) is less than 0.3. Abnormal renovascular
physiology is indicated by a significant decrease in the
glomerular filtration rate with the administration of
captopril, and renal cortical retention of MAG3 (suggestive
of physiologically significant renal artery stenosis).
On giving captopril there is virtually no radionuclide
uptake on DTPA images in a patient with hypertension
receiving captopril therapy. A repeat DTPA renogram
performed in the same patient after cessation of captopril
therapy revealed normal, bilateral DTPA uptake.
The administration of ACE such as captopril inhibitors
prevents the conversion of angiotensin I to the active
vasoconstrictors angiotensin II and angiotensin III. By
inhibiting the compensatory increase in vascular tone at
the postglomerular arteriole, ACE inhibitors decrease
glomerular filtration in the setting of RAS. The
administration of ACE inhibitors in conjunction
with radionuclide renography provides a non-
invasive method for the detection of functionally
significant RAS.
In patients with RAS, effective renal plasma flow
(ERPF) is shown to increase after the administration of
an ACE inhibitor because of the efferent arteriolar
vasodilatation, which increases blood flow through the
renal parenchyma and decreases blood flow through the
glomerulus. 131I-labeled OIH also closely estimates ERPF.
Recently, technetium-labeled mercaptoacetyltri-
glycine (MAG3) has also been used to qualitatively
assess ERPF.
Since the introduction of captopril renography, various
modifications have been made. Some centers only use
one agent, either DTPA or MAG3. A positive captopril
scan indicates that RVHT is present, and it also
implies the existence of hemodynamically
significant RAS (>60–75% of the lumen).
It is important to understand that the criteria for a
positive study depends upon the tracer used. If DTPA
is used, there should be a change in split function if RVHT
is present (since DTPA is dependent upon GFR for uptake
there will be decreased initial uptake in the affected
kidney). If MAG3 is used, split function will usually not
change, but there will be increased cortical retention
(usually measured as 20 minute to maximum ratio) in

the affected kidney. This is because initial MAG3 uptake
is primarily dependent upon tubular secretion rather than
GFR. However, later clearance of MAG3 is dependent
upon GFR (therefore decreased excretion is the primary
finding). Rarely, the split function will change when MAG3
is used in cases of severe RVHT.
Recent preliminary data suggests that aspirin
renography may be as sensitive as captopril reno-
graphy for detecting RAS. Considering that aspirin,
compared with captopril, reduces renal blood flow and
thus tubular tracer delivery in poststenotic kidneys, aspirin
renography is expected to be more useful, particularly
if tubular tracers are used.
Color Doppler
Doppler sonography can be used to measure the
velocity of blood flow. It is a noninvasive technique, and
it has high sensitivity in expert hands. Color flow Doppler
may demonstrate disorganized flow patterns and high
velocity flow stream associated with hemodynamically
significant stenosis.
Normal state: The peak systolic velocity in normal renal
arteries averages 120 cm/s ±12, with an average peak
systolic aortic velocity of 60 m/s ±15. Both velocities
decrease with age. The kidneys offer a low-resistance
vascular bed; thus the Doppler spectral waveform from
the normal kidney is that of a constant forward diastolic
flow. In renal parenchymal disease there is increased
vascular resistance, which in turn causes a decrease in
the diastolic flow component and an increase in the
pulsatility of the Doppler spectral waveform. Parenchymal
diastolic flow velocities less than 20% of the peak systolic
velocities are consistent with renal parenchymal disease.
RAS
The diagnosis of RAS is based on systolic and diastolic
velocity changes throughout the length of the renal artery.
Renal artery flow patterns can be classified into
four categories:
(1) Normal,
(2) Diameter-reducing stenosis less than 60%,
(3) Diameter-reducing stenosis more than 60%, or
(4) Renal artery occlusion.
Renal Vascular Diseases 173
Direct signs:
1. In RAS, the peak systolic velocity increases by
more than 150 cm/s for angles less than 60° or 180
cm/s for angles greater than 70°.
2. Poststenotic spectral broadening may be present
with or without flow reversal. Flow may be absent
during diastole in a stenosis of more than 50%.
3. A ratio of the peak systolic renal artery velocity
to the aortic peak systolic velocity of 3.5 or
more is said to be predictive of a stenosis of more
than 60%.
Indirect signs:
1. Presence of tardus-parvus pulse-demonstrated by
a gradual slope of Doppler waveform during systole
(pulse time increase of greater than 0.07–0.12 s) and
attenuated Doppler waveform amplitude (peak
systolic velocity less than 20–30 cm/s).
2. The acceleration index is determined by dividing
the slope of the systolic upstroke (in kilohertz per
second) by the carrier Doppler frequency, and an
acceleration time is the time interval between the onset
of systole and the initial peak. The acceleration index
in RAS is greater than 3 m/s2.
3. The resistive index in RAS is usually less than 0.56.
The early systolic peak may be absent in RAS.
4. Disorganized flow patterns and a high velocity
flow stream associated with hemodynamically
significant stenosis. A false-negative diagnosis may
occur with accessory renal artery, whereas a false-
positive diagnosis may be made with coarctation of
aorta.
RAS in a transplanted kidney
1. It is seen in about 10% of patients after renal
transplantation, raising the questions of whether RAS
it is the cause of post-transplant hypertension.
2. The site of stenosis is not at anastomotic site in
most patients; this suggests the possibility of focal
rejection (with edema/fibrosis) as the cause of the
hypertension. Duplex and color Doppler sonography
has greatly impacted the diagnosis of RAS.
3. The most reliable Doppler criteria for stenosis
are a high velocity jet and distal turbulence.
174 Uroradiology: Text and Atlas
Limitations:
Doppler sonography has several limitations in the
diagnosis of RAS. These include patient-related factors,
anatomic factors, technical factors, and pathologic factors.
1. Patient factors include bowel gas, obesity,
respiratory renal movements, and poor patient
compliance.
2. Anatomic factors include multiple renal arteries
(16–28%), variation of renal veins (used as imaging
landmarks), horseshoe kidneys, and crossed ectopia.
3. Technical factors include false-positive
examinations due to suboptimal angles, variation in
operator experience, incomplete examination
(because complete renal evaluation is cumbersome),
the need to visualize the entire length of artery,
transmitted cardiac and/or aortic pulsation (which may
obscure renal waveforms), and different emphasis on
variable parameters.
4. Pathologic factors include false tracings (which may
be recorded from large collateral vessels and a
reconstituted main renal artery) and variable causes
of RAS that affects different sites (e.g., atheroma,
fibromuscular hyperplasia, vasculitis, arteriovenous
fistula, retroperitoneal fibrosis, neurofibromatosis).
Conventional Angiography
Conventional angiography remains the criterion standard
for the detection of RAS, although CTA and MRA are
challenging it. The severity of the stenosis and the
presence of collateral circulation to the kidney may be
assessed to determine the hemodynamic significance of
RAS. Lesions occluding more than 50% of the
diameter of the artery are considered significant.
Both the angiographic and the nephrographic phases can
be studied because the latter may better depict ischemic
changes.
Epinephrine may further restrict blood flow to the
kidneys and make the collateral circulation more obvious.
Generally, flush aortography suffices for mainstem RAS,
but if branch stenosis is suspected, selective renal
angiography may better define the lesion. DSA does not
address the hemodynamic significance of RAS.
RAS due to atherosclerosis generally affects the middle
and distal renal artery in 79% of the patients; it affects
a branch renal artery in 4%, or a combination of the
2 in 17%. MFP/FMD is bilateral approximately in 65%;
the left-to-right ratio is 4:1.
Degree of confidence: Renal angiography remains
the criterion standard in the diagnosis of RAS.
Angiography is essential when renovascular
intervention is contemplated. The angiographic
measurement of the size of RAS, an important parameter
in assessing the significance of RAS, is inaccurate.
Angiography provides only anatomic information, and
it does not enable the assessment of blood flow through
the stenosis.
CT Angiography (CTA)
CTA with MIP and quantitative measurement of stenosis
is an accurate noninvasive technique in the
diagnosis of RAS. The advent of spiral and multislice
CT scanning has made CTA feasible. Continuous
scanning through an area of interest during a single breath
hold provides sufficient data to reconstruct 3-dimensional
(3D) images.
Many scanning protocols are available. The general
consensus is that both a timed bolus and rapid injection
rate improves image quality. No positive oral contrast
material should be used because it results in severe
degradation of the image quality. Immediately before the
procedure, the patient ingests water, and glucagon is then
given intravenously to diminish bowel movement and
maximize bowel distention. The three most common
techniques used for 3D reconstruction are MIP, shaded-
surface display (SSD), and volume rendering. MIP is often
the single most useful technique for 3D reconstructions.
Accessory renal arteries are reliably identified by
means of CTA. In either the main stem artery or its
intrarenal branches, RAS is detected with a high degree
of accuracy.
Limitations: CTA or MRA may cause the clinician to
overlook mild cases of FMD that are detectable with digital
subtraction angiography (DSA). Most of the false-negative
and false-positive findings of RAS arise from accessory
renal arteries. MRI is expensive, and its availability is
limited.
Measurements of the size of RAS on angiograms (an
important clinical consideration) are imprecise, and do

not permit assessment of the cross-sectional area or, more
importantly, the flow through the stenotic segment. The
various histologic types of FMD are difficult to distinguish
on angiograms; this limitation has important clinical
bearing from a prognostic point of view.
Standing waves in the renal arteries appear as multiple
serrated indentations, symmetrically distributed at evenly
spaced intervals. These waves are of no pathologic
significance and may represent arterial spasm. They may
also affect intrarenal branches.
A fibrous musculotendinous band may cause extrinsic
compression of the renal artery.
Atheroma, FMD, thrombus, embolus, or arteritis may
cause branch RAS.
Klippel-Trenaunay syndrome is a congenital angio-
dysplasia consisting of a triad of angiomas, osteohyper-
trophy and venous varicosities. Visceral involvement is
not uncommon and may cause life-threatening
complications.
The sensitivity and specificity of the spiral CT in
detecting RAS are approximately 98% and 94%,
respectively. In patients with a plasma creatinine
concentration higher than 1.7 mg/dL, the accuracy is
lower (93% sensitivity, 81% specificity), possibly because
of reduced renal blood flow.
MRA
MRA provides accurate information about the number
of renal arteries, the size of the kidneys, and the presence
of anatomic variants. The obvious advantages of con-
ventional angiography are its usefulness in determining
the clinical importance of suspicious lesions and the ability
to concurrently perform endovascular intervention.
Findings: MRA is fast becoming a clinical standard for
the safe and noninvasive detection of RAS, aneurysms,
and occlusions. A comprehensive examination includes
both 3D dynamic gadolinium-enhanced and 3D phase-
contrast MRA techniques, which allow an evaluation of
the renal arteries and other visceral arteries. The 3D
phase-contrast technique is flow based and subject to
dephasing in the presence of significant arterial stenosis.
The 3D gadolinium-enhanced MRA method produces
excellent contrast angiograms without the risk of iodinated
compounds or radiation exposure.
Renal Vascular Diseases 175
MRA provides accurate information about the number
of renal arteries, the size of the kidneys, and the presence
of anatomic variants.
Gadolinium-enhanced MRA has been proven to have
a high sensitivity for detecting stenosis in the main and
accessory renal arteries. At present, MRA provides
anatomic information regarding a vascular stenosis but
little information is provided about the functional
significance of a stenosis. Recent reports indicate that 3D
MRA with gadolinium-based contrast agents (which have
a low potential for nephrotoxicity) has a sensitivity of
96-100% and a specificity of 71-96% for the detection
of a main RAS of greater than 50%.
When combined with cardiac synchronization, 3D
MRA can sharply delineate the entire length of the major
renal arteries. However, MRA remains suboptimal for the
detection of hemodynamically significant lesions of distal,
intrarenal, and accessory renal arteries, which may cause
physiologically significant RAS.
Limitations of MRA include its costs and lack of avai-
lability. Contraindications to MRA include claustrophobia
and metallic implants, such as a pacemaker or surgical
clip.
INTERVENTION
Interventions appropriate for patients with RAS/RVHT
may include medical therapy, percutaneous transluminal
angioplasty (PTA), vascular stent placement, intravascular
ultrasonography-guided atherectomy, and surgical
revascularization.
Medical Therapy
Treatment with antihypertensive drugs is indicated and
optimal blood pressure control is essential. ACE inhibitors
should be avoided. Other risk factors that should be
addressed include atherosclerosis, smoking, and hyper-
lipidemia. Definitive therapy for the underlying cause
should always be considered to prevent the development
of ischemic nephropathy. In patients with diffuse
atherosclerosis, the complication rate with both surgery
and angioplasty is relatively high. Medical therapy may
be preferred to other treatments.
176 Uroradiology: Text and Atlas
Percutaneous Transluminal Angioplasty
PTA has become the procedure of choice for treatment
of symptomatic stenoses. Patency rates after PTA are
strongly dependent on the size of the vessel treated and
the quality of inflow and outflow through the vessel. RAS
is an established cause of either RVHT or chronic renal
insufficiency. Because of the excellent results obtained
with renal angioplasty, it is the most commonly performed
procedure in symptomatic RAS.
Previously, angioplasty was considered a contra-
indication in patients with a solitary or transplanted
kidney. This is no longer the case and, angioplasty is now
considered the procedure of choice for treatment of RAS
in these patients.
Technical success is achieved in more than 90% of
patients, and patency rates are 90–95% at two years for
MFP and 80–85% for atherosclerosis. Restenosis requiring
repeat angioplasty has been reported in fewer than 10%
of patients with AD and in 8–30% with atherosclerotic
stenosis. Improvement in blood pressure control with
fewer antihypertensive medications is achieved in
30–35% of fibromuscular lesions and in 50–60% of
atherosclerotic lesions. A success rate of 83% has been
reported with PTA in RAS associated with renal
transplantation.
Vascular Stent Placement
Vascular stenting is considered complementary to PTA.
Many vascular stents are now available. Some stents are
metallic devices, which are either self-expanding or
balloon expandable. The US Food and Drug Adminis-
tration (FDA) has approved a few of these for peripheral
coronary work and transjugular intrahepatic
portosystemic shunt (TIPS) procedures.
The ultimate role of stents in the treatment of vascular
disease is not yet established, but these devices have
already had a dramatic impact on the practice of
interventional radiology. In studies from both the US and
Europe, stenting of smaller vessels has resulted in an
unacceptably high incidence of thrombosis. These
problems are being addressed in the development of new
stent materials and coatings.
Intravascular stents placed during angioplasty may
be helpful in the prevention of restenosis and the
management of RAS. Early results suggest that stenting
may prove useful in patients with ostial disease, in those
in whom restenosis occurs after PTA, or in those with
complications (e.g. renal artery dissection) resulting from
PTA. Primary renal artery stenting in patients with
atherosclerotic RAS has a high technical success rate and
a low complication rate.
Intravascular Ultrasonography-guided Atherectomy
In a single reported case, hypertension secondary to AD
was successfully diagnosed with intravascular sonography,
and intravascular sonography-guided renal atherectomy
was curative.
Surgical Revascularization
Currently, surgical revascularization is reserved for patients
in whom the main renal artery appears completely
occluded and in whom the surviving renal parenchyma
is vascularized by collaterals. Surgical revascularization
might also be used when an ostial stenosis is present with
a buttressing atheroma on either side of the ostium. Some
of these lesions may also be amenable to percutaneous
vascular stent placement.
Several surgical options are available. The stenotic
segment may be excised and the artery resutured directly
onto either the aorta or surviving stump. A vein graft
may be transplanted or the kidney resected and
reimplanted in the iliac fossa with the renal artery
anastomosed to the iliac artery. Another novel method
involves a splenectomy and anastomoses of the splenic
artery to the renal artery when RAS involves the left
kidney. The underlying diagnosis determines the results
of this surgery. With advanced diffuse atherosclerosis,
surgery may become less feasible because the certainty
that the RAS is the cause of the hypertension is less and
the prognosis may be determined by comorbidities.
A potential complication is the release of cholesterol
emboli during the surgery; however, 80–90% of patients
undergoing operation for atherosclerotic RAS benefit with
cure or improvement. The perioperative mortality rate
is less than 5%. In patients with AD, the cure rate is as
high as 80%, and morbidity rates are low. However,
similar results can be achieved with the minimally invasive
renal angioplasty technique, at a considerably less

morbidity, mortality, and expense. In patients with diffuse
atherosclerosis, the complication rate with both surgery
and angioplasty is relatively high.
MORTALITY/MORBIDITY
In patients with hypertension, atherosclerotic renal artery
disease is a strong predictor of increased mortality relative
to the general population. In the setting of renal dys-
function, RVHT is associated with the greatest mortality
rate.
Major complications of RVHT include end-organ
damage due to chronically uncontrolled hypertension and
progressive renal insufficiency, which is an important
sequel of chronic renal ischemia.
The prognosis of patients with RVHT is difficult to
ascertain because it varies with the degree of RAS, the
response of the patient to antihypertensive therapy, and
the effectiveness of revascularization procedures.
RENAL VEIN THROMBOSIS (RVT)
INTRODUCTION
In 1840, Rayer first described the entity of renal vein
thrombosis (RVT) and its association with nephrotic
syndrome. Although trauma, infection, and tumor can
cause RVT, nephrotic syndrome is now known to be the
most common cause of RVT.
ETIOLOGY
Primary Cause
Nephrotic syndromes: Among the various etiologies
of nephrotic syndromes, the nephropathy most commonly
associated with RVT is MGN, with MGN in 60% of
patients, with membranoproliferative glomerulonephritis
(MPGN) in 40% of patients, and with focal sclerosis (FS)
in 28% of patients).
Secondary Causes
1. Alterations of renal flow secondary to volume losses
(GI fluid loss, hemorrhage, dehydration, infection) or
functional states of decreased cardiac output and renal
hypoperfusion (congestive heart failure, aortic
insufficiency, constrictive pericarditis) can predispose
individuals to RVT.
Renal Vascular Diseases 177
2. Blunt or iatrogenic trauma, neoplasms such as renal
cell carcinoma, Wilms tumor, transitional and
metastatic disease, drugs (including birth control pills
and exogenous estrogens), hypercoagulable states
such as pregnancy and disseminated malignancy,
septic abortion, and extension of leg or pelvic venous
thrombus all can predispose an individual to
RVT.
3. In addition, extrinsic compression of the renal vascular
pedicle observed in pregnancy, retroperitoneal fibrosis,
lymphomas, tumors, and abscesses may precipitate
thrombus formation in the renal vein or IVC. Finally,
a number of systemic diseases, including polyarteritis
nodosa, diabetic glomerulosclerosis, sickle cell anemia,
and systemic lupus erythematosus, may also be
associated with RVT.
INCIDENCE
Incidence of symptomatic or asymptomatic RVT is
16-42% in patients with nephrotic.
PATHOPHYSIOLOGY
In general, patients with RVT have two primary modes
of clinical presentation: acute and chronic.
Acute RVT
Acute RVT is most commonly observed in infants and
neonates secondary to dehydration. Acute RVT is
characterized by abrupt onset of flank pain, nausea,
vomiting, and gross or microscopic hematuria. Physical
findings may include a palpable kidney and hypertension.
On occasion, acute RVT may be bilateral, resulting in
oliguric acute renal failure and flank pain. RVT results
in an enlarged kidney that is tense, swollen, and cyanotic.
The renal pelvis is usually stretched, distorted, and
blurred. Bilateral acute obstruction in the adult may well
be lethal irrespective of the cause.
A characteristic, although rare, radiographic finding
is notching of the ureter, which usually occurs when
collateral veins in close relation to the ureters become
tortuous and dilated. If swelling continues to increase,
arterial perfusion may be compromised and the kidney
may undergo hemorrhagic infarction and atrophy.
178 Uroradiology: Text and Atlas

Chronic RVT sections of the renal vein or cessation of blood flow if

The chronic presentation of RVT is observed more the lumen is completely obstructed. Recently, power
frequently than the acute form. In general, it is Doppler USG has increased specificity in the diagnosis
asymptomatic, making the true prevalence of chronic RVT of RVT and in the assessment of caval tumor thrombus.
difficult to determine. Patients present with few or no
Computed Tomography
accompanying symptoms and normal renal function,
except for albuminuria, or gradual worsening in those CT findings include decreased nephrographic attenuation,
with nephrotic syndrome and resultant chronic edema. loss of corticomedullary differentiation, a low-attenuating
Many patients with RVT may develop DVT. They can thrombus in the renal vein (Figure 12.1), renal
initially present with pulmonary thromboembolism. DVT enlargement with persistent parenchymal opacification,
and pulmonary embolism are the most common and renal vein enlargement. In the acute stage, capsular
complications of RVT and nephrotic syndrome, with venous collaterals, thickening of the Gerota fascia, and
pulmonary embolism being the most common fatal pericapsular whiskering are also often observed.
thromboembolic complication.
In chronic RVT formation, regardless of the degree
of thrombosis, the collateral circulation always evolves.
Occasionally, evidence of venous collateralization in the
form of a varicocele or retrograde flow in dilated
superficial epigastric veins is observed. The presence of
a varicocele should prompt careful imaging of the kidney
to assess for bland or malignant RVT. In general, patients
with chronic RVT are older than those with acute RVT,
and they have a greater incidence of other thrombo-
embolic phenomena.

ROLE OF RADIOLOGY AND IMAGING

Because the classic presentation of hematuria, flank pain,
and a lumbar mass is rarely seen in RVT, a high index
of suspicion is essential for the diagnosis. Ultrasonography
(US), CT, and MRI have varying levels of sensitivity and
specificity.
Ultrasonography
Currently, USG is the initial study of choice to exclude
RVT. In an acute setting, USG may reveal an edematous
and enlarged kidney with decreased echogenicity caused
by diffuse edema, focal or diffuse disruption of
parenchymal architecture, and/or thrombus within the
renal veins.
In addition, duplex Doppler USG demonstrates
peaked, abruptly decreasing systolic-frequency shifts and
retrograde plateau-like shifts during diastole at the level
of the main renal artery and its proximal branches, with
an absent venous signal. Doppler US may reveal
increased blood velocity and turbulence in narrowed
FIGURE 12.1: Low attenuation thrombus in IVC and left renal vein
Magnetic Resonance Angiography
Recent observations also suggest that magnetic resonance
angiography (MRA) appears to be a useful and accurate
alternative test for the diagnosis of RVT prior to
venography when US findings are equivocal). MRA
produces high contrast between flowing blood, vascular
walls, and surrounding tissues. Other advantages include
the avoidance of contrast material, its noninvasiveness,
and the ability to image both the arterial and venous
phases. Preliminary observations suggest that MRI and/
or MRA may be the diagnostic procedure of choice for
RVT.
Renal Venography
Presently, renal venography remains the diagnostic
criterion standard. Assessing the venous phase of renal

arteriography also helps in making the diagnosis.
However, both are invasive procedures requiring the use
of potentially nephrotoxic contrast agents in patients with
existing renal compromise. US and MRA do not require
the use of contrast agents.
Radionuclide Renography
Radionuclide renography using technetium 99mTc DTPA
also has been proven useful in the assessment of renal
perfusion. Arterial compromise from venous pressure
elevations in acute RVT is undoubtedly the primary factor
determining ultimate organ damage (Keating, 1985). In
such cases, scintigraphy reveals delayed or absent
perfusion to the kidney. When a scan indicates perfusion
arrest, an aggressive therapeutic approach may be
warranted.
TREATMENT
The treatment of RVT has evolved from nephrectomy
to thrombectomy to anticoagulation, which is presently
the standard treatment of choice in RVT. Anticoagulants
act by preventing further propagation of the thrombus
while allowing recanalization through the body’s own
fibrinolytic system and preventing thromboembolic
phenomenon. Standard therapy has consisted of initiating
systemic anticoagulation with intravenous heparin and
later switching the patient to oral anticoagulants.
Physicians recommend that, as long as patients have
significant hypoalbuminemia (defined as a serum albumin
level <2.5 g/L), anticoagulant therapy should be
administered. For autoimmune disease, steroids and other
immunosuppressive drugs are indicated.
Thrombolytic Therapy
Thrombolytic therapy is warranted in patients with
bilateral RVT and acute renal failure, extension of RVT
into the IVC, acute renal failure, a massive clot with high
risk of acute embolic events, pulmonary emboli, or severe
flank pain . In a patient with unilateral RVT and no other
signs of thromboembolic disease, an absence of flank
pain, and normal renal function, the risk-to-benefit ratio
supports the use of anticoagulant therapy alone.
Thrombolytic therapy should also be considered
in patients whose condition fails to improve with
Renal Vascular Diseases 179
heparin therapy. Because heparin works by enhancing
the activity of AT-III, decreased levels AT-III, as observed
in nephrotic syndrome, may be a cause of failure from
heparin use. In general, prolonged therapy of several
days’ duration may lyse more than 90% of those clots.
Many investigators have demonstrated reversal of acute
renal failure after urokinase-mediated thrombolysis.
Currently, one thrombolytic agent does not appear to
have an obvious advantage over another.
Although thrombolytic agents lead to faster and more
complete resolution, they have the potential to cause
bleeding complications: Minor bleeding occurs in
approximately 5% of patients, and serious bleeding
events, such as intracranial hemorrhage, occur in 1%.
Contraindications for the use of thrombolytic agents
include factors predisposing patients to bleeding,
intracerebral cancer, recent cerebral trauma, a prior
history of cerebrovascular accident (CVA), recent surgery,
or GI bleeding.
The decision to choose systemic or local
administration via venous or arterial administration
depends on risk and benefit factors. Systemic
administration is not invasive while local administration
allows for lower lytic dose and shorter infusion times.
Recent reports suggest that systemically administered
thrombolytic therapy is effective and safe if no obvious
contraindications exist, and invasive procedures might
be avoided.
To date, no prospective studies have been performed
to compare anticoagulation and thrombolytic treatment
alone as the treatment of RVT. The general consensus
is that heparin should be used initially. Thrombolytics
should be reserved for second-line treatment when
heparin fails.
Surgical thrombectomy or nephrectomy is rare and
usually reserved for cases that are refractory to medical
therapy. Thrombectomy is indicated in situations of
unrelenting pulmonary emboli and oliguria refractory to
medical therapy from bilateral RVT or thrombosis of a
solitary kidney. Consider nephrectomy in patients that
present acutely with severe toxicity from hemorrhagic
infarction of the kidney (Keating, 1985).
180 Uroradiology: Text and Atlas

MORTALITY AND MORBIDITY

Pulmonary embolus is the most common and most
serious complication in patients with RVT.

RENAL ARTERIOVENOUS MALFORMATIONS

INTRODUCTION
These are somewhat rare clinical entities, may be
congenital, acquired or idiopathic.

CLINICAL FEATURES
The majority of patient experience hematuria. Other signs FIGURE 12.3: T1 W MRI
and symptoms include abdominal or flank bruits, diastolic
hypertension, cardiomegaly, and congestive heart failure.

ETIOLOGY
Renal arteriovenous fistulas are typically due to trauma;
itrogenic, congenital malformations are rare.

ROLE OF RADIOLOGY AND IMAGING (FIGURES 12.2 TO 12.4)

Characteristic features include dilated, tortuous vessels
within the renal collecting system, as well as early visua-
lization (Figure 12.5) of the renal draining vein and IVC.
Symptoms typically include gross hematuria.
Embolization is the non-surgical treatment.

TREATMENT
Small lesions may be successfully treated with
embolization, whereas larger lesions may require partial FIGURE 12.4: DSA image: Pre-embolization AVM
or total nephrectomy.

FIGURE 12.2: T2 W MRI FIGURE 12.5: Post embolization DSA image

 Renal Vascular Diseases 181

FIGURE 12.6: MDCT: Renal artery aneurysm FIGURE 12.8: CT angiogram: Accessory right renal artery supply
upper pole of right kidney

RENAL ARTERY ANEURYSM

See Figure 12.6.

RENAL INFARCT
See Figure 12.7.

ACCESSORY RENAL ARTERY

See Figure 12.8.

FIGURE 12.7: CECT: Wedge-shaped left renal infarct

182 Uroradiology: Text and Atlas

INTRODUCTION AND HISTORICAL ASPECT portable means to first detect most surgical emergencies
The first renal transplantation was performed in 1954. in such cases (Figure 13.1).
The kidney remains the most frequent organ transplanted.
PATHOPHYSIOLOGY
A major breakthrough occurred with the release of
cyclosporin in 1983; this drug helps to control transplant The process of organ transplantation begins with
rejection. With improved surgical techniques and medical the evaluation of patients with end-stage kidney
management of rejection, renal transplantation has
become the treatment of choice for end-stage renal
disease (ESRD).
The use of immunosuppressive agents such as
cyclosporin, OKT3, and FK506 has resulted in a 1-
year survival rate for mismatched cadaveric renal grafts
of 80%. A 90% 1-year graft survival rate has been
reported with nonidentical grafts from living related
donors and a 95% 1-year success rate for grafts with
identical human lymphocyte antigen. The half-life of grafts
from living related donors varies from 13–24 years.
Surgical techniques for transplantation have improved,
and the means by which kidneys are obtained from living
related donors was recently advanced with the use of
laparoscopic surgical techniques.
Perioperative complications occur in 15–20% of
renal transplants. Most initial complications can
be corrected if detected promptly. The radio-
logist should help to select the most effective
imaging methods for evaluating the many
problems encountered in renal transplantation.
Overall, ultrasonography (US) is a safe, rapid, and FIGURE 13.1: Transplanted kidney (For color version see Plate 6)

disease. Chronic renal failure makes the potential
transplant recipient more susceptible to a wide range of
neoplasms, including carcinoma of the kidney. The
significance of an atypical cyst or a small renal deformity
is much greater in chronic renal insufficiency. The renal
transplant recipient is often chronically ill. Pulmonary
hypertension greater than 35 mm Hg has been detected
in more than a third of patients receiving chronic
hemodialysis. Dialysis access-induced venous stenosis is
common. Stenosis of the superior vena cava may result
in severe upper extremity and cervical venous stasis.
The next stage in the renal transplantation
process involves the selection and examination
of a suitable donor. In the best circumstance, the renal
donor is alive and related to the transplant recipient. The
success of transplants involving living related subjects is
much higher than those involving cadaveric transplants.
Generally, kidneys are harvested from living
related donors using a left-flank approach. Hand-
assisted laparoscopic techniques have been reported to
result in shorter operative and warm ischemia times. The
need for excellent preoperative imaging is directly related
to the challenge of the laparoscopic procedure as well
as the additional time (27–30%) needed to transplant
a kidney with two or more renal arteries. Concomitant
surgery has been performed for live donors using a lapa-
roscopic approach. Simultaneous surgical interventions
at the time of kidney donation benefit the donor and
do not compromise the overall transplantation process.
Renal transplantation surgery must address multiple
renal arteries, which may be treated with primary or
secondary anastomosis. The left renal vein is longer
and easier to use; therefore, harvesting of the left
kidney is favored. Recently described techniques allow
for longer arterial length on the harvested renal transplant.
Longer donor kidney vessels potentially make a right renal
donor kidney more acceptable. Dual pediatric donor
kidneys are left connected to the donor aorta, which is
then anastomosed to the external iliac artery. The vessels
of the ureter must be preserved. In general, the ureter
should be straight but not retracted. The distal ureter is
implanted into the bladder through a tunnel without
opening the bladder.
Radiology of Renal Transplant 183
ANATOMICAL BASIS
The anatomic basis for renal transplantation reflects the
need to create an arterial inflow and venous return for
the renal transplant. The transplanted kidney is generally
placed in the upper lateral portion of the pelvis. The ureter
from the transplant is attached into the urinary bladder
via a submucosal tunnel.
The vascular supply to the ureter of the transplanted
kidney is critical as well. The traditional surgical means
of harvesting the transplant kidney allows the selection
of either the right or left kidney. In most cases, the left
kidney is favored because the left renal vein is longer
than the right. The introduction of a laparoscopic
approach for donor nephrectomy has further emphasized
the selection of the left kidney in most cases. Single renal
arteries and veins are most common; however, the donor
kidney can have multiple renal arteries arising from the
aorta from T12 to L4. Multiple renal arteries are noted
in approximately 25–30% of renal grafts. Allografts with
multiple renal ar teries can be successful. The
pretransplantation donor evaluation must include an
accurate assessment of the number and the location of
multiple renal arteries.
Pretransplantation donor evaluations must include
adequate evaluation for accessory renal arteries beginning
from just below the diaphragm and proceeding distally
to include both external iliac arteries. Arterial assessment
should include the possibility of early renal artery
branching. Preoperative assessment is best performed
using a multidetector CT scanner with extensive post
processing using multiplanar reformatted images and 3D
visualization.
Renal veins can be multiple and present frequent
anomalies. The most common venous anomalies include
the retroaortic position of the main left renal vein, multiple
veins, early branching of renal veins, and anomalies of
the anastomosis between the renal veins and the lumbar
and gonadal veins. Anomalies in the potential renal donor
may include urologic collecting system duplication, single
kidneys, crossed-fused kidneys, and hydronephrosis.
(Figure 13.2).
184 Uroradiology: Text and Atlas

Contd...

3. Vascular
Arterial
• Anastomotic stricture (technical)
• Kinking or twisting of vessel
• Lobar vessel occlusion
• Renal artery stenosis
• Arteriovenous fistula
• Pseudoaneurysm
Venous
• Renal vein thrombosis
• Kinking

FIGURE 13.2: CECT: Transplanted kidney with bifid COMPLICATIONS OF RENAL TRANSPLANT
pelvicalyceal system (TABLE 13.1 AND FIGURE 13.3)
1. An incisional hernia was observed in 4% of transplants
The surgical placement of the donor kidney is subject in one series. The presence of large polycystic kidneys,
to variation depending on the size of the kidney compared bladder outlet obstruction, and chronic lung disease
with that of the recipient, the number of renal arteries,
was associated with the development of an incisional
and the presence of preexisting diseases such as polycystic
hernia. Both early and delayed incisional hernias were
renal disease and severe atherosclerotic disease of the
Renal
pelvic arteries. Repeat renal transplantation is influenced 1. Hyperacute rejection
by the location, condition, and size of the initial (failed) 2. Acute rejection
transplant. The primary arterial anastomosis may involve 3. Chronic
4. ATN
the external iliac artery or the hypogastric (internal iliac) 5. Cyclosporin toxicity
artery. Dual pediatric donor kidneys are left connected
to the donor aorta, which is then anastomosed to the
external iliac artery. Peritransplant
collections
Table 13.1: Complications of renal transplant • Pus
• Blood
1. Renal • Urine
Rejection • Lymph
• Chronic
• Acute
• Hyperacute
• Accelerated
Acute tubular necrosis
Cyclosporine A toxicity
2. Urological
Obstruction Urological Obstruction
• ‘Missed’ stone • ‘Missed’ stone
• Blood • Blood
• Pressure from adjacent collection (ureteric/bladder leak) • Pressure from adjacent collection
• Technical problem (ureteric/bladder leak)
• Technical problem
• Ischemic breakdown • Ischemic breakdown
• Anastomotic stricture • Anastomotic stricture
Urine leak
Peritransplant fluid collection: lymph, urine, pus or blood
FIGURE 13.3: Schematic representation of complications
Contd... of renal transplant

noted. Surgical repair was accomplished by primary
facial approximation and polypropylene mesh
reinforcement. Postoperative complications have been
reported secondary to the use self-retaining retractors.
2. Direct trauma may occur due to compression of large
bowel, femoral nerve compression, or other soft tissue
contusions related to the blade position.
3. Lymphocele collections may occur soon after renal
transplantation or they may develop on a delayed
basis. Whether its origin is from the recipient or donor
is rarely identified. A lymphocele may result in urinary
obstruction of the transplant or compromise blood
flow. Treatment generally involves fenestration of the
cavity into the abdominal space or, more recently,
laparoscopic fenestration.
4. Urinoma or urinary fistulas may occur in any renal
transplant patient but are more common in children
in whom urinary tract anomalies are present.
5. The application of bladder augmentation techniques
(ileum, ureter, sigmoid, stomach), incontinent urinary
conduits (ileum, colon), and continent urinary
reservoirs is associated with surgical complications,
including stomal stenosis, stomal prolapse, renal
artery stenosis, urine leaking, enterovesicular fistula,
and wound dehiscence and urinary tract stones.
Similar complications may occur in the older
transplant patient who has undergone bladder or
prostate surgery.
6. In the period immediately after renal transplantation,
hemorrhage may occur around the transplanted
kidney or in the peritoneal or retroperitoneal spaces.
Later, obstructive uropathy may occur because of
stone formation, cross clamp stenosis, or ischemic
stenosis of the ureter or renal pelvis.
7. Renal arterial and venous stenosis may result in
hypertension or graft failure. The primary treatment
opinion is renal arterial or venous angioplasty often
with a stent placement. Surgical repair of transplant
renal artery stenosis has been described using both
direct vascular repairs as well as with preserved
cadaveric iliac artery grafts.
8. Vascular complications occur in up to 3% of renal
transplants. Thrombotic, hemorrhagic, stenotic, and
embolic complications related to the transplanted
kidney have been reported.
Radiology of Renal Transplant 185
9. Occasionally, masses may arise from within the
transplanted kidney. Renal cell carcinoma, focal
fungal disease, and B-cell lymphoma have been
reportedly transmitted within renal transplants.
10. Infections (Figure 13.4).
FIGURE 13.4: CECT: Focal nephritis in a transplanted kidney
PREFERRED INVESTIGATIONS
CONVENTIONAL RADIOGRAPHY AND IVU
Traditionally, the potential donor was examined with
intravenous urography (IVU) and angiography. But,
conventional radiographs provide a limited amount of
useful information about the complex clinical presenta-
tions of renal transplantation. Often, chest radiographic
findings are nonspecific because chronic interstitial
pulmonary disease is difficult to differentiate, whereas
abdominal radiographs may fail to illustrate fluid collec-
tions. Nowadays, preoperative evaluations are performed
with MRI and CT. CTU offers ease of performance and
a high degree of detection of renal stones, anomalies,
and (less commonly) renal masses in the kidneys of
potential donors.
Limitations
Traditionally, the potential donor was examined with IVU
and angiography. That no longer occurs. Although a
number of pretransplantation urologic evaluations have
been recommended in the literature, no one specific
universally accepted protocol exists. The expense and
potential risk of using IV contrast material should limit
duplication of tests.
186 Uroradiology: Text and Atlas

Donor anomalies related to the upper collecting system

and duplicated ureters may make the kidney from a living
related donor unacceptable. This is readily illustrated on
CT and MRI examinations, replacing IVU.

USG AND COLOR DOPPLER

The most commonly used imaging modality in the renal
transplant recipient is USG. To confirm two kidneys with
no gross abnormality, USG can be used as a screening
tool. Immediate complications related to surgery can be
demonstrated. USG enables suitable localization prior to
biopsy in most patients. Duplex USG also provide
important information concerning the vascular status of
the graft in cases of acute rejection. Delayed complications
related to the renal transplant, such as lymphocele, etc
can also be very well documented. Fluid within the
peritoneal space is not a specific finding. Hypoechoic
abdominal fluid may remain after peritoneal dialysis.
Urine, bowel content, sepsis, and hemorrhage may have
variable sonographic appearances.
Features
Diagnostic USG, including duplex vascular study, is the
most commonly performed examination for routine
follow-up after renal transplantation. Typical renal
transplant sonograms demonstrate the following: arcuate
arteries, echo-poor medullary pyramids, hyperechoic
renal sinus, absence of hydronephrosis, stable renal
volume (formula: 0.5 × length × transverse × antero-
posterior dimensions), normal position of renal transplant
anterior to the external iliac vessels, and otherwise normal
echogenicity in the parenchyma, collecting system, and
surrounding tissues.
The measurement of the vascular resistive index (RI)
is a part of the evaluation. The RI measures resistance
to arterial flow within the renal vascular bed. RI is
calculated from the peak diastolic arterial waveform. The
normal RI is less than 0.7–0.8. An RI of greater than 0.9
indicates transplant dysfunction but not the cause. In some
instances a nonfunctioning renal allograft can have
“normal” RI and pulsatility index (PI) (Figure 13.5).
Peritransplant Fluid Collections
Sonographic evaluation of renal transplant complications
is often successful because many of the potential
FIGURE 13.5: Normal flow waveform in transplanted kidney
peritransplant complications are associated with fluid
collections. The superficial nature of a typical renal
transplant allows good resolution with relatively few
reverberation echoes. During the immediate post-
operative transplant period, most fluid collections in and
around the bed of the transplant are hematomas or
urinomas. A hyperacute hematoma often presents as a
hypoechoic fluid-filled mass near the surgical site.
Hematomas may be stable in size but can enlarge rapidly.
The enlarging hematoma may compress the kidney,
resulting in a reduction of urine output. Later, a hematoma
becomes complex with both hypoechoic and echoic areas.
A second possible cause for fluid around the transplant
during the first 24 hours following transplantation is a
urinoma. A urinoma results from a leak between the renal
transplant ureter and the recipient’s bladder. Such a leak
may be the result of surgical failure or from necrosis of
the distal portion of the transplant ureter. A urinoma
enlarges more slowly and remains hypoechoic. If the
urinoma becomes infected the quality of the fluid may
become more complex as an abscess forms. After several
weeks a spontaneous hematoma or a urinoma becomes
less likely.
A lymphocele may form anywhere in the general area
of the renal transplant. While lymphoceles are more likely
to occur soon after the transplant, they may develop long
after the skin wound has healed. An uncomplicated
lymphocele is hypoechoic and remains hypoechoic unless
 Radiology of Renal Transplant 187

it becomes infected. While lymphoceles are slow to neously. Mild tissue rejection may cause transplant edema,
develop, a lymphocele can create significant pressure and a mechanical obstruction may cause hydronephrosis.
resulting in urinary or venous obstruction. Correlation with findings from functional examina-
An abscess may develop at any time during the life tions, including nuclear medicine study and dynamic
history of a renal transplant recipient. Abscesses may be MRA, should be performed whenever US cannot confirm
around the kidney, within the transplant, or in the the cause of the decreased renal function. Changes in
abdominal cavity remote from the transplant. Most native kidneys of renal transplant patients should include
abscesses have complex sonographic qualities. An abscess a survey to detect masses. Cysts frequently develop in
the kidneys of patients with ESRD. New patterns of
can be diagnosed best by comparing the sonographic
internal echoes or rapidly enlargement should be noted.
texture of a fluid collection to the white blood cell count
Correlation with CT, MRI, or aspiration biopsy results may
and the patient’s fever curve. In cases in which an abscess
be necessary to exclude carcinoma or other pathology.
is considered likely, sonographically guided aspiration is
recommended. Diagnostic ultrasound may both initially Limitations:
diagnose the fluid mass as well as guide the surgical or 1. Sonograms may fail to differentiate gas versus
radiologically based drainage. If percutaneous drainage calcifications, and bowel gas may obscure important
results in a recurrence of a lymphocele, laparoscopic findings.
drainage is indicated. 2. In double (pediatric) renal transplantation, one of the
kidneys may be much smaller than the other. The
Acute Kidney Transplant Rejection smaller kidney may be mistaken for a mass. Patients
may undergo more than one renal transplant. The
Sonographic findings include globular enlargement of the
contralateral, or prior, transplant is generally smaller
kidney, swelling and hypoechogenicity of the medullary
and can be mistaken for a mass.
pyramids, an indistinct cortical-medullary junction, and
3. Gas within the vascular or ductal systems may be
hypoechoic foci in the renal cortex. Among the early
interpreted as calcifications. Aneurysms and venous
findings of acute renal transplant rejection is renal
varices may be mistaken for lymphoceles unless
enlargement. The length of a renal transplant should not
duplex signals are routinely assessed. The degree of
increase from the stabilized posttransplantation hydronephrosis may be underestimated in a patient
measurements. with acute transplant rejection.
Although acute transplant rejection must be consi- 4. Tortuous renal arteries may suggest renal artery
dered in all cases of declining renal function after initially
stenosis in the absence of hemodynamically significant
successful renal transplantation, other acute events may
narrowing. Increases in the RI should be interpreted
occur in the immediate postoperative period or later
carefully. Variations in the location of the sampled
clinical follow-up. Perinephric hematoma and acute
arterial signal may suggest elevation of the RI (Figure
hydronephrosis are among the complications than can
13.6).
result in the acute loss of kidney function.
Perinephric hematoma appears as a peripheral,
mixed, hypoechoic rim or ring surrounding the kidney.
The bleeding may proceed away from the kidney. The
extent of the bleeding may be difficult to evaluate at US
because of overlying bowel gas. Acute or chronic
hydronephrosis has a presentation that is generally similar
to hydronephrosis in a native kidney. The central col-
lecting system may be dilated and filled with hypoechoic
fluid (urine), and a variable degree of dilatation is
generally preset in the renal collecting system. Several FIGURE 13.6: Figure on right shows bilateral small malfunctioning
diseases may affect the transplanted kidney simulta- kidneys and figure on left shows transplanted kidney in the same patient
188 Uroradiology: Text and Atlas
CT Scanning and CT-guided Interventions
CT scanning and CT-guided interventions remain an
important means for examining the preoperative renal
donor candidate and for evaluating the complications
that develop in patients who undergo renal transplants.
CT is not limited by bowel gas; however, the use of
IV iodinated contrast material must be limited in many
cases. CT and MRI studies of the abdomen and pelvis
offer similar information. In most cases, CT is preferred
because CT-guided aspiration and drainage procedures
may obviate surgical interventions.
Findings: An increased interest in CT imaging has
paralleled the improvement in the image quality and
speed of the CT examination. With the introduction of
spiral CT imaging, both the resolution and speed of the
available examinations have improved. Concurrent with
improved imaging, the expanded role of interventional
radiologic procedures has created an important role for
CT imaging in transplant recipients (Figure 13.7).
FIGURE 13.7: CECT: Narrowed supplying artery with segmental
infarct in a transplanted kidney
CT of the renal donor may reveal small renal cell
cancers, cysts, upper collecting system duplications, and
partial renal collecting system obstructions. Particularly
important, the CT examination should be performed prior
to the IV administration of contrast agent to look for renal
stones, as well as immediately after administration of the
bolus.
Early postinjection-phase images best demonstrate
the renal cortex, while images obtained approximately
40 seconds after injection of the contrast agent bolus best
show the combined enhancement within the renal
medullary space and the renal pyramids. Nephrogram-
phase images have been shown to be most sensitive in
the overall detection of renal masses. By reexamining
the kidneys, ureters, and bladder after a 2-3-minute delay,
accurate evaluation of the renal collecting system, ureters,
and urinary bladder is possible.
By carefully reviewing the axial CT images obtained
during the first 20–30 seconds after the IV bolus, most
renal artery duplications and many renal vein anomalies
can be detected. Image collimation of 2–3 mm with an
image index of 1–2 mm is necessary to separate small
vessels, which are closely positioned. The patient must
hold his or her breath during the arterial phase of CT
scanning. Special imaging reformatting and reconstruction
methods improve the general diagnostic accuracy of renal
CT angiography and, in selected cases, the demonstration
of small accessory arteries and venous anomalies that
otherwise might not be detected. Such 3-dimensional
(3D) imaging also provides the surgical team with an
excellent overall review of the surgical anatomy.
CT scanning is useful in the evaluation of both
immediate and delayed complications of renal
transplantation. Multidetector CT urography has been
shown superior to conventional IVP in the detection of
urinary leaks and ureteral obstructions. In the immediate
posttransplantation period, perigraft hemorrhage and
urinary leaks can be detected with CT. In most cases,
either USG or functional nuclear medicine imaging should
be performed first. CT scanning is the best means for
surveying the most common intermediate and delayed
surgical complications. CT findings are related to density
differences between areas of hemorrhage, lymphoceles,
and abscesses.
Regarding the donor, after a careful review of the axial
CT images with a cine technique, the evaluation of
maximum intensity projection images in multiple
projections and variable slab thicknesses is useful.
Coronal, curved, multiplanar, reformatted images best
outline the full length of each renal artery.
Immediate complications related to recipient renal
transplantation is best evaluated with combined or
independent renal USG, functional renal nuclear
medicine study, CT, and occasionally MRI. Acute perirenal
collections with a high CT attenuation of 28 Hounsfield
 Radiology of Renal Transplant 189

units (HU) or greater is most likely perinephric Findings: Gadolinium-enhanced MRA is rapidly
hemorrhage. Perirenal or pararenal fluid collections of becoming the technique of choice for imaging the renal
18–24 HU are most likely lymphoceles. Complex fluid arteries. MRA has several advantages compared with
collections anywhere in the abdomen or pelvis of more conventional digital subtraction angiography (DSA). MRI
than 28 HU on a delayed basis may be abscess cavities and MRA are noninvasive and use no ionizing radiation.
Gadolinium-based contrast media are safe to use in
or chronic (liquefying) hematoma. In general, the findings
patients with renal insufficiency because the agents have
of perirenal transplant complications have a pattern
minimal nephrotoxic effects. MRA provides true anatomic
similar to that of diseases of the abdomen in other
images and permits multiplanar reformatting. High-
immunocompromised patients. Multidetector CT performance MR gradient systems allow the acquisition
urography is more complete and precise compared to of 3D volumes in a single breath hold of shorter than
more conventional diagnostic techniques. The overall 30 seconds. Imaging of the renal arteries is important
diagnostic accuracy of CT urography has been reported in the examination of potential renal donors and of
to be 90%. transplant patients with suspected renal artery stenosis
(Figure 13.8).
Advantages of CT over MRI: The layering of excreted
gadolinium into the urinary bladder and ureters generates
artifacts that are less easily managed at MRI than at CT.
During MRI, changing the patient’s position requires
additional time in the scanner. In comparison, prone or
decubitus positioning at CT allows the mixing of contrast
layers, which enables a more complete evaluation of the
urinary bladder, including the anterior bladder surfaces.
In general, CT of the kidneys and urinary bladder is better
in the detection of renal stones and of renal, ureter, and
bladder anomalies. CT with CTA generally costs less than
MRI. In most applications, MRI is reserved for examination
of the transplant recipient, whereas CT and CTA are used
in the potential donors.

MRI
In more recent years, MRI of the abdomen has evolved
into an excellent alternative means for the diagnosis of
most renal transplantation complications and for the
examination of the living related donor. The contrast
agents used for MRI are nontoxic to the transplanted
kidney, and MRI often can be used to assess renal
function, vascular supply, and postoperative complica-
tions. However, MRI remains expensive and may be
contraindicated in certain patients. Whenever 2 or more
diagnostic techniques are used in the diagnosis of renal
transplantation, comparison between the techniques is
often very useful. Comparison of recent, current studies
with remote, prior examinations is critical. New fluid
collects are of greater significance than are slowly resolving
fluid collections.
FIGURE 13.8: CEMRA: Transplanted kidney with
its vascular supply
MRI offers several advantages in the pretransplan-
tation donor and recipient evaluation. MRI offers good
spatial resolution with excellent tissue differentiation. No
adverse effects related to radiation are known, and the
gadolinium-based IV contrast agents can be safely used
in patients with renal insufficiency. MRA with gadolinium
enhancement has been improved by the development
of fast 3D gradient-echo sequences. The T1 shortening
effect of the IV injection of paramagnetic contrast material
significantly improves vessel imaging by eliminating signal
190 Uroradiology: Text and Atlas
loss from saturation effects, minimizing dependence of
the inflow phenomenon, and possibly decreasing
intravoxel dephasing effects.
MRA demonstrates accessory renal arteries using
gadolinium agents with the same degree of accuracy as
CTA. MRA has been successfully applied to the diagnosis
of most of the complications related to acute renal
transplant vascular thrombosis. Gadopentetate
dimeglumine (DTPA), when administered as an IV bolus
during MRA, provides qualitative functional information
concerning the renal transplant. It demonstrates the
morphology in a manner similar to CT and is generally
superior to diagnostic USG.
Limitations: The spatial resolution of MRI is generally
less than that of CT, while the functional information
available is generally qualitative compared with the
quantitative data provided by nuclear renal scans. Patients
with pacemakers, cochlear implants, most intracranial
aneurysm clips, or severe claustrophobia cannot be safely
examined using MRI. The use of conscious sedation in
mildly claustrophobic patients and young children can
be considered in MRI but this adds to the cost.
Nuclear Medicine Scanning
Nuclear medicine scanning and flow studies remain the
primary means for evaluating vascular supply to the
transplant after surgery. The main advantage of nuclear
medicine scans is that they demonstrate the pathophysio-
logy involved. Recent developments in Doppler USG and
MRI show promise in improving the quality of renal
vascular imaging without the use of potentially nephro-
toxic intravenous (IV) contrast materials. There is certainly
complementary role of nuclear medicine studies and USG
in the imaging evaluation of hydronephrosis, renal artery
stenosis, flank pain, renal masses, pyelonephritis, and
kidney transplant.
Findings: Nuclear medicine studies have a role in all stages
of postrenal transplantation evaluation. Immediately after
surgery, nuclear medicine studies can be used to evaluate
diminished renal function. The most immediate cause
of renal transplant failure may be renal artery occlusion.
During the period immediately after the bolus IV injection
of the technetium 99mTc mercaptotriglycylglycine (MAG3)
agent, both images and activity counts are collected from
the area of the abdominal aorta and the renal transplant
site. Visualization of the renal artery and the renal
transplant should occur within 20–30 seconds, with no
significant difference between the time of aortic and renal
visualization.
The causes of diminished renal function include ATN,
rejection, and drug nephrotoxicity. ATN is the most
common cause of delayed graft function. ATN is
associated with prolonged ischemia and reperfusion
injury. ATN occurs after placement of most cadaveric
grafts. Recovery is usually spontaneous within 2 weeks.
ATN is less common in patients whose transplants are
from living related donors.
Functional activity of the renal transplant is assessed
using activity curves obtained from the renal transplant,
aorta, and background. Orthoiodohippurate 131 and
99m
Tc MAG3 studies demonstrate a delayed transit with
a delayed time to maximum activity and a high ratio of
findings at 20 minutes versus those at 3 minutes.
Mechanical leaks from the renal pelvis, ureter, or urinary
bladder can be detected as extrarenal nuclide collections.
Limitations: Although complete thrombosis and renal graft
infarction is easily determined with nuclide studies,
moderately severe transplant renal artery stenosis may
not have a clear pattern on a renal scan. In dual (pediatric)
renal transplants, the delay in the visualization of one
of the kidneys may indicate partial thrombosis or stenosis
of the arterial supply to that kidney. However, in most
cases, only a single renal transplant is present, and
comparing its activity with that of the other kidney is not
possible. The degree of renal dysfunction must be
compared with the known surgical history and the current
laboratory value.
Angiographic Study
Angiographic study of the transplant may involve CT
angiography, MR angiography, or intra-arterial catheter
angiography if therapeutic procedures are to be
performed. The donor evaluation is most likely done with
MRA and CTA.
In general, CT of the abdomen and kidneys is
performed, especially at the time of the evaluation of
the renal vasculature. If MRA is selected for the renal

vascular evaluation, an MRU can follow with sufficient
spatial resolution to obviate the need for a standard IVU.
Conventional angiography was long considered the
criterion standard for the evaluation of the renal arteries
and veins of the living related donor candidate. Today,
as noted before, CTA (with spiral multidetector and
multiplanar reconstruction) and MRA have become the
imaging techniques of choice. If vascular status, severe
arteriosclerosis, or venous abnormalities of the pelvic
arteries is suspected that might complicate the creation
of the renal artery anastomosis, MRA or CTA can be
performed. Angioplasty or stent placement may be
required with a subsequent interventional procedure.
Findings: Conventional angiography has been replaced
by CTA or MRA in many diagnostic applications both
in the pretransplantation and posttransplantation periods.
Cost, potential morbidity, and possible nephrotoxic effects
of iodinated contrast must be considered. In most cases,
digital subtraction angiography (DSA) provides the most
fully diagnostic evaluation of the renal artery, the
recipient’s vascular status, and the patency of the renal
veins.
In select cases, renal transplant angiography may be
preferred to CTA or MRA. In all cases requiring vascular
intervention, DSA angiography immediately precedes the
interventional procedure. The potential diagnoses best
made with angiography include renal artery stenosis, renal
vein thrombosis, aneurysms, and arteriovenous fistula.
Except for a pelvic location, the diagnosis of renal
transplant circulation disease is similar to the diagnosis
of renal artery disease in the native kidney.
Direct visualization of the lumen of a blood vessel
is considered the most accurate means to determine the
presence of arterial stenosis, venous thrombosis, and
arteriovenous malformation (AVM) or arteriovenous
fistula (AVF). Because angiography is generally performed
just before therapy, other testing typically is not performed
to confirm a catheter-proven lesion. Vascular flow
gradients can be assessed at the time of the procedure
to confirm a hemodynamically important lesion prior to
treatment and to confirm the absence of a gradient after
angioplasty with or without stent placement.
Radiology of Renal Transplant 191
INTERVENTION
Many renal transplant patients undergo renal dialysis
during the years prior to receiving the renal transplant.
Interventional techniques used to treat thrombosed
peripheral arteries have been applied to the removal of
clots within arteriovenous (AV) shunts used for renal
dialysis. At other times, double-lumen central venous
access lines may be used to continue renal dialysis in
the event of AV access failure. Interventional radiology
plays an important role in the care and treatment of renal
transplant recipients.
Historically, catheter angiography has been performed
to evaluate the anatomy of the renal arterial and venous
systems of potential renal donors. To lower costs and
reduce risk, CTA or MRA has largely replaced
conventional DSA in the preoperative phase of renal
transplantation. However, image-guided interventional
techniques play a vital role in the relief of mechanical
urinary obstruction, drainage of abscess and cystic fluid
collections, and aspiration biopsy of neoplastic and
infectious processes.
The development of lymphoceles in the surgical site
of a renal transplant is a diagnostic challenge.
Occasionally, lymphoceles enlarge to cause compression
of the renal transplant pelvis and hydronephrosis.
Drainage of lymphoceles enables diagnosis, and it can
relieve a mechanical obstruction; however, lymphoceles
may recur after catheter drainage. Renal transplant
patients’ immunosuppression makes the development of
opportunistic infections more likely. Evaluation of
aspiration biopsy samples in spinal diskitis may reveal
fungal or bacterial infections that are not often seen in
most other patients.
Interventional techniques commonly used to treat
vascular stenosis, including renal artery angioplasty and
renal artery stent placement, may be applied to the
management of renal artery stenosis. Improvements in
the management of transplant rejection have made renal
transplant arterial stenosis less common. Percutaneous
nephrostomy may be applied to temporarily relieve a
mechanical renal outlet obstruction.
192 Uroradiology: Text and Atlas

• Radiological anatomy of urethra Type 3: unrelated to the verumontanum; present in the

• Urethral pathologies membranous urethra; consist of a disc-like membrane
– Urethritis with central pinhole orifice; rare.
– Periurethral abscess
– Urethral stricture CLINICAL FEATURES
– Urethral calculus
Occur only in males.
– Urethral polyps and diverticuli
Posterior urethral valves are the most common cause
– Urethral caruncle
– Congenital urethral lesions of obstructive symptoms and of ascites in the newborn.
– Urethral tumors. Complete obstruction may lead to renal failure,
oligohydramnios, and intrauterine death, calyceal rupture,
POSTERIOR URETHRAL VALVE (PUV) fetal intracapsular, perirenal or intrarenal urinomas or fetal
PATHOPHYSIOLOGY urine ascites. Other symptoms and signs may include
Posterior urethral valves refer to thick valve cusps that palpable kidneys and bladder, abdominal distention,
result from abnormal fusion and insertion of the plicae straining to void, absence of urinary stream and dribbling.
colliculi. Plica colliculi are the inferior extensions of the BUN and creatinine are usually elevated.
midline urethral crest (2-4 in number) that take a spiral Renal function commonly returns to normal after
course and end inferiorly in the membranous urethra. obstruction is relieved. Occasionally, chronic renal failure
The urethral crest is the continuation of the inferior aspect intervenes despite surgical decompression.
of the verumontanum.
Young children may present with symptoms of urinary
CLASSIFICATION tract infection—fever, vomiting, hematuria, or failure to
Young, 1919: thrive-resulting from vesicorenal reflux and pyelonephritis.
Type 1: present in the bulbo-membranous urethra below Older children or young adults with mild obstruction may
the verumontanum; most common type; produce clinical not be diagnosed until infection supervenes. Therefore,
manifestations. posterior valves must be included in the differential of
Type 2: extend proximally from the verumontanum to UTI or outlet obstruction in male infants, children and
the bladder neck; rare. young adults.
 Urethral Diseases 193

ROLE OF RADIOLOGY AND IMAGING

Neonates (Figures 14.1 to 14.3)
Best examined with ultrasound.
Renal isotope studies (99mTc-DTPA or 99mTc-GH) can
assess degree of residual renal function and renal damage,
differential renal function, degree of hydronephrosis, and
site of obstruction. Addition of furosemide will produce
diureris and help distinguish from nonobstructive
hydronephrosis. Excretory urography is less useful in this
age group and is contraindicated in severe renal
impairment.

Older Children and Young Adults

Valves are best demonstrated by voiding cystourethro-
graphy, although catheter insertion may be difficult with
type 3 valves. The valves are recognized by a spinnaker
FIGURE 14.2: MCV: Type 3 PUV with dilated prostatic urethra,
sail sign that consists of the dilated posterior urethra and bladder neck hypertrophy and thick trabeculated bladder wall
a linear radiolucent defect in the bulbo-membranous
urethra. The urinary stream is reduced distal to the valves.
The bladder is of large capacity, trabeculated, and shows
diverticula, reflux and occasionally a periureteric Hutch
diverticulum that shows up best during reflux.
Transrectal voiding sonourethrography may
demonstrate bladder abnormalities and a dilated prostatic
urethra, but the valves themselves will rarely be visualized.

FIGURE 14.3: MCV: Type 1 PUV with grossly dilated posterior

urethra, trabeculated bladder right renal and agenesis left VUR

FIGURE 14.1: Diagrammatic representation of PU valves
(For color version see Plate 6)
In Utero Diagnosis
Fetal outlet obstruction is diagnosed by ultrasonographic
findings of dilated renal pelves, dilated tortuous ureters,
distended bladder, oligohydramnios, and possibly,
pulmonary hypoplasia and a small thorax. Pelvicalyceal
dilatation may be absent if a calyceal fornix has ruptured
194 Uroradiology: Text and Atlas

and decompressed into an intracapsular, perirenal, or

intrarenal urinoma. A dilated posterior urethra is almost
pathognomonic of outlet obstruction due to posterior
valves. Outlet obstruction is an indication for intrauterine
surgery or early fetal delivery to reduce the incidence
of chronic renal failure in infants.

URETHRAL STRICTURES
INTRODUCTION
During urination, the bladder empties through the urethra
and out of the body. Urine passes through an opening
called the bladder neck into a portion of the urethra FIGURE 14.4: Ascending urethrogram tight urethral
stricture at penobulbar region
surrounded by the prostate, called the prostatic urethra.
The next segment of the urethra is called the membranous
urethra and it contains a muscle called the external urinary
sphincter. This sphincter allows a patient to voluntarily
hold urine and to stop during urination. Together, the
prostatic urethra and the membranous urethra make up
the posterior urethra, and are approximately one to two
inches long. The urine then enters the bulbar urethra,
followed by the penile urethra. The penile urethra is the
segment that runs along the bottom surface of the penis.
The exit at the tip of the penis is called the meatus. The
bulbar urethra, penile urethra and meatus make up the
anterior urethra, which is 9 to 10 inches long.
A urethral stricture is a scar in or around the urethra,
which can block the flow of urine, and is a result of FIGURE 14.5: Ascending urethrogram: Urethral stricture with
outline irregularity and spicking urethral carcinoma
inflammation, injury or infection.
penis up into the bladder to allow urine to drain until
ETIOLOGY a repair can be performed. Trauma such as straddle
Stricture disease may occur anywhere from the bladder injuries, direct trauma to the penis and catheterization
to the tip of the penis. can result in strictures of the anterior urethra.
The common causes of stricture are trauma to the In adults, urethral strictures may occur after prostate
urethra and gonorrheal infection. However, in many surgery, removal of kidney stones, urinary catheterization
cases, no cause can be identified. or other instrumentation.
Stricture of the posterior urethra is often caused by In children, urethral strictures most often follow
a urethral injury associated with a pelvic bone fracture reconstructive surgery for congenital abnormalities of the
(e.g. motor vehicle or industrial accident). Patients who penis and urethra, cystoscopy and urethral catheter
sustain posterior urethral injuries from pelvic fracture drainage.
generally suffer a disruption of the urethra, where the
urethra is cut and separated. These patients are ROLE OF RADIOLOGY AND IMAGING
completely unable to urinate and must have a catheter Evaluation of patients with urethral stricture disease
to realign the urethra. The catheter is placed through the includes:

1. Urethral imaging (X-rays or ultrasound) and
2. Urethroscopy.
The retrograde urethrogram is an invaluable test
to evaluate and document the stricture.
Combined with antegrade urethrogram, length of
the stricture can be determined. The retrograde
urethrogram is performed as an outpatient X-ray
procedure and can indicate the number, position, length
and severity of the stricture(s). This study involves
insertion of contrast dye (fluid that can be seen on an
X-ray) into the urethra at the tip of the penis. No needles
or catheters are used. The retrograde urethrogram study
allows doctors to see the entire urethra and outlines the
area of narrowing at the stricture (Figures 14.4 and 14.5).
Ultrasound is performed by placing a small, high
frequency ultrasound probe on the skin over the stricture
to view it and surrounding tissue.
Urethroscopy is a procedure where the doctor gently
places a small, flexible, lubricated telescope into the
urethra and advances it to the stricture. This study permits
the doctor to see the urethra between the tip of the penis
and the stricture.
Recently MRI is also being used for evaluation of
urethral lesions.
OTHER BENIGN URETHRAL LESIONS
Causes can include abscesses, pelvic fractures, straddle
injuries, infections or injury caused by surgical instruments
(e.g., catheters, cystoscopes, resectoscopes, etc.).
BENIGN NEOPLASMS
Linked to the presence of genital warts on the penile shaft,
these lesions are often the product of human papilloma
virus (HPV). Urethral wart-like growths are suspected
when there is bleeding from the urethra, a visible lesion
on the opening of the urethra or changes in the urinary
stream, accompanied by a history of genital warts.
BALANITIS XEROTICA OBLITERANS
Balanitis xerotica obliterans is a chronic condition with
unknown causes that affects the end of the penis and
is marked by pale, shiny, whitish skin around the opening
of the urethra. The scarring and thinning of the membrane
begin (in most cases) in young adulthood and can
Urethral Diseases 195
progress, leading to a narrowing of the urethra and
difficulty passing urine. Other symptoms include soreness
and itching in the area and sometimes ulceration.
URETHRAL POLYPS
A urethral polyp is an irregularity that is usually present
at birth. It is usually composed of fibrous tissue but may
include some smooth muscle, small cysts or nerve tissue
all covered by a thin protective layer of tissue. Symptoms
include a lump in the vulva, blood in the urine or a
blockage. Urethral polyps are diagnosed with cystoscopy,
a fiber-optic technique that allows a urologist to readily
view the polyp, and a voiding cystourethrogram (VCUG).
By combining an X-ray of the urethra with dye in the
area, the doctor can easily view the structures.
PARAURETHRAL CYST
Also known as Skene’s glands, paraurethral glands are
located in the urethrovaginal wall at the opening into
the urethra in females. A paraurethral cyst will be evident
to a doctor by its appearance — a glistening, tense and
bulging yellowish-white mass reducing the size of the
urethral opening. Other symptoms include a misdirected
urinary stream and possibly painful urination.
URETHRAL CARUNCLE
Urethral caruncles are polypoid (or stalk-like) masses,
hanging from one area of the external urethral opening.
The primary sign of this problem is a thin, reddish
membrane protruding from one portion of the urethral
opening. Other symptoms include bleeding and urination
problems such as frequency, urgency and pain. A urethral
caruncle is usually spotted during an examination for
another condition. They are relatively common in the
urethral epithelium of women who do not use hormone
replacement therapy (HRT) after menopause. Marked by
a purplish mucosal mass, this condition can cause a
variety of symptoms, including difficult or painful
urination, blood in the urine and tenderness.
URETHRAL DIVERTICULUM
Urethral diverticulum are outpouchings of urethral
mucosa through their weak walls (Figures 14.6 and
14.7).
196 Uroradiology: Text and Atlas

FIGURE 14.6: MCU: Urethral diverticulum FIGURE 14.9: Urethrogram: Beaded urethrogram-multiple short
segment urethral strictures typical of TB

FIGURE 14.7: MCU: Well defined, smooth, oval filling

defect in mid urethra urethral polyp
FIGURE 14.10: Hypoplastic penis with underdeveloped urethra

FIGURE 14.8: Ascending urethrogram: Normal anterior urethra FIGURE 14.11: MCU: Meatal stenosis
 Urethral Diseases 197

FIGURE 14.12: Plain X-ray: Calculus in prostatic urethra FIGURE 14.13: Ascending urethrogram: Filling defect due to
calculus in penile urethra

FIGURE 14.14: USG: Calculus in prostatic urethra with dense post-acoustic shadow
198 Uroradiology: Text and Atlas

FIGURE 14.15: MCU: Urethral trauma with narrowing of bulbo- FIGURE 14.16: MCU: Large periurethral collection of
membranous urethra and extravasation of contrast periurethrally contrast abscess cavity

DUPLICATION OF URETHRA URETHRAL CALCULUS

See Figures 14.8 and 14.9. See Figures 14.12 to 14.14.

AGENESIS OF URETHRA PERIURETHRAL ABSCESS

See Figure 14.10. See Figures 14.15 and 14.16.

MEATAL STENOSIS
See Figure 14.11.

CLASSIFICATION
• Bladder diverticulum
• Neurogenic bladder
• Vesical calculus
• Emphysematous cystitis
• Bladder carcinoma
• Rhabdomyosarcoma of bladder
• Primary lymphoma of bladder
• Urachal carcinoma
• Bladder outlet obstruction (BOO).
BLADDER DIVERTICULUM
The diverticula are full thickness outpouchings of mucosa,
adventitia, and detrusor muscle. There is usually a
communicating channel with the main bladder lumen.
Diverticula can have wide or narrow necks. The wide
necked variety empty urine readily. The narrow neck types
are slow to empty and therefore, are more likely to have
urinary stasis.
Bladder diverticula are categorized as:
• Congenital or
• Acquired.
Whether congenital or acquired the etiology is
secondary to bladder outlet obstruction.
• If a congenital diverticula (hutch diverticula), the
bladder outlet obstruction is usually secondary to a
Urinary Bladder Diseases 199
congenital urethral valve or urethral stricture. The
congenital variety of diverticula are typically seen in
boys. These diverticula are characteristically located
at the ureteral insertions. Often, vesicoureteral reflux
is resultant. Bladder diverticula most often occur as
a result of outlet obstruction. Occasionally, a congenital
weakness in the bladder wall adjacent to the ureteral
orifice results in a diverticulum. This is termed a
“Hutch” diverticulum.
In children, outlet obstruction causing a diverti-
culum is rare and can be seen with urethral valves.
In men, diverticula are associated with outlet obs-
truction from urethral stricture, prostatic hypertrophy,
prostatic carcinoma, etc. acquired diverticula are rare
in women.
• If it is an acquired diverticula, the bladder outlet
obstruction is usually secondary to BPH, carcinoma,
or prostatitis. Acquired diverticula can occur anywhere
there is a bladder wall weakness, although, as in the
congenital variety, the most vulnerable area for
presentation is at the ureteral insertions.
Diverticula usually occur on the lateral bladder walls,
rarely the dome. They are often multiple. Large diverticula
often displace the bladder and or ureters.
Infection, tumor and stone formation can occur as
a result of urine stasis within a diverticulum. Tumor
formation in a diverticulum is more likely to spread
200 Uroradiology: Text and Atlas

beyond the bladder because the diverticulum wall consists CYSTITIS (Figure 15.2)
only of urothelium without muscle. • Ascending urinary tract infection is extremely common
Bladder diverticula can be evaluated with excretory in sexually active females.
urography, ultrasound, CT and cystoscopy. • Urethritis and cystitis can occur.
CONGENITAL URETHRAL DIVERTICULUM • Burning of micturation is the clinical hallmark
• Wall thickness upto 5 mm may be normal, however
INCIDENCE
thickend, hypoechoic and irregular bladder with
Occurs mainly in male infants and children. echoses in urine may favor cystitism USG.
Female ureteral diverticulum is acquired.
ANATOMICAL BASIS EMPHYSEMATOUS CYSTITIS
Arises from the ventral surface of the anterior urethra
Embryology: result of either failure of closure of urethral
folds or an abortive attempt at urethral duplication (in
which case there are anterior urethral valves in the
penoscrotal junction region).
ROLE OF RADIOLOGY AND IMAGING
Diverticulum fills slowly during voiding and has a narrow
neck. As it fills it may obstruct drainage from the true
urethra, leading to incomplete bladder emptying and
infection. At the termination of micturition, the
diverticulum causes dribbling (Figure 15.1).
TREATMENT
FIGURE 15.2: Ultrasonographic section: Cystitis
Urethroplasty to repair the defect in the urethral floor.
INTRODUCTION
It is a rare entity. Typical patients are immunocompro-
mised or elderly and debilitated, and 50 percent of cases
are seen in diabetics.

CLINICAL FEATURES

Patients may present with anything from no symptoms

to an apparent acute abdomen. Pneumaturia is rare.
Prevalence in females is twice that in males. Often
associated with urinary stasis, and growth of gas forming
organisms (most commonly E. coli, but others include
Enterobacter aerogenes, Proteus mirabilis, Staphylo-
coccus aureus, streptococci. Clostridium perfringens, and
Candida albicans).

ROLE OF RADIOLOGY AND IMAGING

Plain abdominal radiographs are generally sufficient

FIGURE 15.1: MCU: Multiple pseudodiverticuli c ‘pine-tree’
appearance of urinary bladder in a case of neurogenic bladder to confirm the diagnosis. This disease is often not

suspected until discovered on the abdominal radiograph.
Findings include curvilinear gas lucencies throughout the
bladder, often described as a “cobblestone” or
“beaded necklace” appearance. Gas may ascend the
ureters and reveal an air pyelogram. In rare cases, where
plain images are negative despite high clinical suspicion,
CT may show intramural bladder gas.
This appearance differs from that of bladder gas
introduced by trauma, instrumentation, or vesicocolic
fistula, where gas is confined to the bladder lumen, and
does not exhibit the curvilinear appearance.
Treatment of emphysematous cystitis involves early
broad spectrum antibiotics, drainage of the bladder, and
management of hyperglycemia if present.
Prognosis in patients diagnosed and treated early in
the disease process is usually good. The development
of emphysematous ureteritis, nephritis, or adrenalitis
portends a poor prognosis.
TRANSITIONAL CELL CARCINOMA (TCC) OF
URINARY BLADDER
INTRODUCTION
Embryologic derivation of the collecting system of the
urinary tract occurs from the fetal mesonephros. As a
result of this development, tumors of the renal collecting
system arise from cell origins different from the renal
parenchyma. Their classification is based on their
respective mesodermal or epithelial tissue origin. Primary
neoplasms of the renal collecting system represent
10% of the renal tumors, of which approximately 80%
are malignant. Most are transitional cell carcinomas
(TCCs).
Bladder TCC is 50 times more common than renal
pelvic tumors. Often, TCCs are multiple, involving any
part or all of the collecting system. The tumors are
traditionally classified into papillary and nonpapillary
types. Nonpapillary tumors are considered malignant.
INCIDENCE
The true incidence of TCC internationally is not known;
however, regions of the world where schistosomiasis
Urinary Bladder Diseases 201
is endemic are expected to have a higher incidence of
TCC.
PATHOPHYSIOLOGY
Causative Agents
1. Chemical carcinogens act locally on the epithelium,
causing a field change; their action is enhanced by
the contact time (exacerbated by urinary stasis or
diverticulae).
Chemical carcinogens:
Tobacco
Aniline dyes
Benzidine
Aromatic amines
Rubber; and
Azo dyes used in textiles, printing, and plastic
manufacturing.
2. Partial obstruction may account for increased exposure
to the upper tracts (e.g. increased incidence of TCC
in horseshoe kidney).
3. Abuse of analgesics (e.g, phenacetin, which increases
the risk 8 times); cyclophosphamide therapy (6-y lag
time), particularly after drug-induced hemorrhagic
cystitis.
4. Balkan nephritis, with progressive renal failure; and
multiple bilateral tumors (etiology unknown); and
5. Recurrent or chronic infection and urinary calculi
(squamous cell carcinoma [SCC] is the most common
entity in this case).
Polychronotropism
Of great importance is the multiplicity of TCCs of both
synchronous and metachronous natures. This issue
includes a frequent association of papillomas in patients
with TCCs. Almost 25% of patients with renal pelvic
papillomas develop a carcinoma. Of those with multiple
papillomas, 50% develop carcinomas. Ureteric TCC may
be solitary, but TCC has marked propensity for unilateral
multicentricity. The reason is unknown, but this
distribution may result from antegrade and/or retrograde
seeding or the fact that the entire ureteral mucosa is
exposed to the carcinogen.
202 Uroradiology: Text and Atlas

Pathology/Histology
TCCs usually have the following broad classification:
1. Exophytic papillary lesion (85%) with a frond-like
structure and central fibrovascular core lined by an
epithelial layer (broad based and pedunculated);
2. Nonpapillary, noninfiltrating;
3. Infiltrating, usually of higher grade and less common;
and
4. Carcinoma in situ.

STAGING OF TCC
Although no staging method is universally recommended,
the following tumor, nodes, metastases (TNM)–American
Joint Committee on Cancer (AJCC) technique is useful
in upper tract and ureteral lesions:
• Tis 0 indicates an in situ lesion; Ta, noninvasive
papillary carcinoma;
• T1 I, invasion of the subepithelial connective tissue;
• T2 II, tumor confined to the muscularis layer;
FIGURE 15.3: Staging of urinary bladder carcinoma
• T3 III, invasion of the renal parenchyma and/or
peripelvic soft tissues; and
• T4 IV, extension beyond the renal capsule. commonly occurs as a result of edema after endoscopy
and/or endoscopic resection and as a result of fibrosis
A staging classification that incorporates the TMN
from radiation therapy.
and Jewett-Strong-Marshall (JSM) systems is
useful. The stages are as follows:
METASTASES
• T1 A indicates lesions involving the mucosa and
submucosa; Hematogenous spread is less frequent with renal pelvic
• T2 B1, invasion of the superficial muscle layer; tumors than with hypernephromas.
• T3a B2, invasion of the deep muscular wall; Lymphatic supply is extensive, and lymphogenous
• T3b C, invasion of perivesical fat; involvement occurs early in the disease process.
• T4a D1, extension to perivesical organs; Metastases occur to the lung, lymph nodes, and liver,
• T4b, invasion of the pelvic and/or abdominal wall; with direct extension into the retroperitoneum being
and D2, distant metastases (Figure 15.3). common.
Metastases from ureteral TCC are far more common
GRADING OF TCC
than those from bladder cancer partly because the ureteral
The grade is usually correlated with the stage, as follows: wall is thin and acts as a poor barrier. Metastases occur
1. Indicates the cells are slightly anaplastic; in approximately 11% of cases, in the following sites:
2. Intermediate features are observed; and • Retroperitoneal nodes (34%);
3. Marked cellular pleomorphism is present. • Distant lymph nodes (17%);
The stage of tumors in the bladder as assessed by • Liver (17%);
the depth of infiltration is the single most important • Lumbar vertebrae (13%);
prognostic parameter when treatment is initiated. • Lungs (9%);
Clinical staging has an accuracy of 50% when compared • Kidneys (8%);
with that with CT (32–80%) or MRI (73%). Overstaging • Adrenals (4%);

• Spleen (2%);
• Sacral vertebrae (2%);
• Brain (2%);
• Pancreas (2%);
• Skin (2%); and
• Isolated metastases to the colon, broad ligament,
diaphragm, humerus, omentum, pericardium, pleura,
prostate, and vagina.
ANATOMICAL BASIS
Embryologic derivation of the urinary tract collecting
system occurs from the fetal mesonephros. As a result
of this development, tumors of the collecting system of
the renal tract arise from cell origins different from the
renal parenchyma. Their classification is based on their
respective mesodermal or epithelial tissue origin.
The uroepithelium is the mucosal lining of the calyces,
infundibula, ureters, urinary bladder, and portions of the
urethra. The uroepithelium has a characteristic micro-
scopic appearance that is midway between glandular and
squamous tissue and hence, its name transitional epi-
thelium. Following the distribution of the uroepithelium,
TCC can develop anywhere from the calyces down to
parts of urethra with uroepithelial lining.
CLINICAL FEATURES
Sex: The male-to-female ratio is 3–4:1.
Age: The mean age of onset is 50–70 years.
Hematuria is a common symptom that occurs in as
many as 80% of patients; it may be frank or microscopic.
Hematuria may occur early or late in the development
of the disease. For upper tract TCC pain, abdominal mass
and pyuria occur with approximately the same frequency
as that of other renal based tumors. Dysuria and frequency
are more commonly reported with ureteral tumors. Pain
is usually dull and colicky and results from obstruction,
although a second type of pain results from direct tumoral
extension. This is frequently severe, constant, and
penetrating.
Rare instances of spontaneous urinary extravasation
due to rupture have been reported; this often results in
an acute abdomen. Other rare findings include
hypercalcemia, secondary amyloidosis, and elevated
chorionic gonadotropin levels.
Urinary Bladder Diseases 203
PREFERRED EXAMINATION
Elevated urinary lactate dehydrogenase (LDH) levels
have been reported, but this finding is nonspecific.
However, cytology can play a significant role, with a
60% accuracy rate in the diagnosis of renal pelvic and
ureteral TCC. Cytology is particularly useful in more
advanced stage tumors, with an accuracy rate improved
to 80%. Selective lavage, ureteral urine collection, brush
biopsy, or ureteroscopy may be performed to obtain
specimens.
SUGGESTED SYSTEMATIC APPROACH TO EVALUATE
ANY UB MASS AND ITS EXTENSION
• Identify the tumor.
• Identify the capsule and possible invasion.
• Evaluate for periprostatic fat infiltration.
• Evaluate the neurovascular bundles and other
periprostatic vascular structures.
• Evaluate abnormalities within the seminal vesicles.
Determine whether the base of the prostate is involved
and whether extraprostatic extension at the base is
present.
• Identify the apex of the prostate and evaluate for
possible tumor involvement and apical extension.
• Identify any regional or extraregional lymph nodes.
Identify any bone involvement.
ROLE OF RADIOLOGY AND IMAGING
The work-up of patients in whom TCC is suspected
includes ultrasonography and IVU. However, CT scanning
is the best modality for the detection and staging of TCC,
usually without the need for additional imaging.
Plain Radiograph
Plain radiographic findings, such as calcifications, are not
specific in the diagnosis of urothelial tumors, and they
usually contribute little to the diagnosis.
Plain radiographic findings are nonspecific, parti-
cularly the presence of calcification, which has a wide
differential. Filling defects in the renal collecting system
and the bladder, as seen with IVU, CT, and retrograde
pyelography, are present in a number of other patho-
logies. These findings are not specific for TCC.
Findings: Plain radiography may be first study to alert the
radiologist to presence of a renal mass or bladder mass.
204 Uroradiology: Text and Atlas
Occasionally, a large renal outline may be seen in a
completely obstructed kidney. Uncommonly, radio-
graphically discernible areas of punctate calcification may
be seen in TCC. The calcification is on the surface of the
tumor and not within the mass duct. Intrinsic calcifications
suggest an adenocarcinoma or the unusual cell type.
TCC is associated with analgesic nephropathy. Plain
radiographic findings of displacement of renal calcifi-
cations, which occur in analgesic nephropathy, may be
the first sign of TCC. Surface calcification of a bladder
tumor may be seen on plain radiographs in 1%
of cases. Osseous expansive destruction or lung
metastases may be seen in the presence of renal
malignancy.
Intravenous Urography
IVU is a common diagnostic test in patients with
hematuria, although the early detection of small urothelial
tumors may be difficult. A meticulous IVU technique is
required.
Findings: The most common findings in TCC of the kidney
are a single or multiple filling defects in renal pelvis, as
seen in 35% of cases. About 26% of patients with renal
TCC may show a dilated calyx due to partial or complete
obstruction of infundibulum. Amputation of the calyx may
be seen in 19% of cases. No visualization of the affected
kidney may occur in 13–31% of cases. This is usually
secondary to hydronephrosis but can be the result of
tumor infiltrating and replacing functioning kidney or the
occlusion of the renal vein. Hydronephrosis with renal
enlargement due to tumoral obstruction of ureteropelvic
junction may be seen in 6% of cases.
Various signs have been described in renal TCC. The
stipple sign is a rare sign that occurs when contrast
material is trapped within the interstices of a papillary
tumor. When this is seen en face, the tumor appears to
contain multiple stipples. This sign is highly suggestive
of TCC. When this sign is seen, blood clots and
radiolucent calculi are excluded, and further investigations
are superfluous. Punctate calcification on a TCC may
mimic the stipple sign.
Punctate calcification is unusual in TCC, and such
calcification is apparent on the scout image before the
intravenous contrast material is delivered. Occasionally,
contrast material may be trapped within a blood clot
formed in the ureter and then extruded into the bladder
as a stringy mass that may trap contrast material in an
irregular fashion. However, this entrapment is coarser
than that seen with neoplastic stippling.
Fungus balls or mycetoma may also occasionally
entrap contrast material, but the pattern of entrapment
is lamellar and frequently associated with gas formation
(frequently, patients have poorly controlled diabetes with
urinary tract infections). Rarely, stippling may be observed
in tubular ectasia when papillae containing dilated ducts
of Bellini are seen en face. Inspection of the other papillae
may make the diagnosis obvious.
Phantom calyx represents the failure of a calyx to
opacify due to obstruction. Oncocalyx represents calyceal
distension due to the tumor.
In contrast to renal TCC, ureteric tumors show a single
or multiple filling defects in only 19% of cases. This
observation may be associated with hydronephrosis and
hydroureter in 34% of cases or to a nonfunctioning kidney
in advanced cases.
Bladder TCC also shows an irregular filling defect
with broad base and fronds. Increased thickness of the
bladder wall in the region of the tumor should indicate
infiltration.
Retrograde Pyelography
RGP is useful when the kidney cannot be visualized by
means of IVU or when IVU cannot be performed because
of renal disease or an adverse response to the contrast
agent. Retrograde pyelography also has the advantage
that it can be combined with various biopsy techniques.
Findings: Retrograde pyelography in ureteric TCC may
show focal expansion of ureters around and distal to the
mass called the champagne, or goblet, sign. This finding
is helpful in differentiating TCC from other causes of focal
lesions such as calculi or blood clots. Typically, calculi
and blood clots do not demonstrate a goblet sign as they
do not progressively stretch the ureteral wall from slow
growth. Occasionally, the catheter may coil below the
mass during retrograde catheterization; this is called the
Bergman sign.

Retrograde pyelography is useful when the kidney
cannot be visualized with IVU or when an intravenous
approach cannot be performed because of renal disease
or an adverse reaction to contrast agents. Retrograde
pyelography may be combined with brush biopsy for a
highly reliable method in the definitive diagnosis of TCC.
The results are considered diagnostic in 85 percent of cases.
If spot filming is the imaging technique, this should
be performed in an appropriate fluoroscopic digital unit
where serial images can be obtained. This would at both
diuresis urography (infusion IVU with 300 mL of
30% contrast media) or at antegrade/retrograde
pyelography.
Angiography
It has no role in the diagnosis of TCC, but it may have
a role in preoperative planning, particularly when
neoplasm sparring surgery is being considered. However,
here also, CT angiography (CTA) and magnetic resonance
angiography (MRA) are challenging the catheter studies.
Ultrasonography
It is inaccurate for diagnosing early TCC, and it is useful
in the diagnosis of obstructive uropathy. Ureteric lesions
are particularly difficult to visualize unless they cause
hydronephrosis and hydroureter. The other limitation of
ultrasonography is that it is inaccurate in the staging of
bladder TCC, particularly Ta and T1 tumors, and also
in detecting pelvic lymph-node involvement.
Findings: The most common sonographic appearance
of TCC is a hypoechoic renal collecting system mass
splitting the central echocomplex with varying degree of
infundibular dilatation. Focal hypoechogenicity of
adjacent renal cortex reflects local invasion. Occasionally,
the central echocomplex may be only segmentally
amputated.
Ultrasonography is inaccurate for diagnosing early
TCC, and it is useful in the diagnosis of obstructive
uropathy. Ureteric lesions are particularly difficult to
visualize unless they cause hydronephrosis and
hydroureter. The other limitation of ultrasonography is
that it is inaccurate in the staging of bladder TCC,
particularly Ta and T1 tumors, and also in detecting pelvic
lymphnode involvement.
Urinary Bladder Diseases 205
Limitations: On sonograms, calculi may be confused with
high-grade TCCs, which can be densely echogenic. No
sonographic features are specific for TCC, and many filling
defects within the renal collecting system and bladder
may give rise to a nonspecific appearance. Ultrasono-
graphy also has problems in depicting nondilated ureters.
CT
Multidetector-row CT (MDCT) with postprocessing image
manipulation (contour imaging) is rapidly challenging
IVU.
CT is rapidly increasing its sensitivity in staging early
TCC, as noted above. However, developments such as
virtual cystoscopy and postmicturition scanning should
improve the overall accuracy of staging by using CT.
On CT scans, confusion may occur with a blood clot
and a hyperattenuating TCC, particularly in early stages
of the disease. Also, as alluded to above, any cause of
inhomogeneous renal fatty attenuation in a patient with
undiagnosed early-stage TCC may hinder accurate
diagnosis.
Multidetector-row CT is replacing IVU in the
evaluation of hematuria, although IVU is still
being used. The early detection of small urothelial
tumors demands a meticulous IVU technique. Accurate
demonstration of the pelvocalyceal system requires
abdominal compression to distend the collecting systems,
and oblique imaging or tomography may also be
necessary. Diuresis multidetector-row CT with contour
reformatting of the axial records may be useful. This
technique does not require abdominal compression. Early
experience with this method has been most positive
because the CT technique demonstrates not only the
opacified lumen but also the surrounding soft tissue
anatomy.
Findings: Filling defects with dilated calyces are easily
seen and readily diagnosed. Hydronephrosis with renal
enlargement is easily confused with uncomplicated
primary pelvic hydronephrosis, and antegrade/retrograde
pyelography is usually required for diagnosis.
Adequate depiction of the ureters is difficult, and
prone, oblique, or even spot images obtained during
fluoroscopy may be required at urography. If an area
206 Uroradiology: Text and Atlas
of constant narrowing of the ureters is seen on more
than 1 image and if it cannot be explained by a crossing
vessels or peristaltic wave, a tumor must be suspected.
A meticulous urographic examination (radiographic or
multidetector-row CT) can prevent unnecessary
pyelography/ureterography in the majority of cases.
Importantly, if the demonstration of the pelvicalyceal
system at excretion urography or CT is poor, an upper-
tract tumor may be missed, particularly when a decoy
of a bladder tumor is present. The coexistence of upper-
and lower-tract tumors is not rare (Figures 15.4 and 15.5).
The sensitivity and specificity with regard to the upper
urinary tract pathology are 67% and 91%, respectively,
for IVU and 56% and 94%, respectively, for
ultrasonography. For both techniques combined, the
sensitivity and specificity are 79% and 88%,
respectively. IVU has a 70% accuracy rate in the diagnosis
of bladder TCC. The role of radiology is in demonstrating
FIGURE 15.4: Focal bladder wall thickening in a case of
Carcinoma bladder
FIGURE 15.5: Focal bladder wall thickening carcinoma at bladder
bases with coincidental right UVJ calculus
the upper urinary tract, both at the time of the initial
diagnosis and during the follow-up of urothelial cancer.
The statistics for multidetector-row CT are now in
development.
Approximately 5% of ureteric TCCs grow intramurally,
producing a stricture rather than a filling defect.
Radiologically, distinguishing this type of tumor from
stricture is impossible. However at CT, a thickened ureteric
wall with stranding may be seen.
MRI
It has the advantage of high intrinsic soft-tissue contrast,
its direct multiplanar capability, and the availability of
nontoxic renally excreted contrast agents. MRI appears
to be at least as useful as CT in the evaluation of
perivesical fat involvement, and it may be superior to
CT in the detection of invasion of the adjacent organs.
However, MRI cannot depict superficial invasion of the
upper urinary tract TCC well.
Both CT and MRI have been shown to perform better
than cystography in the diagnosis of tumors in the bladder
diverticula that are not depicted on cystograms because
of obstruction at the diverticular orifice.
MRI is expensive and has limited availability. False-
positive diagnosis has been reported. In staging bladder
TCC, tumor extension is overstaged according to the TNM
classification in 7.5% of patients and understaged in
32.5% of patients.
RNI
Isotope renography is an extremely sensitive means of
assessing relative renal function and obstructive uropathy
prior to surgery. Isotope bone scanning is a useful
technique in the investigation of skeletal metastases.
Findings: Isotope renography is an extremely sensitive
means of assessing relative renal function and obstructive
uropathy prior to surgery. Isotope bone scanning is a
useful technique in the investigation of skeletal metastases.
D/D OF FILLING DEFECTS
1. Radiolucent or uric acid stones,
2. Blood clots,
3. Sloughed papilla due to papillary necrosis or

4. Fungal balls in patients with diabetes may mimic
a TCC.
5. Vessel crossing may cause a linear extrinsic
impression; in these cases, oblique or compression
images may help in differentiating them from
urothelial tumors.
6. Tuberculosis can cause narrowed infundibulum and
irregular calices and is the major imaging differential
diagnosis.
7. Other mimics include pyeloureteritis cystica.
8. Renal cell carcinoma invading the pelvicalyceal
system, or
9. Choleastoma
10. Papilloma or polyp
11. SCC is radiographically indistinguishable from TCC;
however, SCC is less likely to be a polypoid tumor.
Although a diagnosis may be made on the basis
of urograms or cystograms, a small bladder tumor,
especially one of the infiltrative types, can remain
undetected. Furthermore, a dense concentration of
contrast material may obscure the intraluminal part
of the urothelial tumor.
INTERVENTION
Nephrostomy may be indicated in renal or ureteric
inoperable neoplastic obstruction or as a stop-gap
procedure prior to surgery to improve renal function. The
conventional and standard technique in the treatment
of TCC is a nephroureterectomy with either a standard
surgical technique or a laparoscopic approach. Percuta-
neous renal endoscopy has been used in the diagnosis
and treatment of TCC affecting the renal collecting system;
however, this approach remains controversial.
In high-risk patients and in those with a solitary kidney,
a less-invasive approach may be considered. A percuta-
neous nephrostomy tract is created to access the tumor,
which is then removed by using a resectoscope with
electrocautery or an Nd:YAG laser.
SPECIAL CONCERNS
Although percutaneous nephrostomy is successful for the
removal of most renal collecting system tumors, the
recurrence rate is high, and nearly one third of patients
have recurrent tumors within two years.
Urinary Bladder Diseases 207
Because of these serious limitations, the percutaneous
method is reserved for high-risk patients with a solitary
kidney low-grade lesion, a negative history of bladder
TCC, and negative preoperative cytologic results in the
upper urinary tract.
Unlike renal cell adenocarcinomas, TCC is prone to
spread after percutaneous interventional procedures (e.g.,
nephrostomy).
MORTALITY/MORBIDITY
Approximately 90% of TCCs are curable in patients with
superficial, confined tumors. Those with deeply invasive
types, which are still confined to renal pelvis and ureter,
have a 10–15% likelihood of cure. Usually, distant
metastases that penetrate the urothelial wall cannot be
cured with current forms of treatment.
SUMMARY
Bladder cancer is most common in ages 50-69, with a
male: female ratio of 3:1. 95% of malignant bladder
cancer is carcinoma, originating from urothelial
(transitional cell), squamous, or glandular cells. 90 percent
are transitional cell, 5% are squamous, and
2% are adenocarcinoma. Less common, non-epithelial
bladder cancers include leiomyosarcoma and lymphoma,
though invasion from carcinoma of the prostate, cervix,
uterus, and sigmoid colon can also occur.
Risk factors for TCC include industrial chemical
exposure (azo or aniline dyes), cigarette smoking,
analgesic abuse, and prior radiation. Most TCC’s originate
in the bladder trigone and posterolateral bladder wall,
and 75 percent are superficial papillary lesions. Upper
tract metachronous tumors occur in 2–3% conversely,
up to 40% of patients with upper tract TCC will develop
bladder TCC.
Risk factors for SCC of the bladder include schisto-
somiasis, neurogenic bladder with resultant chronic
irritation and infection, indwelling catheter, and recurrent
cystitis. Increased risk for adenocarcinoma includes the
presence of urachal remnants and bladder exstrophy.
For TCC, depth of invasion is a good predictor of
recurrence, metastatic disease, and survival. Muscle-
invasive tumors have a poor prognosis due to resultant
lymphatic and distant spread, with 5 years survival
208 Uroradiology: Text and Atlas

dropping to 10–20% in this segment. UVJ obstruction

and hydroureter usually indicate muscular invasion. IV
urography is a useful adjunct to detect synchronous upper-
tract urothelial cancers. CT and MRI are used for staging,
but accurate assessment of the depth of invasion is not
possible. MRI is superior for the detection of invasion
of adjacent organs, and is thought to be better for
evaluating tumors of the bladder dome or base.

RHABDOMYOSARCOMA
INTRODUCTION
It accounts for 5–10% of all malignant tumors in patients
under 15 years and is most common malignant tumor
of the vagina, prostate, and bladder.
FIGURE 15.6: Precontrast T1 WMR
PATHOPHYSIOLOGY
Other sites of involvement include perineal region, head
and neck, skeletal muscle/soft-tissue, protahepatis,
peritoneal.
Most neoplasms of the bladder in children are
malignant, with Rhabdomyosarcoma most common. TCC
and Leiomyosarcomsa are rarely seen. Clinically bladder
tumors present with hematuria and retention and can
cause flank pain secondary to hydronephrosis and
constipation.
Rhabdomyosarcoma appears either as pedunculated
soft-tissue mass with bunch of grapes appearance
(Botryoid) or as focal or diffuse wall thickening.

ROLE OF RADIOLOGY AND IMAGING

On CT asymmetry of fat planes or direct soft tissue into
adjacent organs is useful for assessing stage. Pelvic lymph
nodes may be enlarged indicative of metastatic disease. FIGURE 15.7: Postcontrast T1 WMR-brightly enhancing
Metastatic disease to the nodes, liver, bone, lung, brain. rhabdomyosarcoma of bladder in a child

Distinguishing between localized benign and malignant

MORTALITY/MORBIDITY
tumors of the bladder may not be possible with CT
(Figures 15.6 and 15.7). Three year survival rates are 70–80%.

TREATMENT PRIMARY LYMPHOMA OF BLADDER

Genitourinary rhabdomyosarcoma is initially managed INTRODUCTION
by chemo. Patients with operable tumors undergo It is a rare malignancy of the bladder, and accounts for
surgery and radiation rendered for residual inoperable less than 0.2% of bladder neoplasms. Involvement of the
tumor. bladder by manifestations of systemic lymphoma is more
 Urinary Bladder Diseases 209

common, but still rare. It is generally thought that no

lymphoid tissue is present in the bladder. However, it
is felt that lymphoid tissue can develop in bladders affected
by chronic cystitis and this can give rise to the develop-
ment of lymphoma.

CLINICAL FEATURES

Primary lymphoma of the bladder is more commonly

seen in elderly woman who present with a history of
chronic cystitis. Obstruction of the ureter orifice with
resulting hydronephrosis is uncommon since the tumor
usually does not involve the ureteric orifice.
Patients most commonly present with symptoms of
periodic hematuria of variable intensity. This can be
FIGURE 15.9: CT: Bladder lymphoma adjacent prostate
associated with urinary frequency and dysuria. Associated
urinary tract infection occurs in about 50% of patients.
MORTALITY/MORBIDITY

ROLE OF RADIOLOGY AND IMAGING
Transrectal ultrasound is not able to acceptably stage local
prostate cancer. Ultrasound is unable to consistently identify
the prostate capsule and subtle infiltration of tumor beyond
the prostate. With the use of endorectal surface coil, MRI
is able to routinely identify the tumor, the prostate capsule,
the neurovascular bundles and surrounding periprostatic
structures (Figures 15.8 and 15.9).
TREATMENT
Treatment of bladder lymphoma is generally nonsurgical
with patients undergoing chemotherapy.
Prognosis and treatment of prostate cancer requires
staging. Prostate carcinoma confined to the gland has
a 5-year survival rate of 94%. With extracapsular
extension, the 5-year survival rate is less than 70%.
URACHAL CARCINOMA
INTRODUCTION
It is a rare cancer accounting for less than 0.7% of bladder
cancers. Commonly, urachal carcinoma arises in the
dome of the urinary bladder at the vesicourachal junction.
The tumor commonly invades the anterior abdominal
wall, and most patients have a poor prognosis.
Approximately 85% of urachal carcinomas are
adenocarcinomas, and these are 40% of bladder
adenocarcinomas.

PATHOPHYSIOLOGY

The pathogenesis of urachal carcinoma is poorly

FIGURE 15.8: CT: Bladder lymphoma invading adjacent prostate
understood. Adenocarcinoma is believed to arise from
malignant transformation of columnar metaplasia in as
many as 84% of patients. However, in 3%, it arises within
the transitional cell epithelium, and the transitional
epithelium undergoes metaplasia to become glandular
epithelium. Approximately 70% of urachal carcinomas are
mucin-producing adenocarcinomas, and 15% are
non–mucin-producing adenocarcinomas.
210 Uroradiology: Text and Atlas
INCIDENCE
Urachal carcinomas are rare.
ANATOMICAL BASIS
The urachus is a musculofibrous band that is an extension
of the urogenital sinus. This band extends from the
bladder dome to the umbilicus; in the fetus, it is contiguous
with the allantois. The urachus lies in the space of Retzius,
between the transversalis fascia anteriorly and the
peritoneum posteriorly. In 70% of adults, a small lumen
lined by transitional epithelium remains in the urachus.
The persistence of a urachal lumen can lead to a urachal
fistula, urachal cyst, or urachal sinus. In some patients,
this epithelium can undergo metaplasia to become
glandular epithelium. The result may be malignancy,
usually mucinous adenocarcinoma. Most (90%) urachal
carcinomas are juxtavesical, specifically, supravesical,
anterior to the bladder, or in its midline.
CLINICAL FEATURES
Sex: Approximately 75% of urachal carcinoma cases
occur in men.
Age: Patients usually are aged 40–70 years.
Patients can have mucous micturition, although this
occurs in only 25% of patients. More commonly,
hematuria is present in as many as 75% of patients.
Uncommonly, blood, pus, or mucus can drain from the
umbilicus. Nonspecific abdominal pain is often a
symptom.
ROLE OF RADIOLOGY AND IMAGING
Plain Radiography
Plain radiographic findings usually are normal, although
a few urachal carcinomas can be calcified enough to be
depicted on plain radiographs.
CT
It is the best modality to depict urachal carcinoma,
although MRI can be helpful in select patients. MRI is
helpful for the evaluation of the fluid or mucous content
of the urachal segment and for multiplanar depiction of
the carcinoma.
Findings: A mass, often with relatively low attenuation,
may be depicted at the anterior dome of the bladder in
the midline of the body or just off the midline. A mass
in bladder dome with stippled calcifications is pathogno-
monic for urachal adenocarcinoma. Extension into the
perivesical fat, anterior abdominal wall, and through the
space of Retzius is common. Calcification is easier to
diagnose by using CT than with plain radiography.
Calcifications often are dotted, stippled, or curvilinear.
MRI
The MRI appearance of urachal carcinoma depends on
the composition of the tumor. Many tumors have
extremely high signal intensity on T2 weighted images
because of their mucoid composition.
INTERVENTION
Treatment for localized bladder dome urachal cancer
includes surgery to remove the cancer and the bladder,
in whole or in part. This removal may be accompanied
by en bloc resection of the umbilicus and bilateral pelvic
lymphadenectomy. Many advocate the use of radiation
therapy because the most common area of recurrence
is at or near the bladder dome. The use of chemotherapy
in treating urachal cancer remains experimental.
MORTALITY/MORBIDITY
Mortality is based on the stage at presentation. The
prognosis with urachal carcinoma is poor compared with
that of other types of bladder carcinomas. Early detection
is important in preventing death because urachal cancers
that are found early have a good prognosis. However,
in 50% of patients, the disease is fatal. The 5 years survival
rate of less than 16%. The poor prognosis is a result of
the late presentation of symptoms, a tendency for early
local invasion, and pulmonary and osseous metastasis.
BLADDER OUTLET OBSTRUCTION
Congenital Causes
1. PUV
2. Bladder neck hypertrophy (Marion’s disease)
3. Caecourterocele
4. Meatal stenosis
 Urinary Bladder Diseases 211

FIGURES 15.10A AND B: Cystocele with back pressure changes

Traumatic Causes 2. Ca Prostate

Urethral trauma/rupture 3. Urethral malignancy
Infective causes
Miscellaneous
1. Severe UTI
2. Urethral stricture Cystocele
3. Severe urethritis Urethral calculus
4. Urethral abscess For example, Cystocele (Figures 15.10A and B).
5. Chronic balanoposthitis
NEUROGENIC BLADDER
6. Pimosis
Can be autonomic, automatic bladder due to parasym-
Neoplastic Causes pathetic and sympathetic dysfunction (Figure 15.1).
1. BHP
212 Uroradiology: Text and Atlas

CLASSIFICATION 12. Leiomyoma vaginal tumors

• Benign prostatic hyperplasia 13. Miscellaneous.
• Carcinoma of prostate
• Prostatic utricle cyst BENIGN PROSTATIC HYPERPLASIA (BPH)
• Prostatic abscess Benign prostatic hypertrophy (BPH) is the commonest
• Prostatic calcification cause of bladder outlet obstruction in older men. As the
prostate enlarges, it gradually compresses the urethra.
CAUSES OF BLADDER OUTFLOW OBSTRUCTION Since much of the prostate lies below the bladder base,
1. Benign prostatic enlargement Prostatic cancer there may be considerable hypertrophy and urethral
2. Other prostatic lesions obstruction without much of an impression upon the
3. BPH inferior aspect of the bladder shadow. Conversely, the
4. Wegener’s granulomatosis, lymphomatoid granulo- presence of a classic bladder-base defect from median
matosis, malignant lymphoma, hemangioperi- lobe hypertrophy does not guarantee outlet obstruction.
cytoma, rhabdomyosarcoma For so common a problem as BPH, it is remarkable
5. Malignant schwannoma, fibrous mesothelioma how much confusion and controversy surround the
6. Anatomical versus functional postsurgical, traumatic indications for imaging examinations and the significance
7. Large pelvic tumors of findings.
8. Bladder neck obstruction: Acquired bladder neck
PATHOPHYSIOLOGY
stricture, Bladder-sphincter dyssynergia, hydro-
colpos The cause of BPH is unknown but is believed to be caused
9. Hydrometrocolpos Hematocolpometra by changes in hormonal status (declining levels of
10. Cervix, low uterine segment androgens).
11. Foe example Leiomyoma, fibroma, rhabdomyo-
CLINICAL FEATURES
sarcoma, carcinoma Calculus, Brunn’s cyst,
epidermolysis bullosa, gelatinous plug, trigonal It is present in 50% of men between 40 and 60 years
polyp, prolapsing ectopic ureterocele of age and 95% of men over 70 years of age.

Clinical significant symptoms occur in 5–10% of men over
60 years of age.
Overall the gland is enlarged, often reaching massive
size. Small nodules are present throughout the gland.
Some larger nodules show cystic changes. Infarction of
a nodule is common and may be associated with acute
swelling that may precipitate acute pain and urinary
retention. When infarction of a periurethral nodule occurs,
the patient may develop hematuria.
ROLE OF RADIOLOGY AND IMAGING
Bladder size is readily evaluated with cross-sectional
imaging on the urogram. Massively distended bladders
containing 1500 ml or more are not rare in men with
overflow micturition and decompensated bladders.
Abdominal radiographs may show an oval soft-tissue
shadow in the pelvis displacing gas-filled intestinal loops
upwards. US can immediately confirm the presence of
massive bladder distension.
If the patient empties his bladder as documented by
imaging, we learn only that the bladder has not yet
decompensated. Indeed, there may be serious but
compensated outlet obstruction at the expense of very
high micturating pressure. Lower tract urodynamic
evaluation is important to provide objective data about
the presence or absence of obstruction. The symptoms
of an unstable bladder may overlap those of BPH and
the two conditions often coexist.
The radiographic counterpart of elevated micturating
pressure is bladder wall thickening. Unfortunately there
are no reliable criteria for judging when a bladder wall
is too thick. The apparent thickness (distance between
intravesical contrast and extravesical fat) varies with
bladder filling. Even experienced uroradiologists and
urologists have trouble here.
With detrusor hypertrophy, small outpouchings called
cellules develop between adjacent muscular trabeculae.
Later these may progress to full-fledged diverticula.
Cellules and diverticula are reliable indicators of bladder
wall hypertrophy and certainly suggest bladder outflow
obstruction of some type, either anatomicalor
neuropathic. The size of the intravesical prostate on US
or CT may help to decide on transurethral versus open
resection of the prostate.
Large residual bladder volumes may lead to
hydroureteronephrosis, although fortunately these upper
Diseases of Prostate 213
FIGURE 16.1: USG: Benign prostatic
enlargement with median lobe hypertrophy
tract events are reversible. As an example, consider the
patient who develops acute urinary retention. US at this
stage always shows upper tract dilatation. Catheter
drainage of the bladder reverses the hydrouretero-
nephrosis within minutes in most patients. Those few
whose dilatation persists despite bladder decompression
have partial obstruction of the intramural ureters
secondary to fibrosis or severe muscle hypertrophy.
With time, even these unpromising-looking ureters
return towards normal, although some permanent
functional deficit persists. The same principles apply to
chronic bladder outlet obstruction from other causes and
in other age groups. Men with tight urethral strictures and
boys with posterior urethral valves are examples.
BPH is one of the common cause of BOO in old age
(Figure 16.1).
Complications include development of bladder
diverticula, urinary infection, hydronephrosis and chronic
renal failure. Treatment of prostatic hyperplasia is surgical.
DIFFERENTIATING POINTS FROM
CARCINOMA OF THE PROSTATE
Prostate cancer can cause urinary obstruction in several
ways. Most commonly urethral narrowing comes from
growth of intraglandular tumor. Symptoms resemble those
of BPH. Tumor shrinkage after orchidectomy, hormonal
therapy, or chemotherapy can reverse urethral
obstruction. In the absence of a beneficial response to
therapy, transurethral resection of malignant tissue is
required to establish at least temporary urethral patency.
214 Uroradiology: Text and Atlas
Prostatic cancer, spreading locally around the bladder
base, can block one or both ureters, and metastases
to iliac or periaortic lymph nodes may also displace
and/or obstruct the ureters. The latter is particularly
common at the common iliac artery crossing, but ureteric
obstruction may develop above, even at the renal pelvis.
Like urethral obstruction, ureteric obstruction may resolve
after successful hormonal therapy or chemotherapy.
Temporary percutaneous nephrostomy drainage may
preserve renal function until the tumor regresses and
ureteric patency is re-established.
PROSTATE CANCER
INTRODUCTION
It is an important, growing health problem, presenting
a challenge to urologists, radiologists, and oncologists.
Prostate cancer is the most common nondermatologic
cancer, yet despite this frequent occurrence, the clinical
course is often unpredictable. Many men are found to
have had incidental microscopic foci of prostate cancer
at postmortem examination, and most prostate cancers
are slow growing and do not manifest during the man’s
lifetime. Thus, many men die with prostate cancer rather
than die from prostate cancer; however, some cancers
are aggressive, with a rapidly worsening course.
Currently, many men are identified as having early
prostate cancer through the use of prostate-specific
antigen (PSA) screening, but few indicators currently
distinguish progressive prostate tumors from the indolent
cancers.
The treatment of prostate cancer is controversial, and
different options range from early aggressive treatments,
such as radical prostatectomy and radical radiotherapy,
to deferred treatments, i.e. treating men when and if the
disease progresses and becomes symptomatic.
PATHOPHYSIOLOGY
Approximately 95% of prostate cancers are adenocar-
cinomas developing in the acini of prostatic ducts. Other
rare histopathologic types of prostate carcinoma occur
in approximately 5% of patients; these include small cell
carcinoma, mucinous carcinoma, endometrioid cancer
(prostatic ductal carcinoma), transitional cell cancer,
squamous cell carcinoma, basal cell carcinoma, adenoid
cystic carcinoma (basaloid), signet-ring cell carcinoma,
and neuroendocrine cancer.
Prostate cancer is frequently multifocal within the
prostate. In the prostate, 70% of cancers occur in the
peripheral zone (Peripheral zone), and approximately
20% are found in the transition zone (Transitional zone).
Some have claimed that Transitional zone prostate cancers
are relatively nonaggressive, whereas Peripheral zone
cancers are more aggressive and tend to invade the
periprostatic tissues.
Contemporary biopsy strategies concentrate on the
Peripheral zone and largely ignored cancer in the
Transitional zone. A recent study of 148 patients with
Transitional zone cancers based on radical prostatectomy
specimens revealed the details of Transitional zone tumors.
of the Transitional zone tumors, 80% were organ confined.
A secondary tumor was found in the Peripheral zone in
52% of cases. About 15% of the cases had capsular
penetration, 2.7% had seminal vesicle invasion, and 3.4%
had lymph node metastases.
HISTOPATHOLOGIC DIAGNOSIS OF PROSTATE CANCER
Disturbances of architecture, invasion, and anaplasia are
the important histopathologic criteria for the diagnosis
of prostate cancer. Dysplastic lesions of the prostate occur
and are characterized by loss of cellular polarity, increase
in nuclear size with hyperchromicity, and pleomorphism.
Such dysplastic lesions are termed prostatic intraepithelial
neoplasia (PIN). PIN is a histologic appearance that many
pathologists consider to be a preinvasive stage of some
prostate cancers. In its most severe form, PIN is regarded
as carcinoma in situ. PIN may be classified as low grade
or high grade.
GRADING
Various grading systems have been proposed; the
Gleason system is one of the most widely used
internationally. It recognizes a primary and a secondary
pattern and in each, 5 subpatterns. The sum of the
2 patterns contributes the Gleason score. The scores are
of prognostic significance. Patients with a Gleason score
of 4 or below do well, and patients with a score of
8–9 do poorly.

STAGING
The prostate does not have a true capsule, but it does
have an outer fibromuscular band called the capsule.
Tumor spread outside the prostate may occur by means
of capsular penetration, invasion of the seminal vesicles,
or local extension along the neurovascular bundles. The
usual sites for metastases from prostate cancer are the
lymph nodes, bones, and lungs. Skeletal metastases are
common in advanced prostate cancer, but hepatic
metastases are uncommon.
The spread of prostate cancer to the lymph nodes
involves the obturator and from there to the common
iliac and para-aortic lymph nodes. Pelvic lymph nodes
are involved initially; the inguinal nodes are not involved.
Metastatic spread to bone is common in patients with
advanced prostate cancer; this typically occurs as
osteoblastic sclerotic metastases. Lytic metastases are seen
occasionally.
The TNM (tumor, node, metastasis) staging system
revised in 1997 is considered the international standard
for prostate cancer staging and categorizes the prostate
as follows:
Primary Tumor (T)
TX - Primary tumor not assessable
T0 - No evidence of primary tumor
T1 - Clinically inapparent tumor, not palpable or
visible by imaging
T1a - Incidental histologic finding in 5% or less of tumor
resected (tissue obtained during transurethral
resection for symptoms of outflow tract
obstruction)
T1b - Incidental histologic finding of in more than 5%
of tissue resected (tissue obtained during
transurethral resection for symptoms of outflow
tract obstruction)
T1c - Tumor identified by needle biopsy (performed
because of elevated PSA levels)
T2 - Tumor confined within the prostate
T2a - Tumor involving 1 lobe
T2b - Tumor involving both lobes
T3 - Tumor extending through the prostatic capsule
T3a - Extracapsular extension (unilateral or bilateral)
Diseases of Prostate 215
T3b - Tumor invading the seminal vesicles
T4 - Tumor fixed or invading adjacent structures other
than seminal vesicles, bladder neck, external
sphincter, rectum, levator muscles, and/or pelvic
wall
Regional Lymph Nodes (N)
NX - Regional lymph nodes not assessable
N0 - No regional lymph node metastasis
N1 - Regional lymph node metastasis
Distant Metastasis (M)
MX - Distant metastases not assessable
M0 - No distant metastasis
M1 - Distant metastasis
M1a - Nonregional lymph node metastasis
M1b - Bone metastasis
M1c - Metastasis at other sites.
INCIDENCE
Prostate cancer is the most common nondermatologic
cancer and the second most common cause of cancer-
related deaths in the men.
CLINICAL PRESENTATION
Patients with prostate cancer may be asymptomatic.
Cancer is detected when abnormal digital rectal
examination (DRE) results or elevated PSA levels are
further investigated. Alternatively, cancer may be detected
in tissue obtained during transurethral resection to treat
a urinary outflow tract obstruction. Patients may present
with symptoms of advanced disease with weight loss,
lethargy, bladder outflow obstruction, or bone pain. (Men
with newly diagnosed prostate cancer and PSA levels of
less than 20 ng/mL are unlikely to have skeletal metastases
resulting from prostate cancer.)
Age: The incidence of prostate cancer increases markedly
with age. In fact, the incidence is exponentially related
to age.
Prostate cancer is rare in men younger than 50 years.
One half of all cases occur in men older than 75 years.
The maximum mortality rate occurs in those aged 85
years.
216 Uroradiology: Text and Atlas
ANATOMICAL BASIS
McNeal first proposed the histologic division of the
prostate into an outer Peripheral zone, a central zone
(Central zone), and an inner Transitional zone. In the
young adult prostate, approximately 5% of prostatic
glandular tissue is in the Transitional zone located on both
sides of the prostatic urethra. This is the area where benign
hyperplasia develops in older patients.
The Transitional zone is separated from the Peripheral
zone and Central zone by the surgical capsule, in which
calcified corpora amylacea may be found. The Central
zone is relatively resistant to disease processes and
constitutes approximately 25% of the glandular tissue of
the prostate in the young adult. The Central zone is
situated at the base of the prostate, and the ejaculatory
ducts reach the verumontanum by passing through
Central zone tissue. The Peripheral zone constitutes 70%
of the prostate and lies on the posterior and lateral aspects
of the gland surrounding the Transitional zone. Its ducts
drain into the urethra distal to the verumontanum.
Of all prostate cancers, 70% occur in the Peripheral zone,
and approximately 20% occur in the Transitional zone.
Rhabdomyosarcomas of the prostate and pelvis
represent a childhood malignant tumor. These appear
as soft-tissue masses infiltrating the bladder and prostate.
As such, they have a presentation and radiologic features
completely different from those of prostatic adeno-
carcinomas.
PSA SCREENING
PSA screening is currently the single best test for prostate
cancer, but it does not help in determining whether the
detected cancer will cause clinically significant disease.
Some men with prostate cancer may have normal PSA
levels. PSA is an excellent marker for the follow-up of
patients with established prostate cancer.
PSA is produced by both abnormal and normal
prostate tissue. A moderate elevation of the PSA level
(4 – 10 ng/mL) has a low specificity for prostate cancer.
Some men with prostate cancer have PSA levels in the
reference range. An elevated PSA level is not specific for
prostate cancer, and elevated serum PSA levels may also
be associated with prostatitis, prostate infarction, PIN,
prostate biopsy, transurethral resection of the prostate,
and urethral catheterization.
Serum PSA levels are lowered with finasteride
treatment for benign prostatic hyperplasia, and this
treatment must be considered when PSA levels are
assessed and before the decision to perform prostatic
biopsy is made.
RISK FACTORS FOR PROSTATE CANCER
1. High fat consumption is a possible risk factor. Diets
low in animal fat and protein decrease the risk.
2. A family history of prostate or breast cancer is a risk
factor.
3. Farming or exposure to radiation and cadmium are
risk factors.
4. Race: Blacks are at increased risk for prostate cancer.
5. Neither alcohol consumption nor cigarette smoking
is associated with a risk of prostate cancer.
6. Substances that may offer some protection include
vitamin E, selenium, and lycopene from tomato-based
foods. High soya consumption may be protective
because of the ingestion of plant phytoestrogens.
PREFERRED INVESTIGATION
TNM Staging Algorithm
1. For the staging of prostate cancer, MRI is preferred
to CT because it permits more accurate tumor staging.
2. Both techniques can be used in Nodal staging, and
they have equivalent accuracy.
3. Bone scintigraphy is used in staging of Metastases.
CXR and Skeletal Survey
A chest radiograph may be considered in the evaluation
of a patient with known prostate cancer to assess chest
symptoms, weight loss, localized bone pain, or
constitutional symptoms.
Skeletal radiographs may show sclerotic metastases
or lytic lesions with bone destruction.
Transabdominal Sonography
See Figures 16.2 to 16.4.
TRUS
TRUS plays a central role in the contemporary diagnosis
of prostate cancer because it enables accurate image-
guided biopsy of the gland. Patients are usually referred

FIGURE 16.2: # demonstrates large lobulated
prostate with heterogeneous echotexture
FIGURE 16.3: Bladder base invasion by the prostatic carcinoma
FIGURE 16.4: Invasion of bladder base lead to involvement of
both UVJ and backpressure changes more on left side
Diseases of Prostate 217
for TRUS because of an abnormality is found during DRE
or because the serum PSA level is elevated.
Features: Using TRUS, the prostate is shown to be
divided into an outer gland (Peripheral zone and Central
zone) and an inner gland (Transitional zone). Calcification
in the corpora amylacea in the surgical capsule between
the outer and inner parts of the prostate is common.
Particular attention should be paid to the
Peripheral zone in prostate cancer diagnosis
because about 70-80% of prostatic malignancies
are located peripherally.
The most frequently noted abnormality due to prostate
cancer is a hypoechoic area in the Peripheral zone. Rarely,
cancer may appear as a hyperechoic area.
Both prostate cancer and prostatitis may have
increased vascularity, as shown on color and power
Doppler sonograms. This focal alteration in the prostatic
vasculature is most commonly found in hypoechoic areas
in the Peripheral zone, as depicted on gray-scale images.
No cancer-specific flow pattern has been identified, and
some cancers that are demonstrated clearly on gray-scale
imaging show no focal hypervascularity.
Lymphoma of the prostate tends to present in younger
men, and large hypoechoic masses in both the Transitional
zone and Peripheral zone have been reported.
Prostate cancers frequently demonstrate isoechoic
findings. This observation is the basis for the systematic
biopsy approach in which multiple cores are taken from
both lobes in a standardized manner. Color and power
Doppler results have been disappointing, and they have
not been significantly helpful in detecting cancers that
are isoechoic on gray-scale examination (Figure 16.5).
Advantages:
1. Detailed sonographic appearances of the rarer
histologic variants of prostate cancer can sometimes
be described by TRUS. For example, in comedocarci-
noma, the most malignant form of prostate cancer,
stippled multiple small hyperechoic foci within the
hypoechoic area of the cancer can be found. In
patients with adenoid cystic carcinoma of the prostate,
multiple small cysts in the prostate may be seen.
218 Uroradiology: Text and Atlas

Color or power Doppler may also be used to

identify areas for biopsy under TRUS guidance. In the
future, interventional MRI equipment may be used to
guide needle biopsy of the prostate.

CECT
Features: Arterial-phase multisection CT scanning can
help in differentiating the prostate Peripheral zone and
Transitional zone, but it cannot demonstrate intraprostatic
pathology in the prostate. CT has a limited role in
assessing prostatic cancer, but it may be helpful in
detecting nodal involvement.
FIGURE 16.5: TRUS: Arrows point to the prostatic mass
For the evaluation of lymph node metastases, CT and
MRI depict lymph node enlargement, and both have
similar accuracy. CT can be used to search for lymph
2. TRUS may be used for local staging of prostate cancer
node metastases and to stage the primary tumor by
because it can demonstrate bulges of the prostate
depicting extracapsular spread in patients in whom
capsular outline or overt extracapsular extension.
advanced disease is suspected, particularly when
However, TRUS findings have been found to be
radiation therapy is being planned.
inaccurate in the staging of localized prostate cancer.
CT cannot depict T1 or T2 tumors accurately. T3
However, Peripheral zone tumors with contact with
tumors may show invasion of periprostatic fat or seminal
the fibromuscular rim surrounding the prostate of
vesicles. Evidence-based guidelines for the use of CT in
longer than 2.3 cm on TRUS images may be prostate cancer staging have been produced. CT also may
associated with extracapsular invasion. be used to depict soft-tissue metastases elsewhere in the
3. TRUS is widely available, it has a relatively low cost, body (Figures 16.6A and B).
and it provides the opportunity for accurate biopsy
of the gland. Currently, TRUS offers the best Limitations: Current CT techniques cannot demonstrate
opportunity to demonstrate prostate cancer. intraprostatic pathology, and signal intensity changes in
4. TRUS provides the opportunity for accurate and
comprehensive biopsy of the prostate gland while
providing an imaging examination.
Limitations
1. Although, currently TRUS offers the best opportunity
to demonstrate prostate cancer, it does have major
limitations in compeletely demonstrating prostate
cancers because many prostatic tumors are both
isoechoic and multifocal.
2. Furthermore, TRUS has low specificity because many
pathologic conditions may demonstrate similar appea-
rances as hypoechoic areas in the Peripheral zone of
the prostate. For this reason, diagnostic assessment
of cancer in the prostate must be made by means
of the histologic interpretation of biopsy samples. FIGURE 16.6A: Axial CT: Localized prostatic carcinoma
 Diseases of Prostate 219

be complicated by postbiopsy hemorrhage, and MRI

should not be performed until at least 3 weeks after biopsy.
The current role of MRI is the assessment of
local extracapsular extension and invasion of the
seminal vesicle. The optimal MRI technique for the
staging of prostate cancer has not been established. Signs
of extracapsular spread include the following: irregular
bulging of the prostatic outline, breech of the capsule
with extracapsular spread, asymmetry of the neuro-
vascular bundles, and loss of the rectoprostatic angle.
Contiguous areas of low signal intensity extending into
the seminal vesicles from the base of the prostate are
evidence of invasion of the seminal vesicle. On T2-
FIGURE 16.6B: Axial CT: Prostatic carcinoma weighted images, reduced signal intensity in the seminal
with bladder base invasion
vesicles may be seen after radiation therapy or prostatic
biopsy.
the Peripheral zone on MRIs have a low specificity, as
Endorectal MRI is more accurate than body-
with TRUS.
coil MRI in the local staging of the primary tumor.
Nodal staging relies on assessment of lymph node size,
Dynamic endorectal MRI with gadolinium enhancement
and neither CT nor MRI can demonstrate cancer within
may provide optimal visualization of cancer in the
lymph nodes that are not enlarged. For the evaluation
prostate. Magnetic resonance spectroscopy performed by
of lymph node metastases, CT and MRI have similar
accuracy. CT cannot depict T1 or T2 tumors accurately. using citrate and choline can provide specific information
regarding prostatic metabolism. These data may be
MRI useful in assessing the biological potential of the primary
tumor and the extracapsular extension of the tumor
The most accurate imaging technique for staging prostate
cancer appears to be endorectal MRI, but even this may (Figures 16.7 to 16.9).
cause significant understaging in approximately 30% of
prostate cancers.
Features: MRI can demonstrate the internal anatomy
of the prostate, and it can identify areas of altered signal
intensity, which representing focal pathology in the gland.
MRI provides the most complete evaluation of
patients with prostate cancer because it can be
used to assess primary disease in the prostate and
involvement of the local lymph nodes.
On T1-weighted images, the prostate appears
homogeneous with medium signal intensity. Neither the
zonal anatomy nor intraprostatic pathology is displayed.
These are depicted on T2 weighted images, on which
the cancer appears as an area of low signal intensity in
the hyperintense Peripheral zone. The specificity of this
appearance is low.
As with TRUS, MRI cannot accurately depict cancer
in the Transitional zone. Cancer assessment with MRI may FIGURE 16.7: Normal prostate on MRI with ER coil
220 Uroradiology: Text and Atlas
FIGURE 16.8: Normal prostate T1 MRI
FIGURE 16.9: Normal prostate T2 MRI
MR lymphography: A new technique to detect
clinically occult lymph node metastases using “MR
lymphography” with a highly lymphotropic MR contrast
agent is being used since 2003, in which intravenous
lymphotropic paramagnetic nanoparticles of iron oxide
are administered, and patients are examined by MR 24
hours after contrast administration. Small lymph node
metastases are identified with higher sensitivity than with
conventional MR scanning; this potentially valuable test
needs further evaluation.
Interventional MRI: Although, MRI is used primarily
for staging, but the availability of interventional MRI units
means that MRI is likely to have a future role in the precise
diagnosis of prostate cancer.
RNI
Radionuclide bone scanning after the injection of a
99m
Tc tracer is the standard method for assessing
potential bone metastases from prostate cancer. With
diffuse bone metastases, a so-called superscan may be
seen. This superscan demonstrates high uptake
throughout the skeleton, with poor or absent renal
excretion of the tracer.
Immunoscintigraphy
The use of immunoscintigraphy to assess prostate
cancer is under investigation. With this method,
radiotracer-labeled antibodies to acid phosphatase
and PSA are used. Initial studies used iodine-131–
labeled antiprostatic acid phosphatase antibody, and
subsequent studies have used indium-111–labeled
antibody. The use of labeled anti–carcinoembryonic
antigen antibodies is being investigated. The most
commonly used monoclonal antibody (mAb) is
ProstaScint. This is 111In-labeled mAb 7E11-C5.3
(CYT-356, which recognizes an intracellular epitope of
PSMA. This technique is approved for the imaging of
soft-tissue metastases from prostate cancer but not bone
metastases. The sensitivity and specificity of this method
for lymph node metastases is 62 and 72%, respectively.
The sensitivity and specificity for prostatic fossa recurrence
is 49 and 71%, respectively.
Positron Emission Tomography
Positron emission tomography (PET with 18-fluoro-2-
deoxyglucose (FDG) may have a role in the detection
of lymph node metastases from prostate cancer,
particularly in patients with relapsed disease after primary
treatment. Localized disease within the prostate and pelvic
lymph nodes can be difficult to image because of the
proximity of activity of the bladder. The sensitivity of
FDG PET for detection of recurrence after radical
prostatectomy currently is less than 50%. C11-acetate

and C11-choline have shown promise as alternatives to
FDG in prostate cancer, but are less readily available than
FDG. FDG PET has a repor ted sensitivity of
approximately 50% for the detection of skeletal prostatic
metastases. In general, FDG PET has an excellent
detection rate for lytic skeletal metastases, but it has a
poor detection rate for sclerotic metastases. Disease
localizing within the prostate and pelvic lymph nodes can
be difficult to image because of the proximity of activity
of the bladder. The sensitivity of FDG PET for detecting
disease recurrence after radical prostatectomy is currently
less than 50%. Carbon-11 acetate and carbon-11 choline
imaging have shown promise as alternatives to FDG
imaging in prostate cancer, but these are less readily
available than FDG techniques.
INTERVENTIONS
TRUS-guided Biopsy
The original systematic approach for biopsy included the
acquisition of 6 cores, 3 cores from each of the lobes
of the prostate at the base, mid gland, and apex in a
parasagittal plane. Current practice is to obtain an
increased number of cores, i.e. lateral Peripheral zone
cores, mid gland cores, or Transitional Zone cores, in
addition to the standard 6 cores. A 10-core biopsy
incorporating the traditional 6 parasagittal samples and
2 lateral samples from the right and left prostatic lobes,
is now a standard technique for systematic biopsy.
Systematic biopsy may be supplemented with cores
obtained through hypoechoic Peripheral zone lesions.
Focal areas of hypervascularity in the Peripheral zone
of the isoechoic prostate, as shown on color Doppler
examination, may also be targeted.
Opinion differs regarding whether Transitional zone
cores should be routinely obtained during an initial biopsy
procedure or whether the samples may be obtained
during repeat biopsy in a patient with an elevated PSA
level after the initial systematic biopsy results are negative
for malignancy.
Most Transitional zone cancers are found by analyzing
systematic biopsy cores specifically obtained from the
Diseases of Prostate 221
transitional zone. Little attention has been paid to assessing
hypoechoic areas in the Transitional zone because of the
lower frequency of cancer in the Transitional zone and
the perceived lower potential for metastatic spread of
primarily Transitional zone cancer. No specific studies in
the literature report the biopsy results in focal Transitional
zone hypoechoic areas or in areas of specific focal
alterations of Transitional zone vascularity, as identified
by using color or power Doppler imaging.
FUTURE PERSPECTIVES OF
IMAGING IN PROSTATIC CANCER
1. Currently, research studies are underway to investigate
whether sonographic contrast agents have a role in
the identification of cancer in the prostate and whether
by demonstrating tumor vascularity they have a role
in establishing prognosis of a patient with biopsy-
detected prostate cancer. The use of ultrasonographic
contrast agents increases the time and cost of
sonography-guided prostate biopsy procedures. No
marked improvement has been found in the accuracy
of prostate cancer diagnosis with contrast agents.
These agents remain experimental, and they have not
been adopted into standard uroradiologic practice.
The impact of sonographic contrast agents on
radiologic practice could be considerable if future
research proves that they enable the quantitative
preoperative assessment of microvascular density or
that they provide prognostic information in an
individual patient.
FIGURE 16.10: Prostatic utricle cyst
222 Uroradiology: Text and Atlas

FIGURE 16.11: Prostatic abscess

2. Research studies are also being conducted to assess FIGURE 16.12: Prostatic calcification
the value of elastography in the diagnosis of prostate
cancer; however, the role of this technique is still PROSTATIC ABSCESS
unclear. See Figure 16.11.

PROSTATIC UTRICLE CYST PROSTATIC CALCIFICATION

See Figures 16.10. See Figure 16.12.
 Urorenal Interventions 223

VARIOUS INTERVENTIONAL URORADIOLOGY 3. Obstruction causing renal failure

TECHNIQUES Benign
• FNAC and biopsy of renal masses a. Stones
• Percutaneous nephrostomy b. Sloughed papillae
• Percutaneous nephrolithotomy c. Iatrogenic—operative damage to the ureter pro-
• Percutaneous endopyelotomy ducing edema/stricture
• Percutaneous resection of urothelial tumors of renal d. Retroperitoneal fibrosis
pelvis Malignant
• Renal cyst puncture a. Retroperitoneal tumor
• Ureteric stone manipulation b. Pelvic tumor.
• Percutaneous balloon dilatation of ureteric strictures
Elective Percutaneous Nephrostomy
• Therapeutic ureteric occlusion
• Prostatic dilation and stenting 1. Obstruction with minor symptoms before treatment
• TRUS guided biopsy of prostate 2. Diversion of urine to heal urinary fistula
• ESWL. 3. Pressure flow studies for equivocal upper tract
obstruction
4. Percutaneous access for manipulation within kidney
PERCUTANEOUS NEPHROSTOMY
or ureter. Careful clinical supervision is required to
INDICATIONS
ensure that there is adequate fluid replacement.
• Emergency PCN Thus, broadly PCN is commonly indicated for one
• Elective PCN. of following reasons:
• Relief of urinary obstruction
Emergency Percutaneous Nephrostomy • Urinary diversion
1. Obstruction and infected urine • Access for therapeutic interventions
2. Obstruction and severe pain • Access for diagnostic interventions
224 Uroradiology: Text and Atlas
The first indication is the most common and occurs
when bilateral obstruction has occurred or in the
individual with only one functioning kidney. It is especially
important when the patient demonstrates hydronephrosis
in the setting of obstruction and fevers, leukocytosis or
evidence of frank sepsis. The most common indication
for percutaneous nephrostomy is relief of urinary
obstruction. This may be secondary to either acute or
chronic obstruction. Common causes include uretero-
lithiasis, extrinsic compression from abdominal or pelvic
neoplasms, or direct invasion from malignancies.
The second indication, diversion of urine, may be
necessary when there has been trauma to the urinary
system.
The third indication, access for diagnostic inventions,
includes biopsy, antegrade pyelograms and the Whitaker
test.
Access for therapeutic interventions includes stricture
dilatation, stent placement, foreign body removal and
stone therapy.
Relief of urinary obstruction is necessary to preserve
renal function. Most often, only one kidney is affected,
but bilateral disease does occur. In an effort to maximally
preserve renal function, treating the least affected side
first is recommended.
TECHNIQUE
Percutaneous nephrostomy can usually be performed
under local anesthesia with the patient in the prone
position. Anxious patients requiring bilateral
nephrostomy may require intravenous sedation, and
young children always require general anesthesia. The
puncture may be guided by fluoroscopy alone, having
used ultrasound beforehand to establish the site and depth
of the collecting system before puncture, or preferably
by real-time ultrasound.
Two techniques:
• Single-puncture technique
• Double-puncture technique.
Fluoroscopy Guided
The general rule that the simpler a technique is, the more
effective it will be, applies to percutaneous nephrostomy.
If renal function is adequate, intravenous contrast medium
given before the puncture will give additional fluoroscopic
aid to the ultrasound-guided puncture.
If intravenous contrast medium opacifies the
pelvicaliceal system, then it is simple and quick to use
a 19 gauge sheathed needle for the caliceal puncture,
so that a 0.35 guide wire can be advanced into the renal
pelvis. With a poorly functioning kidney an initial puncture
with a fine needle allows opacification of the system so
that a calyx may be selected for the fluoroscopically
guided, sheathed-needle puncture. This double-puncture
technique is usually used if the first two or three passes
with the sheathed needle fail.
Ultrasound Guided
An ultrasonically guided puncture requires a certain
degree of expertise, but is the best method of guidance
for puncturing a posterior calyx. When obstruction is
severe, ultrasound is required to localize the dilated
collecting system. It can be used before cleaning and
draping the patient to enable surface markings to be made
and to give some idea of the angle and depth of the
collecting system. With a small system and a difficult
puncture, ultrasound can be used to direct the needle
during the procedure, using a sterile sheath over the
ultrasound probe. Some operators like to use a guide
attachment on the ultrasound probe to direct the needle,
while others prefer to puncture ‘freehand’ with the needle
in one hand and the ultrasound probe in the other.
SUMMARY
During the procedure, the patient is placed in the prone
position. Conscious sedation is recommended for this
procedure. Ultrasound is used to confirm dilation of the
collecting system and to guide placement of the needle
into a posterior calyx. Posterior calyces are desired
since accessing them is associated with less
chance of vascular injury than does accessing an
anterior calyx or infundibulum. Once the percutaneous
needle is in place, a small amount of contrast is injected
to confirm appropriate access to the kidney. Oblique
images are then obtained to demonstrate that the needle
does not pass through the colon. Guidewires and dilators
precede placement of percutaneous nephrostomy drains.
The tube is then secured by coiling its tip within the renal
pelvis and suturing the drain to the patient’s flank.

CONDITIONS
• Retroperitoneal fibrosis
• Prune belly syndrome
• Tuberous sclerosis
• VHL.
RETROPERITONEAL FIBROSIS (RPF)/
ORMOND’S DISEASE
INTRODUCTION
The French urologist Albarran first described retroperi-
toneal fibrosis (RPF) in 1905, but with Ormond’s publi-
cation in 1948, the disease became an established clinical
entity.
In most patients (approximately 68%), no etiologic
factor is found. Therefore, the term idiopathic RFP is used.
Recent evidence suggests that RPF is an autoimmune
response to an insoluble lipid called ceroid that has leaked
through a thinned arterial wall from atheromatous
plaques. Other implicated causes include drugs,
abdominal aortic aneurysm, ureteric renal injury,
infection, retroperitoneal malignancy, postradiation
therapy, and chemotherapy. No genetic predominance
is seen in malignant retroperitoneal fibrosis.
RPF can be diagnosed on the basis of the history and
the radiologic observations. At times, the diagnosis is not
established firmly until surgical exploration. The use of
Miscellaneous Genitourinary Conditions 225
steroids in RPF remains controversial; however, some
authors believe that steroids can be used as an adjuvant
to surgical ureterolysis. More recently, immunosuppressive
drugs, such as azathioprine, cyclophosphamide, and
tamoxifen, have been used to treat RPF.
PATHOPHYSIOLOGY
Grossly, RPF appears as an exuberant mass of white,
woody, fibrous tissue covering the retroperitoneal
structures such as the aorta, vena cava, ureters, and psoas
muscle. It may extend from the renal pedicle to below
the pelvic brim. The center of the plaque is usually located
at the level of the fourth or fifth lumbar vertebra, overlying
the aortic bifurcation. Not uncommonly, the fibrous tissue
bifurcates and follows the common iliac arteries. Rarely,
the fibrous process extends into the root of the mesentery
or passes through the crura of the diaphragm to continue
as fibrous mediastinitis.
Histologically, the predominant finding is a fibrous
tissue consisting of collagen fibrils and fibroblasts. A
subacute nonspecific inflammatory reaction is often
present, or completely hyalinized fibrosis may be the only
finding. The cellular infiltrate includes polymorphonuclear
cells, lymphocytes, eosinophils, or plasma cells. In the
chronic phase, the only finding may be an acellular fibrosis.
The coexistence of RPF with primary biliary cirrhosis,
fibrosing mediastinitis, panhypopituitarism, glome-
rulonephritis, rheumatoid arthritis, systemic lupus
226 Uroradiology: Text and Atlas
erythematosus (SLE), polyarteritis nodosa, ankylosing
spondylitis, and Riedel or Hashimoto thyroiditis support
the hypothesis of an immune-mediated mechanism. The
association of RPF with the prolonged use of certain drugs
and with the improvement of clinical symptoms (in most
instances after cessation of the drug therapy) indicates
that the fibrotic process is the end stage of vasculitis
resulting from a hypersensitivity reaction to various
antigens such as drugs and diseases. Drugs implicated
in causing RPF include methysergide, beta-adrenergic
blockers, lysergic acid diethylamide, methyldopa,
amphetamines, phenacetin, pergolide, and cocaine.
INCIDENCE
RPF is relatively uncommon, with an incidence of 1 case
per 200,000 population.
CLINICAL FEATURES
Race: No racial preponderance has been recorded.
Sex: The disease is three times more common in males
than in females; however, methysergide-related RPF has
a female-to-male ratio of 2:1. No sex predominance is
noted in malignant RPF.
Age: The age range of patients is 7–85 years, with
predominance in patients aged 40–60 years.
Most patients present with nonspecific symptoms of
less than 12 months’ duration. Children may present with
hip or gluteal pain.
In the early stage, signs and symptoms originate from
the disease process; in the advanced stage, clinical features
represent the effects of obstructive uropathy and renal
failure. The most common presentation is pain (92%)
occurring in the flank (42%), the back (32%), the scrotum
(8%), or the lower abdomen (28%). Other presentations
include fever, weight loss (38%), nausea and vomiting
(32%), malaise (18%), polyuria (18%), polydipsia (18%),
anorexia (15%), nocturia (13%), oliguria (10%), urinary
frequency (8%), and hematuria (2%).
Laboratory findings include anemia, azotemia, and
an increased erythrocyte sedimentation rate (ESR).
Elevated white cell counts and pyuria can occur. The
diagnosis of RPF often is delayed because of its
nonspecific presentation.
PREFERRED INVESTIGATIONS
Plain Radiography and IVU and RGP
On plain abdominal radiographs, the psoas shadows may
not be visible. The renal outline may be enlarged if
hydronephrosis has occurred. Features related to the
complications of RPF may be visualized; these include
bowel dilatation due to obstruction and splenomegaly
secondary to portal hypertension. Findings related to
associated bone conditions may be seen. Such findings
include metastasis, ankylosing spondylitis, and
tuberculosis of spine.
On chest radiographs, signs of noncardiogenic
pulmonary edema may be seen secondary to fluid
overload. Pulmonary fibrosis can occur if associated with
SLE and ankylosing spondylitis. Mediastinal widening
may occur due to a soft-tissue mass associated with
mediastinal fibrosis.
The findings in RPF are nonspecific, and most findings
are related to the late complications of fibrosis, such as
bowel obstruction and pulmonary edema secondary to
renal failure. Contrast-enhanced studies, such as barium
follow-through and barium enema examinations, can
show the level of bowel obstruction. The diagnosis of
RPF has often been suggested on the basis of the excretory
urographic findings due to extensive changes in the
urinary tract. Retrograde pyelography is used in patients
with severely impaired renal function.
Limitations
Findings on plain radiography and contrast-enhanced
studies are nonspecific, demonstrating the late effects of
fibrosis. Excretory urography helps in establishing a
diagnosis in the early stage of the disease.
Characteristically, medial deviation of the ureter is
present, usually at the middle third, beginning at the level
of the third or fourth lumbar vertebra. The medial
deviation of the ureter is not a constant finding in patients
with RPF, and approximately 20% of patients with normal
urographic findings have medial deviation of ureters
without demonstrable evidence of pathologic change in
the urinary tract. Most retroperitoneal neoplasms displace
the ureters in a lateral direction, but medial deviation
can occur. Other causes for medial displacement of the
ureters include aneurysm, metastatic tumors, and bladder

diverticulum. Medial displacement may be seen after
abdominoperineal resection and removal of pelvic
malignancy.
Retrograde pyelography is an invasive technique with
no additional value compared with excretory urography.
Excretory Urography
Characteristically, medial deviation of the ureters occurs,
usually at the middle third, beginning at the level of third
and fourth lumbar vertebrae. Varying degrees of ureteric
obstruction with resultant hydronephrosis, hydroureter,
and tapering of the ureter at the level of L4-L5 vertebrae
may be evident.
Retrograde Pyeloureterography
Small ureteral catheters can be passed easily beyond the
obstruction, despite the appearance of complete occlusion
on excretory urograms, because of restricted peristalsis
rather than intraluminal constriction.
Aortography, Venography, and Lymphangiography
Aortography, venography, and lymphangiography help
in assessing the level and extent of occlusion; however,
findings from these examinations can be normal in
advanced disease.
Findings: Angiography and venography help in
assessing the level and degree of obstruction. Abdominal
aortic aneurysm can be demonstrated on angiograms.
Lymphangiographic findings in RPF include a delay
in the passage of contrast material through the aortic and
para-aortic lymphatics. Lymphatic flow may be obstructed
at the L3-L4 vertebral level, resulting in nonvisualization
of the lymphatics above the fourth lumbar vertebra, filling
of collateral lymphatic channels, and small irregular filling
defects in the mesenteric and para-aortic lymph nodes.
The absence of lymph node metastasis helps in excluding
malignancy.
Lymphangiography can be a complementary study
to excretory urography. The retroperitoneal lymphatics
are delicate structures; therefore, obstruction of the
lymphatics occurs before compression of the ureters or
major vessels. Angiography often causes underestimation
of the size of the aorta; therefore, aneurysms cannot be
excluded.
Miscellaneous Genitourinary Conditions 227
Ultrasonography
Ultrasonography can be used as a noninvasive technique.
Sonograms may or may not help in identifying the
retroperitoneal mass, but they can readily demonstrate
the degree of obstruction to the ureters and kidneys.
Attempts have been made to differentiate benign RPF
from malignant RPF by using color Doppler imaging.
On sonograms, RPF may appear as a relatively echo-
free mass centered on the sacral promontory. Imaging
the retroperitoneum may not be possible, particularly in
obese patients or in those with excessive bowel gas.
Findings: On sonograms, RPF may appear as a well-
defined, smooth-marginated, hypoechoic, retroperitoneal
soft-tissue mass encasing the aorta and inferior vena cava.
Distal extension beyond the sacral promontory and the
absence of lobulation suggest a benign etiology.
Ultrasonography may demonstrate dilatation of the
pelvocalyceal system and the ureters. Sonograms may
show features of coexisting primary biliary cirrhosis, bile
duct dilatation due to common bile duct stricture, portal
hypertension due to portal vein compression, focal or
diffuse pancreatic mass due to sclerosing pancreatitis, and
dilated bowel loops due to obstruction.
Some have attempted to use Doppler ultrasonography
to differentiate benign RPF from malignant RPF. However,
recent findings suggest that color Doppler ultrasonography
has no role in differentiating benign masses from
malignant retroperitoneal masses.
Ultrasonography is not a sensitive examination
compared with CT or MRI. Color Doppler imaging is not
helpful in differentiating benign masses from malignant
masses because they have no distinguishing features.
CT
CT is the imaging modality used to diagnose RPF and
to perform follow-up studies. CT scans help in assessing
the extent of disease and in studying the effects on other
organs. Differentiating benign RPF from malignant RPF
may not be possible.
Findings: On CT scans, RPF may appear as a rind of
soft tissue around the aorta and inferior vena cava
extending between the renal hilum and sacral promon-
tory.
228 Uroradiology: Text and Atlas
Laterally, RPF spreads to involve the ureters, causing
varying degrees of obstruction.
The fat plane between the mass and the psoas muscle
may be obliterated.
The mass tends not to displace the aorta anteriorly.
The attenuation value of the mass is similar to that
of muscle and shows variable degrees of enhancement
depending on the stage of the disease.
Certain CT features can help in differentiating benign
masses from malignant masses. The mass in RPF may
be bulky but not as massive as neoplastic lesions; however,
some exceptions exist. The presence of enlarged
mesenteric nodes and displacement of the aorta from
the spine by the periaortic mass favors malignancy,
although some displacement can occur in RPF. Unlike
RPF, most retroperitoneal neoplasms displace the ureters
laterally.
RPF does not produce local bone destruction.
The CT value and contrast enhancement have no role
in distinguishing benign masses from malignant masses.
MRI
Findings: RPF appears as a mass with low signal intensity
on T1 weighted images and variable signal on T2
weighted images, depending on the activity of the disease.
On T2-weighted images, RPF may appear hyperintense
when active inflammation is present and hypointense in
end-stage fibrosis. In homogeneous signal intensity on
T2-weighted MRIs suggests malignancy.
Isotope Renography
Isotope renography is useful in the serial assessment of
renal function. Gallium scintigraphy may demonstrate
increased uptake, depending on the activity of inflam-
mation. The use of 2-[fluorine 18]-fluoro-2-deoxy-D-
glucose positron emission tomography (FDG-PET) in
differentiating benign from malignant RPF is promising.
With CT and MRI, the fibrosis can be shown in more
detail. The symmetric distribution and geometric shape
are highly suggestive of RPF. CT scans may not be helpful
in differentiating benign RPF from malignant RPF. MRI
may help in differentiating the two, but the diagnosis
cannot be certain by using MRI.
RNI
Findings: In the early inflammatory stage of the disease,
gallium-67 scintigraphy may show increased uptake. Little
or no uptake may occur in the later stages of the disease.
Therefore, gallium imaging may be helpful in predicting
the therapeutic response to steroids and to monitor the
response to treatment. The absence of gallium uptake
in the mature stage of the disease makes the lesion less
likely to be of malignant origin. Both benign inflammation
and malignancy can show increased uptake.
On FDG-PET scanning, benign RPF masses exhibit
low uptake, whereas malignant masses exhibit increased
uptake.
The role of nuclear medicine studies is yet to be
defined. Such studies may be useful in assessing the
activity of the disease and in monitoring the response
to treatment. The use of FDG-PET scanning is still in
the preliminary stages.
DIFFERENTIAL DIAGNOSIS
RPF must be differentiated from other conditions that
can cause ureteric obstruction and renal failure, such as
retroperitoneal abscess, infections, inflammation, pelvic
surgery, and radiation therapy. Unusual causes that can
cause ureteric obstruction include barium granuloma after
colon perforation, use of sclerosing agents for treatment
of inguinal hernia and hemorrhoids, and methyl
methacrylate cement used for joint replacement.
Imaging appearances similar to those of RPF can be
demonstrated by abdominal aortic aneurysm; tumors
inducing desmoplastic response, such as lymphomas,
sarcomas, and pancreatic carcinomas; and metastatic
malignancies from the breast, lung, stomach, colon,
kidney, bladder, prostate, and cervix. Other conditions
that may simulate RPF include periaortic hematoma and
amyloidosis.
INTERVENTION
Biopsy can be performed under CT guidance to differen-
tiate benign masses from malignant retroperitoneal
masses. Drainage of the upper urinary tract can be
performed as a temporary measure. Percutaneous
nephrostomy and the insertion of a double-J stent helps

restore renal function and allows time to improve fluid,
electrolyte, and acid-base balance prior to surgery.
The use of steroids in RPF remains controversial;
however, some authors believe that steroids can be used
as an adjuvant to surgical ureterolysis. More recently,
immunosuppressive drugs, such as azathioprine, cyclo-
phosphamide, and tamoxifen, have been used to treat
RPF.
In drug-related RPF, cessation of the drug therapy can
result in restitution of the urinary tract and disappearance
of the symptoms.
MORTALITY/MORBIDITY
Although fatalities do occur, a satisfactory outcome can
be expected if renal impairment is not too severe.
Unlike idiopathic (nonmalignant) RPF, a distinctly poor
prognosis is associated with malignant RPF, which occurs
in response to metastatic tumor cells in the retro-
peritoneum.
Most patients live only 3–6 months after receiving a
diagnosis of malignant RPF, although prolonged survival
has been reported. Close follow-up care is critically
important to ensure the absence of progressive or
recurrent disease.
PRUNE BELLY SYNDROME (EAGLE BARDETT
SYNDROME)
INTRODUCTION
A classical triad consisting of absent abdominal
musculature, undescended testicles, and urinary tract
abnormalities. The full syndrome only develops in males.
PATHOPHYSIOLOGY
Precise cause is disputed: Theories:
1. The muscular defect is secondary to a distended
urinary system that prevents abdominal muscle
development
2. prostatic dysgenesis and transient neonatal ascites
3. mesodermal deficiency leads to urinary tract abnor-
malities and abdominal wall defect.
CLINICAL FEATURES
Syndrome is detected at birth due to abdominal mus-
culature defect, which typically affects the lower
Miscellaneous Genitourinary Conditions 229
abdominal wall, leaving the upper abdominal musculature
with a normal appearance. The muscular defect may be
partial or asymmetric.
The overlying skin has a wrinkled appearance like
a prune. Older children may instead demonstrate a
“potbelly” appearance.
ROLE OF RADIOLOGY AND IMAGING
The kidneys are asymmetrically affected: one tends to
be normal while the other is dysplastic. The ureters are
tortuous and dilated resulting from a deficiency in smooth
muscle. Vesicoureteral reflux is common and
hydronephrosis is often present. The bladder is typically
very large and may be associated with a patent urachus.
The prostatic urethra is dilated secondary to prostatic
hypoplasia, and it tapers rapidly at the membranous
urethra, giving rise to an appearance resembling that of
posterior urethral valves. The anterior urethra is normal.
An association with megalourethra has been described.
The cryptorchid testes usually lie in an abdominal
location. Extraurinary abnormalities include intestinal
malrotation, microcephaly, imperforate anus, congenital
heart defects, and musculoskeletal deformities such as
polydactyly, hip dislocation, and scoliosis.
An incomplete manifestation of the syndrome exists,
consisting of urinary tract abnormalities, but normal
abdominal musculature.
TUBEROUS SCLEROSIS
INTRODUCTION
It is a neuroectodermal syndrome characterized by
formation of hamartomatous tumors in the skin, brain
and viscera, including most commonly lungs and kidneys.
INCIDENCE
Incidence of tuberous sclerosis has been reported be as
rare as 1 in 150,000 and as common as 1 in 10,000.
It has significant morbidity and mortality with 75 percent
of patients dying by the age of 20 - either from CNS,
cardia, or renal complications.
CLINICAL FEATURES
The mean age of presentation of renal lesions is about
9 years.
230 Uroradiology: Text and Atlas
The most common renal lesion is the angiomyolipoma
(AML) which is present in about 80 percent of cases. The
second most common renal lesion is renal cysts.
ROLE OF RADIOLOGY AND IMAGING
Ultrasound, CT and MRI can all be used for evaluation
of renal tuberous sclerosis. CT is the most sensitive and
specific imaging modality for evaluating renal tuberous
sclerosis. The finding of multiple, less than 3 cm, often
bilateral cysts with fat-containing tumors is highly
suggestive of tuberous sclerosis. AMLs of tuberous
sclerosis are not prone to malignant degeneration and
so no yearly follow-up is needed. However, AMLs of
tuberous sclerosis can grow very large and are prone to
hemorrhage. Therapy for very large AMLs can include
prophylactic arterial embolization or tumors.
VHL
INTRODUCTION
It is a neurocutaneous syndrome characterized by
cerebellar hemangioblastoma, retinal phakomas/
angiomas, renal and pancreatic cysts, and bilateral RCC
in few cases.
ROLE OF IMAGING
CT is the most sensitive and specific technique for
evaluating renal component of VHL.

RECENT ADVANCES
• CT urography (CTU)
• MR urography (MRU)
• TRUS and guided biopsies
CT UROGRAPHY (CTU)
INTRODUCTION
IVU is associated with a substantial radiation dose.
Ultrasound is good for imaging the kidney parenchyma
and for detecting hydronephrosis, does not require the
administration of iodinated contrast, and avoids radiation
exposure. However, ultrasound is not good for detecting
urinary tract calculi, and does not adequately image the
renal collecting system or ureters. For these reasons,
multidetector CT imaging has become the gold
standard for the diagnosis of urinary tract calculi,
the investigation of hematuria, and the charac-
terization of renal masses and has largely replaced
both plain film excretory urography and ultrasound
examinations for these purposes.
Dedicated CT protocols have been developed for
these new high speed machines for different clinical
indications including “stone protocol” for the evaluation
of urinary tract calculi, CT urography for the evaluation
of patients with hematuria and “renal mass protocol” for
the characterization of known renal masses.
Recent Advances in Uroradiology 231
INDICATIONS
CT urography is most vital for the evaluation of patients
with hematuria. The main causes of hematuria are:
• Urinary tract calculi
• Renal tumors, urothelial tumors and
• Urinary tract infections.
CT urography is the best single diagnostic
examination for diagnosing all of these pathologies, with
the exception of infection, which is effectively diagnosed
in most cases by microbiological analysis of the urine.
CT urography offers ease of performance and a high
degree of detection of renal stones, anomalies, and (less
commonly) renal masses in the kidneys of potential
donors before consideration of renal transplant surgery.
TECHNIQUE OF CTU
CT urography requires the use of contrast agent to opacify
the collecting system, the ureters, and the bladder. In
addition to optimal opacification, distension appears to
be an important requirement for thorough evaluation of
the renal collecting system and ureter. For this reason,
intravenous saline is given at the same time as the contrast
material to aid in the detection of subtle filling defects
and the discrimination between urothelial neoplasms
and other filling defects. Image reconstruction tech-
niques are used to create images of the entire length of
the urinary system from the kidneys to the bladder.
232 Uroradiology: Text and Atlas
Multiplanar 3 D reconstruction can provide the anatomic
detail required to correlate the finding with retrograde
ureterography or to perform an endoscopic evaluation.
ADVANTAGES
The advantages of multidetector CT urography over
conventional plain film excretory urography (also known
as IV pyelography and IV urography) and ultrasound for
the evaluation of the urinary tract are numerous.
1. CT has been shown to detect parenchymal masses
in the kidney with a sensitivity of 94 percent, compared
to 67 percent for plain film excretory urography and
79 percent for ultrasound.
2. Another potential advantage of CT is that recons-
tructed images can show tumors in a filled bladder
opacified with contrast agent (“virtual cytoscopy”).
However, conventional cytoscopy remains the gold
standard for the detection of tumors of the bladder,
as it will detect early color-changing mucosal lesions
that do not deform the contour of the bladder wall.
In addition, cytoscopy has the added capability of
biopsy of suspicious lesions.
3. Multidetector CT scanning is fast, taking around 15
seconds for image acquisition from the kidneys to the
bladder during a single breath-hold.
4. The images have good spatial resolution, little
misregistration due to respiratory movement, and the
acquisition of multiple thin slices allows excellent two-
and three-dimensional reconstructions of the abdo-
minal anatomy, making it possible to detect pathologies
outside the urinary tract as well those within.
DISADVANTAGES
1. Although, Iodinated contrast agents are not usually
required for the detection of renal stones, but are
routinely used in CT urography.
2. In comparison to CT, Conventional IVU offers
excellent delineation of calyceal and papillary
anatomy, the ureters and bladder, but it is inferior
to multi-detector CT for imaging of the kidney
parenchyma.
3. Both CT and plain film excretory urography are
associated with a substantial radiation dose.
MAGNETIC RESONANCE UROGRAPHY (MRU)
INTRODUCTION
Interest is rapidly growing in the use of magnetic reso-
nance (MR) imaging to assess genitourinary diseases,
particularly with the advent of faster imaging times
allowing breathhold image acquisitions and contrast
material-enhanced studies with dynamic measurements.
Intravenous excretory urography (IVU) has been
regarded as the imaging modality of choice for the
detection of urinary tract disorders in patients with acute
flank pain. Functional as well as anatomical details are
provided by this imaging technique. The use of ionizing
radiations and contrast material are considered to be the
major drawbacks of IVU.
Recently, the use of magnetic resonance urography
using half-Fourier acquisition single shot turbo spin-echo
(HASTE) and rapid acquisition with relaxation
enhancement (RARE) sequences has been described in
patients with urinary tract disease. High resolution images
call be achieved with breath-hold and rapid acquisition
sequences. The HASTE and RARE can demonstrate acute
urinary obstruction and show perirenal high intensity
signal, however, information about renal function is not
achieved. Small calculi are difficult to detect and non-
dilated urinary tract is not fully visualized. In this aspect
Gadolinium enhanced three-dimensional fast low angle
shot (3D FLASH) sequence provides an alternative rapid
imaging technique for urinary tract evaluation.
Gadolinium enhanced 3D FLASH MRU is a highly
sensitive and specific imaging modality in investigating
patients with acute flank pain and could replace
Conventional IVU when the later is contraindicated or
undesirable. MRI also offers the possibility to screen the
abdominal cavity and retroperitoneal space to rule out
other pathological conditions. The combined use of both
HASTE and 3D FL4SH sequences will ensure better
confidence in the evaluation of acute suspected renal colic.
TECHNIQUE
MR urography has been perfor med with both
T1 weighted and heavily T2 weighted pulse sequences
(e.g. rapid acquisition with relaxation enhancement, fast
spin-echo [SE], and half-Fourier acquisition turbo SE).

Gadolinium-enhanced excretory MR urography
supplemented with low-dose diuretics such as furosemide
has been proposed as an accurate alternative to
conventional excretory urography for imaging the
morphology of the urinary tract.
Gadolinium-enhanced MR imaging to differentiate
obstructive from nonobstructive hydronephrosis,
employing a renogram-like dynamic format to depict
signal intensity (SI) changes in the cortex and medulla
in normal and hydronephrotic kidneys.
A strategy for estimating single-kidney hemodynamic
functions by using MR imaging with gadopentetate
dimeglumine enhancement to determine the single-
kidney filtration fraction has also been described.
ADVANTAGES
MRU provides detailed anatomic, dynamic, and
functional information on normal and abnormal kidneys.
No technique other than MR imaging has the potential
for accomplishing all of these goals.
Currently used MR contrast agents, such as gadopen-
tetate dimeglumine and gadoversetamide, are small
molecules, similar to inulin, that after intravascular
injection are distributed initially in the vascular space and
then rapidly into the extracellular space. These agents
can serve as extracellular fluid markers and are freely
filtered in the glomeruli. Since they are neither secreted
nor absorbed, they are an excellent indicator of renal
function, serving as an “MR-visible inulin”.
MR contrast agents also produce a T1 effect on
images, rendering the calices, ureters, and bladder highly
visible on T1-weighted MR images. A previously
unexploited value of these molecules is their effect on
the T1 of moving blood, which is linearly related to their
concentration in blood . Thus, the T1 of the incoming
blood in the renal artery will be different from that of
the outgoing blood in the renal vein, in a relationship
that reflects the percentage of plasma filtered, the FF. Pulse
sequences used to determine renal blood flow, performed
Recent Advances in Uroradiology 233
simultaneously or closely in time, could provide a rapid
determination of split glomerular filtration rate (GFR),
a fundamental index of renal health and viability.
Coronal breath-hold images of the kidney (three or
four sections, 8 mm thick) are to be acquired before and
after bolus injection of contrast material to simulate
nephrotomogram.
DISADVANTAGES
1. Only a limited spectrum and intensity of hydro-
nephrosis. Obstructive hydronephrosis was diag-
nosed in only two patients, and none had acute
obstruction.
2. Greater clinical experience will be required for
assessing the strengths and weaknesses of dynamic
and functional MR urography. The compatibility of
the dynamic MR renograms with known renal
physiology, radionuclide renograms, contrast medium
renal pharmacokinetics, and laboratory reports
provides support for these preliminary findings.
COMPARISON WITH IVU, CTU, USG, AND RNI
Nuclear medicine renography provides functional
information but relatively poor spatial resolution.
US has better spatial resolution than nuclear medicine
but provides no functional information, although new
US contrast agents could be promising for the study of
renal dynamics.
CT offers excellent spatial resolution and the potential
to assess renal dynamics, but multiple exposures would
be needed, resulting in inordinately high radiation doses.
CT also requires iodinated contrast agents, with an
increased risk of systemic and renal toxicity.
With use of predominantly breath-hold pulse
sequences, the potential for MR to provide excellent pre-
and postcontrast anatomic images, tomographic coronal
dynamic images with renograms, and unilateral renal FFs
as a measure of kidney function not available with any
other clinical technique.
234 Uroradiology: Text and Atlas
CONTRAST MEDIA
INTRODUCTION
Iodinated contrast media are widely used today in many
radiological procedures.
Nonionic low-osmolar iodinated (iopamidol, iohexol,
etc.) contrast media are preferred over ionic (sodium and
meglumin salts of diatrozoate).
PRECAUTIONS FOR A CONTRAST MEDIUM INJECTION
• Explain to the patient about the examination and risk.
• Anxiety-free examination atmosphere.
• Secure that first line drugs and instruments are
available.
• The patient should be well hydrated.
• Determine whether the patient is at risk of any contrast
medium reaction.
• Patients at risk should be carefully monitored during
the examination.
• When absorption or leakage into the circulation is
possible (for example after intracavitar use) take the
same precautions as for intravascular administration.
CIN (CONTRAST MEDIA-INDUCED NEPHROTOXICITY)
The findings of contrast media-induced nephrotoxicity
(CIN) include persistent bilateral, diffuse nephrograms
and occasionally vicarious excretion of contrast by the
biliary system.
It occurs iatrogenically after the administration of
intravascular contrast. The underlying pathophysiology
is usually acute tubular necrosis. A common definition
of CMN is impairment, either transient or permanent,
in renal function (rise of at least 1.0 mg/dL) within two
to five days after exposure to contrast.
Risk factors for development of CMN include
preexisting renal insufficiency (especially diabetic
nephropathy), decreased renal perfusion (congestive
heart failure, diuretics, etc.), hypertension, age over 60,
concurrent nephrotoxic medications, and repeated
exposure to contrast within a 72 hour period. Intraarterial
contrast administration places patients at higher risk for
CMN than does intravenous administration.
The risk of CMN in patients with normal renal function
is less than 0.5%. Prospective studies have found the risk
of CMN in patients with renal impairment to be 12–27%.
CMN occurs after the use of both low-osmolality contrast
media (LOCM) and high-osmolality contrast media
(HOCM); however, studies show that there is generally
a decreased risk of CMN with LOCM, especially diabetic
patients with renal insufficiency.
N-acetyl cysteine has been found to be very helpful
in treating CIN.
Methods for prevention of CMN include vigorous
hydration, careful patient selection, and increased interval
between contrast examinations.
 Radiological Contrast Media 235

Main risk factors and prophylactic measures on use of contrast media in imaging
Adverse reaction Risk factors/conditions Measures to reduce the risk
Previous generalized • Previous adverse reaction, either moderate Use non-ionic contrast media.
contrast medium reaction (e.g.urticaria, bronchospasm, moderate hypotension) Corticosteroids may be given :
or severe (e.g. convulsions, servere bronchospam, Prednisolone 30 mg orally 2 hours or
pulmonary edema, cardiovascular collapse) – Methylprednisolone 32 mg orally 12 and 2 hours
anaphylactoid reactions. before injecting contrast medium.
• Asthma Effects of antihistamines [H1 and H2] are not
• Allergy requiring medical treatment. definitely proven.
Contrast medium • Raised s-creatinine levels, particularly secondary • Make sure that the patients is well hydrated
induced nephrotoxicity to diabetic nephropathy. [give at least 100 ml. (oral (e.g. soft drinks) or
• Dehydration intravenous (normal saline) depending on the
• Congestive heart failure clinical situation) per hour starting 4 hours before
• Concurrent administration of nephrotoxic drugs, to 24 hours after contrast administration – in warm
e.g. non-steroid anti-inflammatory drugs areas increase the fluid volume]
• Age over 70 years old. • Use non-ionic contrast media
• Stop administration of nephrotoxic drugs for
at least 24 hours
• Consider alternative imaging techniques,
which do not require the administration of iodinated
contrast media.
Lactic acidosis Patients treated with biguanide-type anti diabetics • Serum creatinine level measurement < 1 week
• Serum creatinine normal
• Stop biguanide intake, give contrast medium
• Serum creatinine abnormal
• Consider alternative imaging techniques, which do
not require the administration of iodinated contrast
media.
Postpone contrast medium examination for 48 hours.
Anxiety Nervousness, sweating, etc. Consider benzodiazepines
Iodine induced • Patient with Graves’ disease In very selected high-risk patients prophylactic therapy
hyperthyroidism • Multi-nodular goiter with thyroid autonomy, especially may be given by endocrinologists in advance.
elderly patients and patients living in areas of iodine
deficiency
Extravasation • Pressure injector with insufficient fixation of Appropriate injection site, careful injection
needle placement Prefer non-ionic contrast medium in combination with
• Fragile or damaged veins pressure injector
Risk for late reaction • Previous contrast medium reaction Patient should be informed and observed
(1 hour to 7 days) • Interleukin-2 treatment
Hypotension Dehydration Hydrate adequately
236 Uroradiology: Text and Atlas

First line treatment of contrast medium adverse reactions

Subsequent steps if needed should be taken by care of resuscitation team.
Acute adverse reactions ( < 1 hour ).
Nausea/Vomiting Moderate, transient : Supportive treatment
Severe, protracted : Appropriate antiemetic drugs (e.g. odansetron, dimenhydriant )
Urticaria Scattered, transient : Supportive treatment including observation
Scattered, protracted : Appropriate H1 antihistamine (e.g.clemastine) intramuscularly or intravenously should be
considered. Drowsiness and/or hypotension may occur.
Profound : Consider Adrenaline 1:1000, 0.1-0.3 ml. (0.1–0.3 mg.) intramuscularly in adults, 0.01 mg/kg
intramuscularly up to 0.3 max. in children. Repeat as needed.
Bronchospasm 1. Oxygen by mask (6-10 l/min)
2. B-2-agonist metered dose inhaler, 2–3 deep inhalations
3. (e.g. salbutamol)
4. Adrenaline intramuscularly depending on blood pressure
Normal blood pressure
1:1,000, 0.1–0.3 ml (o.1–0.3 mg) [use smaller dose in a patient with coronary artery disease or elderly patient]
In children : 0.01 mg/kg; mad dosage : 0.3 mg
Decreased blood pressure
1:1000, 0.5 ml (0.5 mg), in children : 0.01 mg/kg max. dosage : 0.3 mg
5. For further treatment : resuscitation team.
Laryngeal edema 1. Oxygen by mask (6–10 l/min)
2. Intramuscular adrenaline (1:1000), 0.5 ml (0.5 mg) for adults, repeat as needed
3. Intubation via resuscitation team.
Hypotension Isolated hypotension
1. Elevate patient’s legs
2. Oxygen by mask (6–10 l/min)
3. Intravenous fluid : rapidly, normal saline of lactated Ringer’s solution
4. If unresponsive : adrenaline : 1:1000, 0.5 ml (0.5 mg) intramuscularly, repeat as needed
Vagal reaction (hypotension and bradycardia)
1. Elevate patient’s legs
2. Oxygen by mask (6–10 l/min)
3. Atropine 0.5–1.0 mg intravenously, repeat if necessary after 3-5 min, to mg total (0.04 mg/kg) in adults
In pediatric patients give 0.02 mg/kg
Intravenously (max. 0.6 mg/dose) repeat if necessary to 2 mg total
4. Intravenous fluids : rapidly, normal saline or lactated Ringer’s solution
Hypotension and tachycardia
1. Elevate patient’s legs
2. Intravenous fluids : rapidly, normal saline or lactated Ringer’s solution
3. Oxygen by mask (6–10 l/min)
Anaphylactoid 1. Call for resuscitation team
generalized reaction. 2. Suction airway as needed
3. Elevate patient’s if hypotensive
4. Oxygen by mask (6–10 l/min)
5. Intramuscular adrenaline (1:1000), 0.5 ml (0.5 mg) in adults. Repeat as needed.
In pediatric patients 0.01 mg/kg to 0.3 mg max. dose.
6. Intravenous fluids rapidly (e.g. normal saline, lactated Ringer’s)
7. H1-blocker, e.g. diphendydramine 25–50 mg intravenously
Seizures, Convulsions Diazepam 5–10 mg rectally (or intravenously)
 Radiological Contrast Media 237

Late adverse reactions ( 1 hour – 7 days)

Symptomatic and similar to the management of other drug-induced skin reactions
Extravasation • Conservative management is adequate in most case
Limb elevation
Apply ice packs
Careful monitoring
• If a serious injury is suspected, seek the advice of a surgeon
Iodine induced Very late reaction (several days/weeks)
hyperthyroidism Seek the advice of an endocrinologist
Contrast medium induced Symptomatic
nephrotoxicity Close monitoring as in any other patient with reduced renal function (due to other causes)-Consult a nephrologists
Dialysis seems to have no effect on the incidence on contrast media induced nephropathy
Lactic acidosis • Monitor renal function ( serum creatinine), serum lactic acid and pH of blood
• Look for symptoms of lactic acidosis (vomiting, somnolence, nausea, epigastric pain, anorexia, hyperpnea,
lethargy, diarrhea and thirst). Blood test results indicative or lactic acidosis: pH < 7.25 and lactic acid
> 5 mmol
 References 239

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47. Zagoria KJ, Tung GA. Genitourinary Radiology, The Requisites. St. Louis: Mosby, 1997.
 Index

A Adult polycystic kidney disease 46 B

clinical features 47
Abdominal ectopy 35 incidence 47 Beckwith-Wiedemann syndrome 51
Accessory renal artery 181 pathophysiology 46 Beer-drinker’s hydronephrosis 31
Acute infections 103 preferred investigation 47 Benign urethral lesions 195
acute pyelonephritis 103 angiography 48 balanitis xerotica obliterans 195
causative organism 103 CT scanning 48 benign neoplasms 195
role of radiology and imaging 103 MRI 48 paraurethral cyst 195
emphysematous pyelonephritis 105 plain radiographs 47 urethral caruncle 195
clinical features 106 RNI 48 urethral diverticulum 195
etiological agents 106 ultrasonography 47 urethral polyps 195
incidence 105 mortality/morbidity 48 Bilateral large kidneys 161
intervention 107 Agenesis of urethra 198 causes 161
pathophysiology 106 Alport syndrome 88, 161 Bilateral small kidneys 161
predisposing factors 105 Anomalies of urorenal tract 27 causes 161
preferred investigations 106 kidney 27 Bladder 1, 33
treatment 107 anomalies of form 27 congenital bladder diverticula 33
types 106 anomalies of fusion 27 exstrophy 33
pyonephrosis 104 anomalies of number 27 Bladder diverticulum 63, 199
renal abscess 105 anomalies of position 27 Bladder duplication 69
features 105 Antegrade urography 9 Bladder exstrophy 68
Acute urinary obstruction 92 advantages 11 associated anomalies 68
anatomical basis 94 disadvantages 11 clinical features 68
clinical features 93 indications 10 incidence 68
etiology 93 Aphorism 59 management 68
incidence 93 Ascent of the kidneys 27 pathophysiology 68
intervention 100 Aspirin renography 173 role of radiology and imaging 68
pathophysiology 92 Autosomal recessive polycystic kidney Bladder outlet obstruction 210
role of radiology and imaging 94 disease 44 congenital causes 210
KUB and IVU 94 anatomical basis 45 neoplastic causes 211
urographic findings in acute obstruction classification 44 traumatic causes 211
96 clinical features 45 Bochdalek’s hernia 37
urographic findings in chronic incidence 45 Bosniak classification of renal masses 75
obstruction 96 mortality/morbidity 46
nephrographic density 96 pathophysiology 44
C
parenchymal thickness 96 preferred investigations 46
pyelogram 96 CT 46 Calyceal diverticulum 52
renal size 96 MRI 46 treatment 53
ureter 96 ultrasonography 46 types 53
242 Uroradiology: Text and Atlas
Captopril renography 173
Captopril scan 172
Caroli disease 51
Chronic infections 108
malacoplakia 119
renal tuberculosis 112
clinical features 113
incidence 113
mortality/morbidity 117
pathophysiology 112
preferred examination 113
radiological findings 113
schistosomiasis (bilharziasis) 117
clinical features 118
differential diagnosis 118
frequency 118
mortality/morbidity 119
pathophysiology 118
role of radiology and imaging 118
treatment 119
xanthogranulomatous pyelonephritis
108
clinical features 109
differential diagnosis 111
incidence 109
intervention 111
pathophysiology 108
role of radiology and imaging 109
stages 109
treatment 111
Chronic urinary obstruction 101
additional note on ureteral obstruction
101
hydronephrosis 101
differential diagnosis 101
non-obstructive causes 101
mortality/morbidity 101
Cobra-head deformity 61
Column of Bertin 6
Complete urinary collecting system
duplication 53
clinical features 54
differential diagnosis 54
pathophysiology 53
role of radiology and imaging 54
treatment 54
varieties 54
Congenital bladder diverticulum 68
Congenital PUJ obstruction 30
clinical features 31
differential diagnosis 31 pathophysiology 214
incidence 30 preferred investigation 216
pathophysiology 30 PSA screening 216
role of radiology and imaging 31 risk factors 216
treatment 31 staging 215
Congenital urethral diverticulum 200 prostatic abscess 222
anatomical basis 200 prostatic calcification 222
incidence 200 prostatic utricle cyst 222
role of radiology and imaging 200 Drooping lily sign 56, 61
treatment 200 Duplicated collecting systems 54
Congenital uterovesical fistula 70 anatomical basis 56
Crossed fused renal ectopia 28, 37 clinical features 55
clinical features 38 incidence 55
age 38 mortality/morbidity 58
anatomical basis 34 pathophysiology 55
etiology 38 preferred investigations 56
incidence 38 antegrade pyelography 57
pathophysiology 38 arteriography 58
preferred investigations 38 CT with contrast 57
MRI 39 IVU/excretory urography 56
ultrasonography 39 magnetic resonance urography 57
Cystic disease of kidney 71 MCU/VCUG 57
classification 71 plain radiography 56
genetic cystic diseases 71 scintigraphy 58
nongenetic cystic diseases 71 ultrasound 57
pathophysiology 71 terms relevant to duplex collecting
Cystitis 200 systems 56
Cystography and cystourethrography 22 bifid system 56
ascending urethrogram 22 double ureters 56
combined ascending urethrogram and duplex kidney 56
MCU 22 duplex system 56
MCU 22 upper and lower pole ureters 56
upper or lower pole 56
D Duplication anomalies 29
Duplication of urethra 198
Diseases of prostate 212
benign prostatic hyperplasia 212
E
clinical features 212
differentiating points from carcinoma Ectopic orifices 31
of the prostate 213 Ectopic ureteral 58
pathophysiology 212 associated anomalies 58
role of radiology and imaging 213 clinical features 58
prostate cancer 214 embryology 58
anatomical basis 216 imaging 58
clinical presentation 215 incidence 58
grading 214 Ehlers-Danlos syndrome 51
histopathologic diagnosis of prostate Embryology 27
cancer 214 Emphysematous cystitis 200
incidence 215 clinical features 200
interventions 221 role of radiology and imaging 200
 Index 243

Excretory urography 11 H M
bowel preparation 14
Horseshoe kidney 28, 39 Malrotation 29
contraindications 14
anatomical basis 41 Meckel diverticulum 80
contrast administration 17 clinical features 40
bolus versus infusion 17 Medical renal disease 161
horseshoe kidney with associated
dosage 17 anomalies 40 differential diagnosis 162
demerits 21 isolated horseshoe kidney 40 role of radiology and imaging 162
exposure factors 15 complications 41 MRI 162
film sequencing 17 incidence 40 USG 162
intervention 44 Medullary sponge kidney 50
general considerations 17 pathophysiology 40
indications 13 associated syndromes 51
preferred investigations 41
informed consent 14 clinical features 50
CECT 42
limitations 21 IVU 41 incidence 50
limited urogram 20 MRI 43 intervention 52
modifications 21 plain radiographs 41 mortality/morbidity 52
RNI 43 pathophysiology 50
patient preparation 14
ultrasonography 42 preferred examination 51
dehydration 14
physiology 12 CT 52
plain film of abdomen 15 I IVU 51
postvoid film 20 MRI 52
Interventional uroradiology
psychological preparation 14 plain radiograph 51
techniques 223
tailoring 20 RNI 52
Intrathoracic kidney 35, 37
tomography (adult) 19 USG 51
Intravenous urography 11, 16
compression 19 Megapolycalicosis and primary megaureter
introduction 11
Extracorporeal shock wave lithotripsy 78 megapolycalicosis 66
Ischial spine 4
pathogenesis 66
primary megaureter 67
F K differential diagnosis 68
Fibromuscular band 5 Kidney 1 potential complications 68
Foley balloon 63 mesonephros 1 role of radiology and imaging 66
Fused pelvic kidney 28 metanephros 1 Mesodermal tumors 63
pronephros 1 Metal stenosis 198
G Milk-alkali syndrome 88
MR anatomy of prostate 5
Genetic cystic disease 76 L
MRI 26
ARPKD 77 Leukopenia 30 MR urography 26
infantile 77 Levator ani muscle 5 Müllerian ducts 2
juvenile 77 Lymphoma of kidneys 152 Multicystic dysplastic kidney 29, 49
neonatal 77
anatomical basis 153 differential diagnosis 50
perinatal 77
incidence 153 imaging findings 49
autosomal dominant polycystic kidney
intervention 156 CT/MR findings 49
disease 76
Genitourinary manifestations of diabetes mortality/morbidity 156 nuclear scintigraphy 49
166 pathophysiology 153 ultrasound 50
diabetic nephropathy 166 preferred investigation 153 incidence 49
causes 166 angiography 155 intravenous urography 50
complications 167 CT 154 prognosis 50
imaging 167
IVU 153 retrograde ureterogram 50
incidence 166
reproductive system 167 MRI 155 Multilocular cystic nephroma 144
risk factors 166 RNI 155 cystic Wilms’ tumor 145
role of investigations 166 ultrasonography 154 clinical issues 146
244 Uroradiology: Text and Atlas
gross pathologic-surgical features
145
microscopic features 145
pathology 145
prognosis 146
treatment 146
Muscular hypertrophy 63
N preferred investigation 159
Nephroblastomatosis 143
role of radiology and imaging 143
treatment 143
Nephrocalcinosis 87
causes of medullary nephrocalcinosis 88
clinical features 89
incidence 89
pathophysiology 87
causes of cortical nephrocalcinosis
88
disorders of calcium metabolism 87
preferred investigations 89
computed tomography 90
MRI 90
RNI 91
ultrasonography 90
Neurogenic bladder 211
Nongenetic cystic kidney disease 72
acquired cystic renal disease 76
calyceal diverticulum 75
treatment 76
types 75
cortical renal cysts 72
Bosniak classification 73
clinical features 72
complications 73
incidence 72
pathology 72
role of radiology and imaging 72
dysplasia/cystic dysplasia/multicystic
dysplastic kidney 75
medullary sponge kidney 75
Normal anatomy 3
anatomy of 3
kidney, ureter and bladder 3
prostate 3
retroperitoneum 3
Normal variants (pseudotumors) 6
Nubbin sign 56
O Prenatal (fetal) hydronephrosis 101
bilateral pathology 102
Oncocytoma 158 differential diagnosis 101
anatomical basis 159 unilateral pathology 101
clinical features 159 Primary lymphoma of bladder 208
frequency 159 clinical features 209
intervention 160 mortality and morbidity 209
mortality/morbidity 160 role of radiology and imaging 209
pathophysiology 158 treatment 209
Prune Belly syndrome 70
angiography 160 Prune Belly syndrome (Eagle Bardett
CECT 159 syndrome) 229
KUB radiograph 159 clinical features 229
limitations of techniques 160 pathophysiology 229
MRI 160 role of radiology and imaging 229
PET scan 160
RNI 160
R
USG 159
Radiological contrast media 234
P Radiology of renal transplant 182
anatomical basis 183
Page kidney 126 complications 184
Pelvic kidney 35 historical aspect 182
Penis and urethra 33 intervention 191
duplication of urethra 34 pathophysiology 182
epispadias 34 preferred investigations 185
hypospadias 34 limitations 185
phimosis and paraphimosis 34 USG and color Doppler 186
posterior urethral valves 34 acute kidney transplant rejection 187
urethral meatal stenosis 34 angiographic study 190
urethral stricture 34 CT scanning and CT-guided
Percutaneous nephrostomy 223 interventions 188
indications 223 features 186
elective percutaneous nephrostomy MRI 189
223 nuclear medicine scanning 190
emergency percutaneous peritransplant fluid collections 186
nephrostomy 223 Radiolucent urolithiasis 86
technique 224 Ranal arteriovenous malformation 180
fluoroscopy guided 224 clinical features 180
ultrasound guided 224 etiology 180
Peripheral zone 5 role of radiology and imaging 180
Periurethral abscess 198 treatment 180
Plain KUBU radiograph 7 Recent advances in uroradiology 231
mimics of renal colic 7 CT urography (CTU) 231
Posterior urethral valve 192 advantages 232
classification 192 disadvantages 232
clinical features 192 indications 231
pathophysiology 192 technique 231
role of radiology and imaging 193 magnetic resonance urography 232
Potter’s syndrome 27 advantages 233
 Index 245

disadvantages 233 pathophysiology 163 intravascular ultrasonography-

technique 232 preferred examination 164 guided atherectomy 176
Renal agenesis 34 CT 165 medical therapy 175
associated anomalies 35, 36 MRI 165 percutaneous transluminal
bilateral renal agenesis 35 plain radiographs 164 angioplasty 176
clinical features 36 retrograde pyeloureterography 165 surgical revascularization 176
incidence 35 ultrasound 165 vascular stent placement 176
pathophysiology 35 Renal scintigraphy 26 mortality/morbidity 177
role of radiology and imaging 35, 36 arteriography 26 pathophysiology 168
angiography 37 dynamic scan 26 arterial dysplasia 170
CT 37 renal cortical scintigraphy 26 atherosclerosis 170
ultrasound 36 static scan 26 congenital stenosis 171
urography 36 Renal trauma 120 development of RVHT 168
Renal angiomyolipoma 156 clinical features 121 evolution of RVHT 170
clinical features 156 incidence 121 incidence 171
findings 157 management of renal injury 129 neurofibromatosis 171
follow-up 158 mortality/morbidity 129 transplant RAS 171
incidence 156 pathophysiology 120 role of radiology and imaging 172
mortality/morbidity 158 causes 120 color Doppler 173
pathophysiology 156 features 120 conventional angiography 174
preferred investigations 157 grading 120 CT angiography (CTA) 174
treatment 158 preferred investigations 121 hypertensive urography 172
Renal artery aneurysm 181 angiography 128 MRA 175
Renal cell carcinoma 146 intravenous urography 121 RAS 173
anatomical basis 147 MRI 128 RNI 172
clinical details 148 radiography 121 Retrocaval utreter 33
differential diagnosis 152 retrograde pyelography 122 Retrograde urography 8
incidence 147 RNI 128 indications 9
intervention 152 ultrasonography 122 Retroperitoneal fibrosis /Ormond’s disease
mortality/morbidity 152 VCUG 122 225
pathophysiology 146 radiologic intervention 129 clinical features 226
preferred investigations 149 Renal vein thrombosis 177 differential diagnosis 228
angiography 152 etiology 177 incidence 226
CECT 150 primary cause 177 intervention 228
intravenous urography 149 secondary causes 177 mortality/morbidity 229
MRI 151 incidence 177 pathophysiology 225
plain radiography 149 mortality and morbidity 180 preferred investigations 226
RNI 151 pathophysiology 177 aortography 227
USG 149 acute 177 CT 27
risk factor 146 chronic 178 excretory urography 227
staging 146 role of radiology and imaging 178 isotope renography 228
Renal dysplasias 29 computed tomography 178 lymphangiography 227
Renal ectopia 28 radionuclide renography 179 MRI 228
Renal hypoplasia 29 ultrasonography 178 plain radiography and IVU and RGP
Renal infarct 181 treatment 179 226
Renal papillary necrosis 163 thrombolytic therapy 179 retrograde pyeloureterography 227
anatomical basis 163 Renovascular hypertension 168 RNI 228
clinical features 163 clinical features 171 ultrasonography 227
mortality/morbidity 166 intervention 175 venography 227
246 Uroradiology: Text and Atlas

Rhabdomyosarcoma 208 clinical features 229 RNI 61

mortality and morbidity 208 incidence 229 ultrasound 60
pathophysiology 208 role of radiology and imaging 230 voiding cystourethrography 60
role of radiology and imaging 208 Urethra 1
treatment 208 U Urethral calculus 198
Role of MDCT in urologic diseases including Urethral strictures 194
the imaging protocols 23 Ultrasonography 22 etiology 194
hematuria protocol 24 advantages 22 role of radiology and imaging 194
indications 23 disadvantages 22 Urethral trauma 133
renal mass protocol 24 Unilateral small kidney 161 anatomical basis 134
stone protocol 24 causes 161 clinical details 134
nephrolithiasis 24 Urachal abnormalities 69 incidence 134
urolithiasis 24 anatomy/embryology 69 intervention 138
clinical features/complications 69 mortality/morbidity 138
complications 70 role of radiology and imaging 135
S
incidence 69 CT 137
Sacral kidney 35 role of radiology and imaging 70 MRI 137
Sickle cell disease 88 varieties of abnormalities 69 retrograde urethrography 135
Space of Retzius 210 patent urachus 69 ultrasonography 137
Stenosis 31 urachal cyst 69 Urinary bladder trauma 129
Supernumerary kidney 27 urachal diverticulum 70 anatomical basis 131
urachal sinus 69 classification 130
T Urachal carcinoma 209 clinical features 130
anatomical basis 210 mechanism 129
Transitional cell carcinoma of urinary
clinical features 210 mortality/morbidity 133
bladder 201
incidence 210 preferred investigations 131
anatomical basis 203
intervention 210 CT cystography 132
clinical features 203
mortality/morbidity 210 CT retrograde cystograms 132
incidence 201
pathophysiology 209 limitations of techniques 133
intervention 207
role of radiology and imaging 210 retrograde cystography 131
mortality/morbidity 207
pathophysiology 201 CT 210 ultrasonography 132
causative agents 201 MRI 210 Urogenital septum 1
pathology/histology 202 plain radiography 210 Urolithiasis 78
polychronotropism 201 Ureter 30 clinical features 79
preferred examination 203 Ureterocele 32, 58 differential diagnosis 80
role of radiology and imaging 203 classifications 58 incidence 79
angiography 205 clinical features 59 intervention 85
CT 205 differential diagnosis 62 mortality/morbidity 86
intravenous urography 204 incidence 60 pathophysiology 78
MRI 206 intervention 62 predisposing factors 78
plain radiograph 203 mortality/morbidity 62 role of radiology and imaging 80
retrograde pyelography 204 pathophysiology 59 conventional radiography 81
RNI 206 role of radiology and imaging 60 CT 83
ultrasonography 205 antenatal ultrasonography 60 CT protocol for calculus disease 84
staging of TCC 202 CT 61 intravenous urography 82
grading of TCC 202 intravenous urogram 61 MRI 85
metastases 202 MRI 61 RNI 85
Tuberous sclerosis 229 renal/bladder ultrasonography 61 ultrasonography 82
 Index 247

special considerations 86 mortality/morbidity 66 genetics 141

types of renal calculi 78
calcium stones 78
cystine stones 79
magnesium ammonium phosphate
(struvite) stones 79
matrix stones 79
orotic acid stones 79
several other less common forms of
urolithiasis 79
uric acid stones 79
xanthine stones 79
V
Vesicoureteral reflux 32, 63
anatomical basis 63
clinical features 64
grades 64
incidence 63
pathophysiology 63
role of radiology and imaging 64
angiography 66
intravenous urography 64
RNI 65
ultrasonography 65
VCUG 64
Vesicourethral canal 1
Vestibule 2
VHL 230
role of imaging 230
W Xanthogranulomatous pyelonephritis 80
Weigert-Meyer rule 54, 59
Wilms’ tumor 80, 51
Wilms’ tumor/nephroblastoma 140
associations 141
incidence 140
mortality and morbidity 141
pathophysiology 141
role of radiology and imaging 141
computed tomography 142
magnetic resonance imaging 143
plain radiography 141
ultrasound 142
staging 141
Wolffian duct 2, 55
X
Z
Zonal anatomy 5
Zuckerkandl’s fascia 3