Chapter 9
The Kidney and Ureter
Paul Babyn
Marilyn J. Siegel
Computed tomography is an easily performed imaging
examination that often offers unique information about the kidney and
its collecting system (1). With current
multidetector helical scanners, fast scan times, high spatial
resolution and thin collimation are possible, even in children who are
unable to suspend respiration. The rapid data acquisition times,
combined with short interscan delays, allow images to be obtained
during multiple phases of parenchymal enhancement after administration
of a single bolus of intravenous contrast material (2).
The high spatial resolution and thin-slice collimation enable isotropic
voxels and excellent quality three-dimensional (3D) reformations of the
renal arteries and veins and the collecting system (2). These reconstructions can potentially obviate conventional angiography and urography.
The kidneys are most commonly imaged as part of an
abdominal CT examination. However, there are various specific clinical
indications for renal CT, including evaluation of suspected renal
masses, trauma, complicated infections, obstructive uropathy,
congenital anomalies, and vascular disease. Computed tomography is not
only important in diagnosis, but it also plays a role in treatment
planning and follow-up of children with renal diseases. This chapter
reviews the techniques of renal CT in children, characteristic CT
features of common renal diseases, and pitfalls in diagnosis.
Computed Tomography Technique
The CT examination needs to be individualized for each
specific clinical indication. Decisions need to be made about the use
of intravenous contrast and oral contrast agents, the number of imaging
phases, and the timing of the examination (3,4,5). This is important to minimize radiation exposure to the patient and to ensure diagnostic quality studies.
Intravenous Contrast Agents
Intravenous contrast material improves the visualization
of abdominal and pelvic organs and identification of pathology.
However, some indications, such as nephrolithiasis, urolithiasis, and
retroperitoneal hematoma, may not require the use of intravenous
contrast agent.
Both hand and power injection techniques provide optimal
opacification if contrast administration is via a large peripheral vein
and there is an adequate flow rate. Flow rates vary with angiocatheter
size; typical flow rates are 1.5 to 2.5 mL per second for a 22-gauge
catheter and 3 to 4 mL per second for a 20-gauge catheter (see Chapter 1 for more details). The conventional dose of contrast agent is 2 mL/Kg, not to exceed 125 mL (3).
Oral Contrast Agents
Standard protocols for abdominal CT scanning usually
include oral administration of diluted iodinated contrast medium 45 to
60 minutes before the CT scan and then again immediately prior to the
initiation of the examination to ensure adequate small bowel
opacification. Failure to opacify the bowel adequately can lead to
difficulties in interpretation because unopacified bowel loops may
simulate a juxtarenal mass lesion or adenopathy. However, in some
scenarios, such as evaluation of urolithiasis or an obtunded trauma
patient, oral contrast agent may be contraindicated. In CT angiography,
in which dense oral contrast agent can degrade 3D rendering, negative
oral contrast agents, such as water or milk, may be useful to distend
the bowel.
Noncontrast CT
Noncontrast scans are obtained to evaluate urolithiasis,
detect acute hematoma, and acquire baseline attenuation measurements of
renal masses. Noncontrast CT scans are widely accepted as the primary
imaging study to identify urinary calculi.
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Phases of Renal Enhancement
There are four phases of contrast enhancement depending on the image acquisition time (6). Arterial phase imaging
is performed to evaluate arterial anatomy and pathology (such as
stenosis and thrombus). It occurs 15 to 20 seconds after the start of
contrast administration. Either a standard delay (15 to 20 seconds) or
a bolus-triggering method, triggering off the aorta at a threshold
value of 120 HU, can be used for arterial-phase imaging. In the
arterial phase of enhancement, enhancement of the cortex as well as the
arteries can be seen. Scanning is limited to the area of the kidneys.
The corticomedullary phase
is performed to evaluate renal masses, traumatic injuries, and venous
anatomy. It begins approximately 30 to 40 seconds after the start of
the contrast medium injection and continues for approximately 60
seconds. The authors use a 30 to 40 second delay to obtain
corticomedullary phase images of the kidney. In this phase, the cortex
enhances intensely while the medulla remains relatively less enhanced.
The extent of scanning (i.e. the kidney alone or the entire abdomen and
pelvis) depends on the clinical indication for the examination.
The nephrographic phase is
optimal for the evaluation of the renal parenchyma (especially small or
subtle abnormalities such as nephrogenic rests, small cysts, and
pyelonephritis) and for detection of focal masses arising in the cortex
or medulla. This phase begins 75 to 100 seconds after the start of
contrast medium injection. The authors use a 75 to 90 second delay
(shorter scan times for smaller patients) to obtain nephrographic phase
images of the kidney. In the nephrographic phase, the renal cortex and
medulla enhance uniformly and the contrast medium has not yet been
excreted into the renal collecting system. The extent of scanning (i.e,
the kidney alone or the entire abdomen and pelvis) depends on the
clinical indication for the examination.
The excretory or urographic phase
is used to evaluate the renal collecting system and ureters. It begins
3 to 5 minutes after the start of the contrast medium injection. The
authors use a 5 to 10 minute delay to obtain nephrographic phase images
of the kidney. In this phase, the density of the nephrogram decreases
and contrast excreted from the renal tubules begins to fill the
pelvises, calyces and ureters. Scanning extends from the kidneys
through the pelvis to evaluate the ureters and bladder.
While each phase of enhancement contributes different
types of information, the value of multiple acquisitions needs to be
balanced against the potential deleterious effects of the radiation
exposure. The approach for scanning needs to be tailored for each
patient, so the abdomen and pelvis are scanned only once or at the most
twice. The choice of enhancement phase varies with the clinical
indication for the CT examination.
Technical Factors
Slice collimation and pitch vary with detector
technology and the size of the structure of interest. For a 16-row
detector, 0.75- to 1.5-mm collimation with a pitch of 1 to 1.5
suffices. For a 64-row detector, 0.6- to 1.25-mm collimation and a
pitch of 1 to 1.5 suffice. Thinner collimation is used to improve
visualization of small renal lesions, vessels, and ureters. A 3- to
5-mm section thickness is usually adequate for routine viewing of the
volumetric data. Thin (1- to 2-mm) reconstructions are used if
multiplanar and 3D reconstructions are needed. (See Chapter 1 for more detailed discussion of techniques.)
Most diagnoses can be made from review of the axial
image set. Multiplanar reformations can be useful for demonstrating the
craniocaudal extent of neoplasm, inflammatory lesions, or traumatic
abnormalities. 3D reconstructions, particularly thick slab
maximum-intensity projections and volume rendering, are most useful for
evaluation of vessels (CT angiography) and ureters (CT urography) (Fig. 9.1).
Normal Anatomy
Despite the relative paucity of perirenal fat in
children, the cross-sectional anatomy of the normal kidneys is readily
recognizable on CT scans. The kidneys lie in the retroperitoneum in a
slightly oblique position, with the lower poles sloping laterally and
anteriorly to the upper poles. Slight rotation around the long axis is
also present so that the vascular pedicle is directed anteromedially.
The left kidney is often located slightly more cranial than the right
kidney. On nonenhanced CT images, the renal parenchyma is of
homogeneous soft tissue attenuation, usually measuring between 30 and
60 Hounsfield units (HU). The renal sinus is usually directed
anteriorly and medially, representing an extension of the perinephric
space centrally enclosed by the renal parenchyma. It contains fat,
linear fluid-attenuation renal vessels, and the water-attenuation
collecting system (8). The cortex, medulla, and calyces usually cannot be distinguished without contrast administration.
Renal volume can be calculated by using the region of
interest cursor to obtain a cross-sectional area on each image slice,
multiplying this calculation by the thickness of the slice to obtain
the slice volume, and then adding the volumes of the individual slices.
Normative renal growth curves have been described (9).
The appearance of the kidneys varies with the phase of renal enhancement (6).
In the arterial phase (15 to 20 seconds after start of the contrast
medium injection), there is maximum enhancement of the renal arteries (Fig. 9.2A). The cortex also enhances, with attenuation values approaching 70 HU. In the corticomedullary
phase (30 to 60 seconds), there is maximum enhancement of the cortex, owing to preferential glomerular filtration of the contrast material. Cortical attenuation may reach 140 HU. The attenuation of the medulla also increases, but it is <60 HU (Fig. 9.2B). The renal veins show maximum opacification in this phase. In the nephrogram phase (80 to 120 seconds), cortical and medullary enhancement are similar owing to tubular filtration of contrast material. Parenchymal attenuation is 80 to 120 HU (Fig. 9.2C). In the excretory phase (3 to 4 minutes after injection), the medulla is brighter than the cortex and contrast material opacifies the collecting system and ureters (6).
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phase (30 to 60 seconds), there is maximum enhancement of the cortex, owing to preferential glomerular filtration of the contrast material. Cortical attenuation may reach 140 HU. The attenuation of the medulla also increases, but it is <60 HU (Fig. 9.2B). The renal veins show maximum opacification in this phase. In the nephrogram phase (80 to 120 seconds), cortical and medullary enhancement are similar owing to tubular filtration of contrast material. Parenchymal attenuation is 80 to 120 HU (Fig. 9.2C). In the excretory phase (3 to 4 minutes after injection), the medulla is brighter than the cortex and contrast material opacifies the collecting system and ureters (6).
 |
Figure 9.1. 3D Reconstructed images. A: CT angiogram. Axial volume-rendered image shows normal caliber renal arteries bilaterally (arrows). B:
CT urography. Coronal volume-rendered image shows a dilated left renal
pelvis with a normal caliber ureter consistent with congenital
ureteropelvic junction obstruction. (See color insert.) |
 |
Figure 9.2. Contrast enhancement patterns. A:
Arterial phase (15 seconds after start of contrast injection). The
cortex is enhanced, while the medulla is unenhanced. There is good
opacification of the renal arteries. B:
Corticomedullary phase in another patient (50 seconds after start of
contrast injection). There is marked enhancement of the cortex, while
the medulla remains relatively less enhanced. The renal veins are well
opacified at this time. The renal arteries no longer enhance. C: Nephrographic phase, same patient as in B
(approximately 100 seconds after start of contrast injection). The
cortex and medulla have similar attenuation, so that the parenchyma
appears homogeneous. |
The renal margins are usually smooth, except in areas of
renicular fusion (see discussion below on cortical lobulations). The
renal capsule and the underlying parenchyma cannot be distinguished on
CT. The layers of the perirenal fascia may be visualized separately
from the renal capsule. The fascia appears as a soft tissue–
attenuation structure surrounding the kidneys (10).
The anterior renal fascia usually appears as a thin line between the
kidney and the pancreas. It is more often seen on the left than on the
right. The posterior renal fascia is multilayered and is commonly seen
bilaterally. The fascia is particularly easy to see when it is
infiltrated by fluid.
The renal arteries, which arise from the aorta below the
origin of the superior mesenteric artery, course anterior and medial to
the kidney (Fig. 9.2A). At the renal hila, the
arteries typically divide to form dorsal and ventral branches. The
longer left renal vein passes anteriorly to the aorta to reach the
inferior vena cava. The shorter right renal vein courses superiorly and
obliquely to reach the vena cava (Fig. 9.2B).
Normal Variants
Variations in renal morphology and position occur during
normal fetal development; these need to be recognized to avoid
mistaking them for pathology. Two common anatomic variations are fetal
lobulations and enlarged columns of Bertin. The normal kidney is formed
by the fusion of multiple embryonic renunculi or lobes. Each lobe
consists of a medullary pyramid and its surrounding cortex. Eventually,
the lobes fuse forming a single kidney with irregular lobulated
margins, referred to as fetal lobulations. During late fetal
development, the lobulations usually regress and the renal contour
becomes smoother. Occasionally, these fetal lobulations persist into
postnatal life, appearing on CT as cortical indentations (Fig. 9.3).
Fetal lobulations should not be mistaken for renal scarring. The latter
is associated with parenchymal thinning; the former is not associated
with parenchymal loss.
The column of Bertin refers to a thickened appearance of the renal cortex, again occurring at the site of renuncular fusion (11).
This prominent area of cortex may simulate a mass, particularly on
sonography, but it can be distinguished from a pathologic mass on
contrast-enhanced CT. The column of Bertin extends from the renal
cortex into the renal sinus, is located between two renal sinuses, and
has attenuation similar to that of normal renal parenchyma on both
precontrast and postcontrast CT scans (Fig. 9.4). The absence of renal contour
abnormality is a useful feature in differentiating a hypertrophied column of Bertin from a true mass.
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abnormality is a useful feature in differentiating a hypertrophied column of Bertin from a true mass.
 |
Figure 9.3. Fetal lobulations. Cortical indentations (arrows) between renal lobes represent fetal lobulations. |
 |
Figure 9.4. Column of Bertin. Axial image during the corticomedullary phase reveals a prominent area of renal cortex (arrow) extending toward the renal sinus. The attenuation of the column of Bertin is the same as that of the normal cortex. |
Congenital Anomalies
Congenital anomalies can be classified as abnormalities
in number (renal agenesis), position (ptosis or ectopia), and fusion
(horseshoe kidney, renal duplication) (12).
Generally most renal anomalies can be well evaluated by sonography, and
CT is not needed for diagnosis. However, they can be found incidentally
on studies performed for other clinical indications, and thus, they
need to be recognized. They are usually easily identified on
contrast-enhanced CT by their tissue enhancement and excretion
patterns, which are identical to those of normal kidney.
Renal Agenesis and Hypoplasia
A solitary kidney may reflect renal agenesis, renal
aplasia, or spontaneous involution of a multicystic dysplastic kidney.
Renal agenesis is complete failure of the kidney to form, whereas renal
aplasia refers to the presence of a small, nonfunctioning mass of
undifferentiated or poorly differentiated tissue that may involute (13).
Both abnormalities are rare, and bilateral involvement is lethal. CT
findings of renal agenesis are an empty renal fossa, compensatory
hypertrophy of the contralateral kidney, and adjacent organ
displacement (Fig. 9.5). On the right, the
proximal small bowel, hepatic flexure, liver, or pancreatic head may
fill the empty renal fossa. On the left, small bowel loops, the splenic
flexure, or the pancreatic tail fill the corresponding space. Other CT
findings seen in renal agenesis and renal aplasia include thin
elongated adrenal glands, absence of the ipsilateral renal artery and
vein, inferior vena caval anomalies (13),
anomalous drainage of the left adrenal vein into the inferior vena
cava, and genital anomalies, including absence of the seminal vesicles
or vas deferens, seminal vesicle cysts, Gartner duct cysts (14), undescended testes, uterine and/or vaginal duplication, and imperforate vagina with secondary hydrometrocolpos.
 |
Figure 9.5. Renal agenesis. The empty right renal fossa is occupied by air-filled bowel loops (arrow). |
Renal Ectopia
Simple Ectopia
Renal ectopia, or abnormal location of the kidney, may
be simple or crossed. In simple ectopia, the kidneys and ureter are on
their expected sides of the spine. The simple ectopic kidney is most
commonly located in the pelvis. The ectopic pelvic kidney is often
malrotated, and the renal pelvis is positioned near the surface of the
kidney, not in the deeper parenchyma, as occurs in the normal kidney (Fig. 9.6). The ureters are typically short.
Crossed Fused Ectopia
In crossed ectopia, both kidneys are located on the same
side of the spine. The crossed ectopic kidney is smaller than the
orthotopic kidney and malrotated, and it usually lies caudal to the
orthotopic kidney. The upper pole of the ectopic kidney is usually
fused to the lower pole of the orthotopic unit. The ureter draining the
ectopic kidney enters the bladder at the contralateral trigone, whereas
the ureter of the orthotopic component enters the ipsilateral trigone.
Horseshoe Kidney
Horseshoe kidney is a common anomaly with an incidence of 0.2% to 0.25% (12).
The lower poles of the kidneys are usually fused and connect by an
isthmus that may contain functioning parenchyma or fibrous tissue. The
ureters descend from anteriorly positioned renal pelves. The arterial
supply is from either the lower aorta or from the common iliac
arteries. Other genitourinary abnormalities associated with horseshoe
kidney include ureteropelvic junction obstruction, duplicated
collecting system, vesicoureteral reflux, and renal dysplasia.
Horseshoe kidney also is associated with increased risk of infection,
stone formation, Wilms tumor, and renal cell carcinoma. On CT, the
kidneys and isthmus enhance after administration of intravenous
contrast agent (Fig. 9.7).
Duplication Anomalies
Duplication of the renal collecting system is another common renal anomaly (15,16). Partial duplication anomalies are more common than complete duplications. The
spectrum of partial or incomplete duplication ranges from a bifid renal pelvis to duplicated proximal ureters with the two ureters fusing somewhere along their course, producing a single common ureter distally. In complete duplication, the kidney has two pelvicalyceal systems and two ureters that enter the bladder through separate orifices (16). The ureter from the lower pole collecting system is normally located in the trigone. The ureter from the upper pole moiety can have a normal or ectopic site of insertion and often is obstructed (see Ureteral Duplication below).
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spectrum of partial or incomplete duplication ranges from a bifid renal pelvis to duplicated proximal ureters with the two ureters fusing somewhere along their course, producing a single common ureter distally. In complete duplication, the kidney has two pelvicalyceal systems and two ureters that enter the bladder through separate orifices (16). The ureter from the lower pole collecting system is normally located in the trigone. The ureter from the upper pole moiety can have a normal or ectopic site of insertion and often is obstructed (see Ureteral Duplication below).
 |
Figure 9.6. Pelvic kidney. A: CT scan through the upper abdomen shows absence of the left kidney. Small bowel loops occupy the empty renal fossa. B: Coronal multiplanar reformation shows the malrotated left pelvic kidney. The feeding artery and draining vein (arrows) arose from the left common iliac vessels. |
 |
Figure 9.7. Horseshoe kidney. Axial CT scan (A) and coronal multiplanar reformation (B) demonstrate fusion of the lower renal poles and the isthmus (arrow) of renal parenchyma extending across the midline. There is a large neuroblastoma anterior to the horseshoe kidney (arrowheads). |
Renal Cystic Disease
A wide variety of diseases and syndromes are associated
with renal cysts or a cystic appearance. Accurate diagnosis often
requires clinical, radiologic, genetic, and pathologic correlation.
Common abnormalities include autosomal dominant or recessive polycystic
disease, simple cysts, calyceal diverticula, multicystic dysplastic
kidney, tuberous sclerosis, and cystic neoplasms. Important
considerations that help in diagnosis are location of the cysts (e.g.,
whether cortical or medullary), extent of involvement (unilateral or
bilateral), and associated abnormalities (17,18,19).
Unilateral Cystic Disease
Simple Cysts
Simple cysts are rare in children, with an incidence of <1% (19,20).
Pathologically, they are unilocular masses lined by a single layer of
flattened epithelium and containing clear serous fluid. Simple cysts
arise in the renal cortex, do not communicate with the collecting
system, and are more often solitary than multiple. They are usually
asymptomatic and detected during CT examinations performed for other
indications. Diagnostic CT findings include sharply marginated
contours, smooth round shape, homogeneous near-water-attenuation
(<20 HU) contents, imperceptible walls, and no enhancement following
intravenous contrast medium administration (Fig. 9.8).
Bleeding or infection can increase the attenuation of the fluid
contents or the wall thickness. Hyperdense cysts have attenuation
greater than the adjacent renal parenchyma on unenhanced CT, commonly
measuring 40 to 90 HU. Some hemorrhagic cysts may show a fluid–fluid or
fluid–debris level. Rarely, renal carcinomas may appear as a hyperdense
cyst.
Bosniak has described a classification scheme for
complex cystic renal masses that can be useful in diagnosis and
clarifying the risk of malignancy (21,22).
A Bosniak type I lesion meets criteria of a simple cyst. A type II cyst
has thin septations, calcifications, or a central location. A type III
Bosniak cyst contains thicker calcifications or thicker septations and
may show a small amount of rim enhancement. A type IV Bosniak cyst has
thick walls, thick septations, and/or calcifications and shows
enhancement of solid contents in the lesion. The risk of malignancy
increases with increasing Bosniak classification.
 |
Figure 9.8.
Simple cyst. Contrast-enhanced CT scan shows a round, homogeneous,
water-attenuation cyst (C) in the upper pole of the right kidney. |
Calyceal diverticula need to be distinguished from
simple cysts. Diverticula are cystic spaces that are lined by
transitional epithelium and communicate with the collecting system
through a narrow orifice. On noncontrast CT, they are usually of water
attenuation, although they may show a higher density if they contain
calculi or milk of calcium. Most diverticula demonstrate some filling
with contrast on excretory-phase CT images, allowing a correct
diagnosis (23,24).
Multicystic Dysplastic Kidney
Multicystic dysplastic kidney is characterized by a
cluster of noncommunicating cysts, nonfunctioning parenchymal tissue
containing primitive dysplastic elements, and an atretic ureter.
Usually diagnosed in neonates or young infants, it presents as a large
mass on prenatal sonography or a palpable mass on postnatal physical
examination. Most dysplastic kidneys regress or involute completely by
early childhood. Rarely, involution is incomplete, leaving a residual
cystic remnant, which usually is asymptomatic and detected incidentally
during an examination performed for other clinical indications (19,25,26,27). CT findings include a uniloculated or multiloculated cystic mass with no discernible normal parenchyma and no contrast
excretion (Fig. 9.9). Calcifications may be noted in the cyst walls or in the septations between cysts (Fig. 9.9B) (19). The contralateral kidney usually shows compensatory hypertrophy and may have vesicoureteral reflux, ureteropelvic or ureterovesical junction obstruction (26,27).
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excretion (Fig. 9.9). Calcifications may be noted in the cyst walls or in the septations between cysts (Fig. 9.9B) (19). The contralateral kidney usually shows compensatory hypertrophy and may have vesicoureteral reflux, ureteropelvic or ureterovesical junction obstruction (26,27).
 |
Figure 9.9. Multicystic dysplastic kidney. Two patients. A: Arterial-phase contrast-enhanced CT scan reveals a multiloculated cystic mass (arrows) with no identifiable parenchyma and no contrast enhancement in the left renal fossa. The right kidney excretes normally. B: Enhanced CT scan in another patient shows a cystic structure with a calcified rim (arrow), representing the atrophied dysplastic right kidney. |
Multilocular Cystic Renal Tumor
Multilocular cystic renal tumor, previously called
multilocular cystic nephroma, benign cystic nephroma, cystic hamartoma,
cystic Wilms tumor, cystic lymphangioma, and partially polycystic
kidney, is a nonhereditary cystic mass. It has a biphasic age and sex
distribution, affecting boys younger than 4 years of age and women
older than 40 years of age. Characteristic pathologic findings are an
encapsulated mass containing multiple noncommunicating epithelial-lined
cysts separated by fibrous septa. Histologically, there are two types:
cystic nephroma, characterized by mature septal elements, and cystic
partially differentiated nephroblastoma, which contains immature septal
elements (blastemal cells) (28). Foci of Wilms may be found in the septa or cyst wall (29,30,31).
Patients usually present with a palpable abdominal mass or hematuria,
which results from herniation of a portion of the tumor into the renal
pelvis.
 |
Figure 9.10. Multilocular cystic renal tumor. A, B: Contrast-enhanced CT scans in two patients show low-attenuation masses with thin septations. |
On CT, both forms of multilocular cystic renal tumor appear as a well-circumscribed, intrarenal mass containing
multiple fluid locules and interspersed septa (28,29,31). The cystic spaces have attenuation equal to water or slightly higher than that of water and do not enhance after administration of contrast medium (Fig. 9.10). The septa are usually thin and may show minimal enhancement. Septal or wall calcification also can occur. Thickened, nodular or intensely enhancing septa or walls should raise a suspicion of malignancy (e.g., Wilms tumor) (31,32,33). Most multilocular cystic nephromas are successfully treated by nephrectomy alone.
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multiple fluid locules and interspersed septa (28,29,31). The cystic spaces have attenuation equal to water or slightly higher than that of water and do not enhance after administration of contrast medium (Fig. 9.10). The septa are usually thin and may show minimal enhancement. Septal or wall calcification also can occur. Thickened, nodular or intensely enhancing septa or walls should raise a suspicion of malignancy (e.g., Wilms tumor) (31,32,33). Most multilocular cystic nephromas are successfully treated by nephrectomy alone.
Bilateral Cystic Disease
Polycystic renal disease can be classified into autosomal recessive and autosomal dominant types (34).
The former disease was previously known as infantile polycystic kidney
disease and the latter as adult polycystic renal disease. In both forms
of polycystic disease, sonography usually suffices for diagnosis, but
CT may be used to assess complications.
Autosomal Recessive Polycystic Disease
Autosomal recessive polycystic disease, as the name
implies, is inherited as a recessive characteristic. Pathologic
sections have shown numerous small cysts, 1 to 2 mm in diameter, in
both the cortex and medulla. Microdissection and high-resolution
sonography have shown that the cysts are actually fusiform dilatations
of the interstitial portions of the collecting tubules; the nephrons
are normal or minimally altered (35). Virtually
all patients with autosomal recessive cystic disease have hepatic
abnormalities, characterized by biliary ductal ectasia and periportal
fibrosis. The clinical features of autosomal recessive polycystic
disease are dependent on patient age at time of presentation (36).
Infants tend to have more severe renal disease and milder hepatic
disease. Patients who survive the neonatal period and come to clinical
attention later in life have milder renal disease and more severe
hepatic disease (usually portal hypertension). The disease also may be
diagnosed in utero, manifesting as renal enlargement and
oligohydramnios.
 |
Figure 9.11. Autosomal recessive polycystic disease. A: Neonate. Contrast-enhanced CT shows bilateral renal enlargement and tubular opacification, creating a striated appearance. B:
Adolescent. Contrast-enhanced CT scan shows multiple small renal cysts,
representing ectatic tubules, in the upper pole of the right kidney (arrow)
and dilated intrahepatic bile ducts. Note also splenomegaly (S) and
hypertrophy of the left hepatic lobe, related to hepatic fibrosis and
cirrhosis. (Part A courtesy of Peter Choyke, MD.) |
On CT, a spectrum of abnormality also exists with the
relative amounts of renal and hepatic involvement varying inversely. In
neonates, the kidneys are large and demonstrate a prolonged nephrogram
phase. Delayed scans show excretion into the dilated collecting
tubules, causing a striated appearance, which persists for several
hours (Fig. 9.11A) (36).
Dilated bile ducts may also be seen. In older children and adolescents,
renal size is often normal, although excretion may still be delayed.
Medullary cysts and bile duct ectasia may be seen (Fig. 9.11B). Manifes-tations of portal hypertension, such as irregular hepatic margins, splenomegaly, and esophageal varices, also occur.
Autosomal Dominant Polycystic Disease
Autosomal dominant polycystic disease is another
hereditary renal cystic disorder. It has been associated with at least
two genetic loci: the PKD1 locus mapped to chromosome 16 and the PDK2
locus on chromosome 4 (37). Pathologically,
multiple cysts of varying size are present in the cortex and medulla
with islands of normal parenchyma interspersed between the cystic
areas. The
cysts communicate with the nephrons as well as the collecting tubules. Autosomal dominant polycystic disease usually becomes apparent in the fourth or fifth decade of life when hypertension or hematuria develops. Rarely, it presents in the neonate as abdominal masses or in older children as hematuria, flank pain or urinary tract infection. The diagnosis also may be made at screening sonography of the offspring of an affected individual.
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cysts communicate with the nephrons as well as the collecting tubules. Autosomal dominant polycystic disease usually becomes apparent in the fourth or fifth decade of life when hypertension or hematuria develops. Rarely, it presents in the neonate as abdominal masses or in older children as hematuria, flank pain or urinary tract infection. The diagnosis also may be made at screening sonography of the offspring of an affected individual.
 |
Figure 9.12. Autosomal dominant polycystic disease in a 6-year-old boy A, B:
Two contrast-enhanced CT scans performed for hematuria and a palpable
abdominal mass demonstrate multiple low-attenuation cysts in both
kidneys. The cysts are of varying size and more extensive in the lower
pole of the right kidney. |
CT may be performed if there is clinical concern for complications, such as stone, infection, or mass (19).
Characteristic CT findings include multiple cysts of varying size
throughout the cortex and medulla. The renal margins may be smooth or
lobulated. Renal size may be normal or enlarged. Bilateral involvement
is usual, and the disease can be asymmetric (Fig. 9.12).
High-attenuation cysts may be seen, resulting from hemorrhage. Cysts
are found not only in the kidney but also in the liver, spleen, and
pancreas (19).
Localized cystic disease, also known as segmental cystic
disease, is a nonhereditary cystic lesion characterized by a
conglomeration of nonenhancing simple cysts separated by normal or
atrophic renal tissue without a capsule (38). It is unilateral and segmental.
Other Congenital or Hereditary Cystic Diseases
Uremic medullary cystic disease (juvenile
nephronophthisis) is a familial disorder inherited as an autosomal
recessive or dominant trait. Patients present in adolescence with renal
failure, polyuria, polydipsia, salt wasting, and anemia.
Pathologically, the kidneys are small and contain multiple cysts in a
medullary distribution. Although CT can demonstrate the cystic changes,
sonography usually suffices for diagnosis (19).
Tuberous sclerosis is an autosomal dominant hereditary disorder associated with abnormalities of chromosomes 9 and 16 (39).
Classic clinical features result from cerebral, cutaneous, and visceral
hamartomas and include seizures, mental retardation, and cutaneous
lesions. Renal lesions include cysts, angiomyolipomas, and rarely,
renal cell carcinoma (39,40,41). Both cysts and angiomyolipomas become more evident with advancing patient age (39).
The renal cysts can vary in number and may be unilateral or bilateral.
Occasionally, numerous cysts may be present, mimicking autosomal
dominant polycystic disease (Fig. 9.13).
 |
Figure 9.13.
Tuberous sclerosis in a 2-year-old girl. Contrast-enhanced CT scan
shows cysts of varying sizes in both kidneys, with more extensive
involvement on the right than the left. This appearance is
indistinguishable from that seen in autosomal dominant polycystic and
von Hippel–Lindau diseases. |
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Von Hippel–Lindau disease is an autosomal dominant
hereditary disorder associated with various malignant and benign
neoplasms, most frequently retinal, cerebellar, and spinal
hemangioblastomas; renal cell carcinoma; pheochromocytoma; and
pancreatic tu-mors. Renal cysts may be seen in Von Hippel–Lindau
disease (42). CT findings are similar to those
seen in autosomal dominant polycystic disease and tuberous sclerosis;
correlation with family history and clinical findings usually permit
the correct diagnosis to be established.
Acquired Renal Cystic Disease
Acquired cystic disease of the kidney occurs in patients
on chronic hemodialysis or peritoneal dialysis. The incidence increases
with the years on dialysis, and it has been reported to be as high as
80% after the third year (6). Microdissection
studies show hyperplasia of tubular epithelium, leading to blockage and
dilatation of nephrons. It is these dilated nephrons that are the cysts
of acquired renal cystic disease. Early in the disease process, the
kidneys are small and smooth with only a few cysts, which are
completely intrarenal. As the length of dialysis increases, the kidneys
become larger and the cysts increase in number and size (43). Eventually, the kidneys may have an appearance simulating autosomal dominant polycystic disease (Fig. 9.14).
Complications include hemorrhage into the cysts or into the subcapsular
or perinephric areas and an increased incidence of renal carcinoma.
Calcification of the cyst walls can occur after many years of dialysis.
 |
Figure 9.14. Acquired cystic disease. Numerous cysts are seen on unenhanced CT scans of a patient who has been on chronic hemodialysis. |
Obstructive Uropathy
Although not required for the diagnosis of
hydronephrosis, CT can be useful if sonography fails to define the
level and cause of renal obstruction. CT also may be requested to
evaluate ureteral-vascular relationships for operative planning and
complications of obstruction. Common causes of obstruction include
ureteropelvic junction and ureterovesical obstruction, renal
duplication with an obstructed upper moiety, and posterior urethral
valves.
The dilated collecting system is easily detected by CT,
appearing as a fluid-filled structure with an attenuation value close
to that of water. The appearance of the kidney after administration of
intravenous contrast medium varies with the degree of obstruction and
the amount of functioning residual renal parenchyma. With mild or
moderate obstructive uropathy, contrast-enhanced CT scans show delayed
function and excretion into a dilated collecting system with a
urine-contrast level; with severe obstruction, excretion may be absent
or minimal.
Ureteropelvic Junction Obstruction
Ureteropelvic junction obstruction is a term that refers
to obstruction of urine flow at the level of the renal pelvis and
ureter. It may be the result of an anatomic abnormality, such as
intrinsic stenosis or extrinsic compression from a band, adhesion or
aberrant vessel, or it may be functional owing to abnormally developed
muscle fibers at the ureteropelvic junction. Usually the diagnosis is
made on in utero sonography. However, patients may present with a
palpable abdominal mass or with complications of obstruction, including
flank pain (often intermittent), hematuria, and urinary tract
infection. CT findings include a dilated upper collecting system, a
normal-size ureter, and parenchymal thinning (44,45) (Fig. 9.15).
Characteristically, the renal pelvis dilates more than the calyces.
Rarely there may be massive hydronephrosis, which may simulate a cystic
renal neoplasm (46).
A dismembered pyeloplasty, in which the redundant renal
pelvis is trimmed and reinserted into the ureter, usually is the
treatment of choice for repair of ureteropelvic junction obstruction.
In some adolescent patients, endopyelotomy has replaced the
pyeloplasty. Endouro-logic repair is associated with an increased risk
of vascular complications because of the blind incision into the
periureteral tissues. CT angiography can depict crossing vessels at the
ureteropelvic junction and their relationship to the site of ureteral
obstruction, aiding in planning surgical management (44,45).
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 |
Figure 9.15. Ureteropelvic junction obstruction. A: Nephrographic phase scan demonstrates a dilated urine-filled left renal pelvis (RP) and calyces (arrows) along with cortical thinning. B:
Coronal CT scan in another patient during the excretory phase shows no
opacification of the dilated left renal pelvis (RP). The right kidney
shows normal excretion. |
A large extrarenal pelvis needs to be differentiated
from ureteropelvic junction obstruction. CT findings of an extrarenal
pelvis are symmetric contrast excretion bilaterally, normal parenchymal
thickness, and absence of calyceal dilatation (Fig. 9.16).
With obstructive uropathy, there is dilatation of the renal collecting
system, delayed excretion, and on occasion parenchymal loss (Fig. 9.15).
 |
Figure 9.16. Extrarenal pelvis. Contrast-enhanced CT scan shows a prominent left renal pelvis (arrow). Absence of calyceal dilatation, preserved cortical thickness, and symmetric contrast excretion exclude obstructive uropathy. |
Megaureter
Megaureter refers to ureteral dilatation. Ureteral
dilatation can be due to an anatomic obstruction (distal ureteral
stenosis or valves), functional obstruction (dysfunctional muscle),
reflux, or high volumes of urine flow associated with diabetes
insipidus. Characteristic CT findings are a dilated intrarenal
collecting system and ureter (Fig. 9.17). There may be disproportionate dilatation of the lower ureter with respect to the upper ureter and renal pelvis.
Ureteral Duplication
As noted above, ureteral duplication can be partial or
complete. The latter is more likely to be obstructed. In complete
ureteropelvic duplication, the kidney has two pelvicalyceal systems and
two ureters with separate insertions. The ureteral orifice of the upper
pole moiety is ectopic, lying medial and inferior to the orifice of the
ureter draining the lower pole segment (Weigert–Meyer rule); it usually
is the obstructed system. The obstructed upper pole system may insert
ectopically into the bladder base (ectopic ureterocele) or into the
vestibule, vagina, or urethra in girls
and into the posterior urethra, epididymis, or the seminal vesicles in boys. The ureter from the lower pole moiety inserts into the trigone, but it has an oblique course predisposing to reflux. The diagnosis is usually made by in utero sonography. Patients may also present later in life with signs of urinary tract infection. Girls also can present with incontinence if the ureter inserts below the external sphincter (47).
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and into the posterior urethra, epididymis, or the seminal vesicles in boys. The ureter from the lower pole moiety inserts into the trigone, but it has an oblique course predisposing to reflux. The diagnosis is usually made by in utero sonography. Patients may also present later in life with signs of urinary tract infection. Girls also can present with incontinence if the ureter inserts below the external sphincter (47).
 |
Figure 9.17. Ureterovesical junction obstruction. A: Contrast-enhanced CT scan demonstrates mild hydronephrosis of the left collecting system. B: A more caudal scan shows a dilated proximal ureter (arrow). C: CT scan through the bony pelvis shows the dilated ureter (arrow) coursing posterolateral to the bladder (B). |
The CT features of an obstructed ureteral duplication
include a hydronephrotic upper pole moiety, a normal or mildly dilated
lower pole moiety, parenchymal loss in the upper pole, and two separate
ureters. Rarely, the ob-structed upper pole moiety is small and
atrophic rather than dilated. Delayed images after administration of
intravenous contrast medium may help to demonstrate a dysplastic
component. A ureterocele, if present, is seen as a round, thin-walled,
urine- or contrast-filled mass at the bladder base (Fig. 9.18). Occasionally, the ureterocele obstructs the contralateral ureter, causing it to dilate.
Posterior Urethral Valves
Posterior urethral valves are the most common cause of
urethral obstruction in boys. Pathologically, urethral valves are folds
of embryonic tissue; they may or may not have a small aperture. The
disease usually presents in the neonatal period or early infancy with
signs of obstruction, although it can present in later childhood when
infection, voiding abnormalities, or failure to thrive occurs. The
characteristic CT appearance is: bilateral hydronephrosis and
hydroureter, parenchymal thinning, a thickened bladder wall, and
posterior urethral dilatation (Fig. 9.19). Associated findings include urinary ascites and subcapsular or perirenal urinomas, resulting from forniceal rupture.
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 |
Figure 9.18.
Ectopic ureterocele. The contrast-filled ureterocele (U) occupies the
base of the bladder (BL). The low-attenuation rim represents the wall
of the ureter. This patient had a duplicated left kidney with an
obstructed upper pole moiety. |
Retrocaval Ureter
The infrarenal vena cava arises from the supracardinal
vein, which lies posterior to the ureter. In some individuals, however,
the infrarenal segment of the vena cava arises from either the
postcardinal or right subcardinal veins, both of which lie anterior to
the ureter. The retrocaval ureter may be clinically silent or produce
symptoms related to ureteral obstruction. On CT, the retrocaval ureter
lies posterior and medial to the inferior vena cava. Other findings
include hydronephrosis, proximal ureteral dilatation, and a normal
caliber distal ureter.
 |
Figure 9.19. Posterior urethral valves in a 3-month-old boy. CT was performed to rule out a retroperitoneal abscess. A: Contrast-enhanced CT scan shows bilaterally dilated calyces (C), a dilated right ureter (arrowheads), and ascites. B: A scan through the pelvis demonstrates a thick bladder wall, bilateral ureterectasis (arrowheads), and a large amount of ascites. Air in the bladder is secondary to catheterization. Arrow, catheter in bladder. |
Acquired Obstruction
Acquired causes of obstruction include calculi (Fig. 9.20),
inflammatory masses, usually owing to appendicitis or Crohn disease,
and retroperitoneal or pelvic tumors. CT can be useful to demonstrate
the cause and level of obstruction.
Renal Masses
Sonography remains the initial imaging modality of
choice for evaluation of a suspected renal or abdominal mass. If
sonography shows a solid or complex renal mass, cross-sectional imaging
with CT can be performed for better characterization, determination of
tumor extent, and delineation of the relationship of the tumor to the
pelvicalyceal system, ureters, adjacent organs, renal vein, and
inferior vena cava (48). CT is useful to
identify the presence of contralateral tumors and to detect metastases
to regional lymph nodes, liver, or lung. Scans are usually obtained
during the corticomedullary or very early nephrographic phase of
contrast enhancement. For some relatively small renal lesions where
partial nephrectomy is a treatment option, later nephrographic phase
imaging may increase detection of medullary lesions (49). Multiplanar and 3D reconstructions are useful to demonstrate
the craniocaudal extent of tumor and may help in planning nephron-sparing surgery.
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the craniocaudal extent of tumor and may help in planning nephron-sparing surgery.
 |
Figure 9.20. Ureteral calculus. Unenhanced axial CT scan (A) and coronal multiplanar reformation (B) show a calcification (arrows) in the proximal right ureter and hydronephrosis. |
Malignant Tumors
Wilms Tumor
Wilms tumor is one of the most common childhood
abdominal tumors and the most common renal malignancy. Affected
children are usually younger than 5 years of age (mean age, 3 years) (31,32,50,51). Rarely, Wilms tumor is encountered prenatally or in the neonatal period (52).
Most children present with a palpable mass and less frequently with
abdominal pain, fever, or microscopic or gross hematuria. Rare
manifestations are pulmonary emboli (53) and varicocele, which occurs when the tumor obstructs the left gonadal vein (54).
Syndromes with increased incidence of Wilms tumor
include overgrowth syndromes (Beckwith–Wiedemann syndrome and
congenital hemihypertrophy), WAGR syndrome (Wilms tumor, sporadic
aniridia, genital malformations, and retardation), Drash syndrome (male
pseudohermaphroditism and nephritis) and Perlman syndrome (fetal
gigantism, hypotonia with multiple congenital abnormalities) (51,55).
Other associated genitourinary tract anomalies with increased incidence
of Wilms include renal ectopia, ureteral duplication, renal hypoplasia,
cryptorchidism, and horseshoe kidney (56).
On gross examination, Wilms tumor is a bulky mass that replaces most of the involved kidney (57).
It arises within the cortex and grows in an exophytic fashion, with the
bulk of the tumor protruding from the kidney. The tumor is surrounded
by a rim of compressed renal tissue, termed a pseudocapsule, and often
contains foci of necrosis or hemorrhage.
On microscopic examination, Wilms tumor is classified as
having favorable or unfavorable histology. Approximately 85% of Wilms
tumors have favorable triphasic histology, containing primitive
blastema, stroma, and epithelial elements. Patients with favorable
histology have an excellent prognosis and an overall survival rate
approaching 90%. The 15% of Wilms tumor with unfavorable histology have
anaplastic or sarcomatous elements. Anaplasia is characterized by
large, hyperchromatic nuclei and increased mitoses, is associated with
high resistance to chemotherapy and poor prognosis with survival rates
of only 20% to 30% (58).
Imaging Features of the Primary Tumor
On unenhanced CT scans, Wilms tumor characteristically
appears as a large (mean diameter 11 cm), spherical, at least partially
intrarenal mass, with an attenuation value slightly lower than that of
surrounding normal renal parenchyma. Following contrast administration,
the tumor enhances less than the surrounding normal parenchyma (Fig. 9.21).
Most tumors (approximately 80% of cases) are heterogeneous with
low-attenuation areas representing necrosis, hemorrhage, or cystic
degeneration (31,50,59,60).
Fewer than 15% of Wilms tumors contain calcification or fat, generally as a minor component (Fig. 9.22) (61,62). Fatty components can be seen within the rare teratoid Wilms tumor, which has features of both teratoma and Wilms (62).
Approximately 10% of kidneys with Wilms tumors show poor or absent
contrast excretion, resulting from invasion or compression of the hilar
vessels or the
collecting system or from extensive infiltration of tumor throughout the kidney. Rarely, the bulk of the tumor can occupy the renal pelvis and even extend down the ureter to the bladder (63,64,65). This intrapelvic polypoid tumor is called botryoid Wilms tumor because of its similarity to botryoid rhabdomyosarcoma.
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collecting system or from extensive infiltration of tumor throughout the kidney. Rarely, the bulk of the tumor can occupy the renal pelvis and even extend down the ureter to the bladder (63,64,65). This intrapelvic polypoid tumor is called botryoid Wilms tumor because of its similarity to botryoid rhabdomyosarcoma.
 |
Figure 9.21. Wilms tumor in a 2-year-old boy. A, B:
Two axial contrast-enhanced CT scans demonstrate a large soft tissue
mass (M) distorting and displacing the enhancing parenchyma (arrows) in the lower pole of the right kidney. The tumor enhances less than normal parenchyma. C: Coronal volume-rendered image shows the craniocaudal extent of the tumor (T). The inferior vena cava (IVC) is patent. (See color insert.) |
Wilms tumor may occur in extrarenal sites, such as the retroperitoneum, inguinal region, pelvis, or thorax (66,67,68,69). These tumors are not usually associated with a primary renal tumor (Fig. 9.23).
Local Tumor Spread
Although the staging of Wilms tumor is based on surgical
findings, determination of the extent of extrarenal disease is
important for operative planning. Wilms tumor spreads intra-abdominally
either by direct extension through the renal capsule into perinephric
tissues, lymph nodes, or adjacent organs, or by invasion of vessels
with extension into the renal vein or inferior vena cava. Perinephric
extension appears as a thickened renal capsule or as nodular or streaky
soft tissue densities in the perinephric space (Fig. 9.24).
Demonstration of extracapsular extension is not critical since the
treatment for Wilms tumor is radical nephrectomy, which includes
removal of the kidney, perirenal fat, and fascia.
Organ invasion appears as a parenchymal soft tissue mass
surrounding or distorting vessels. The presence of fat planes between
the neoplasm and adjacent structures militates against gross invasion,
but the absence of fat planes may be normal or due to tumor adherence
or invasion. When the loss of fat planes is associated with an
eccentric soft tissue mass, a confident diagnosis of extension can be
made. Tumor invasion of the
peritoneal cavity, omentum, and mesentery also can occur. CT findings include plaquelike thickening or nodular implants in the omentum (subdiaphragmatic area) or mesentery (70).
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peritoneal cavity, omentum, and mesentery also can occur. CT findings include plaquelike thickening or nodular implants in the omentum (subdiaphragmatic area) or mesentery (70).
 |
Figure 9.22.
Calcified Wilms tumor. Coronal multiplanar image shows a large soft
tissue–attenuation mass containing scattered calcifications (arrows) in the right kidney. |
Tumor extension to lymph nodes occurs in about 20% of
children with Wilms tumor. Lymph node involvement appears as enlarged
perirenal, paracaval, para-aortic, retroperitoneal, or retrocrural
lymph nodes. Although small nodes can be normal in adolescents and
adults, such nodes are rarely seen in infants and young children. Any
retroperitoneal lymph node, regardless of size, should be regarded with
suspicion in a young child. Not all enlarged nodes, however, contain
tumor and some are enlarged as a result of reactive hyperplasia. Thus,
retroperitoneal nodes are sampled routinely as part of the surgical
treatment in children with Wilms tumor.
 |
Figure 9.23. Extrarenal Wilms tumor. A large retroperitoneal soft tissue mass (M) is seen separate from the normal left kidney (LK). |
 |
Figure 9.24.
Wilms tumor with perinephric extension. There is a large, heterogeneous
mass in the left kidney with associated thickening of the renal fascia (arrow) representing tumor extension into the perinephric space. |
Tumor extension into the renal vein and inferior vena
cava has been reported in 5% to 10% of patients with Wilms tumor.
Extension of thrombus into the right atrium occurs in about 30% of
patients who have tumor in the inferior vena cava. Most patients with
vascular involvement are asymptomatic. On occasion, patients present
with hepatomegaly owing to hepatic vein occlusion or with congestive
heart failure from an occlusive atrial thrombus. Preoperative knowledge
of tumor extension above the level of the hepatic veins is important
because it may necessitate cardiopulmonary bypass to prevent pulmonary
embolism. Tumor below the hepatic veins can be removed by an abdominal
approach. On CT, tumor thrombus is seen as a low-attenuation mass in
the renal vein or inferior vena cava (Fig. 9.25).
Enlarged paravertebral collateral vessels and a prolonged nephrogram
may be observed if the renal vein or the vena cava is completely
occluded.
Care must be taken not to confuse unopacified blood
returning from the lower extremities with tumor thrombus in the
inferior vena cava. This artifact is particularly common with the use
of helical CT and acquisition of early images. Administration of
contrast medium through a foot vein also can cause flow artifacts in
the inferior vena cava.
 |
Figure 9.25.
Wilms tumor with caval invasion. Contrast-enhanced CT scan shows a mass
in the right kidney and tumor thrombus in the dilated right renal vein (black arrow) and inferior vena cava (white arrow). Gallbladder wall edema is related to hepatic failure secondary to tumor extension into the hepatic veins. |
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Between 5% and 10% of children with Wilms tumors have
bilateral disease. Bilateral tumors are more commonly synchronous
(occurring simultaneously) rather than metachronous (occurring at
different times). Patients with bilateral tumors may have a dominant
mass with a smaller contralateral tumor or a dominant mass in each
kidney (Fig. 9.26).
 |
Figure 9.26. Bilateral Wilms tumor. A:
Coronal multiplanar reformation. A large Wilms tumor in the lower pole
of the right kidney obstructs the renal pelvis, which is dilated (white arrow). A smaller nonenhancing tumor (black arrow)
is present in the lower pole of the left kidney. This appearance is
indistinguishable from that of a Wilms tumor with contralateral
nephrogenic rest and tissue sampling is required for diagnosis. B: Axial CT scan in another patient shows large bilateral tumors. |
Metastatic Disease
Wilms tumor metastasizes most often to the lungs (12% to 20% of cases) and occasionally to the liver (8% to 10% of cases) (Fig. 9.27). CT is the method of choice to detect pulmonary metastases.
Staging and Treatment
The staging of Wilms tumor is based on surgical and pathologic examinations (Table 9.1) (51,71,72,73).
Conventional treatment of Wilms tumor is radical nephrectomy and
chemotherapy. Treatment of stage V (bilateral) disease with a dominant
tumor and small contralateral nodule(s) is excision of the kidney with
the dominant tumor and wedge resection of the contralateral nodule(s).
Treatment of stage V disease with large bilateral tumors is
preoperative chemotherapy with delayed resection after tumor shrinkage.
Partial nephrectomy or nephron-sparing sur-gery, or radiofrequency
ablation may be performed for small lesions (74,75).
Follow-up Imaging
Following therapy, CT can be used to detect local or distant recurrence (76). Most tumor recurrence occurs within three years of completion of therapy. Patients with
incomplete resection of tumor, lymph node involvement, or vascular invasion have the highest recurrence risk. Tumor recurrence most often appears as a soft tissue mass in the empty renal fossa, enlarged lymph nodes, or ipsilateral psoas muscle enlargement (Fig. 9.28). A peritoneal or pelvic mass can be seen if tumor spillage occurred at surgery (Fig. 9.29). Recurrence within the kidneys can be associated with partial nephrectomy.
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incomplete resection of tumor, lymph node involvement, or vascular invasion have the highest recurrence risk. Tumor recurrence most often appears as a soft tissue mass in the empty renal fossa, enlarged lymph nodes, or ipsilateral psoas muscle enlargement (Fig. 9.28). A peritoneal or pelvic mass can be seen if tumor spillage occurred at surgery (Fig. 9.29). Recurrence within the kidneys can be associated with partial nephrectomy.
 |
Figure 9.27.
Wilms tumor with metastasis to liver. Contrast-enhanced CT in a patient
with a left Wilms tumor shows a hypoattenuating lesion (arrow) in the right hepatic lobe. Wilms metastases are typically hypovascular. |
Nephrogenic Rests and Nephroblastomatosis
Nephrogenic rests are foci of persistent embryonal renal
tissue persisting beyond 36 weeks of intrauterine gestation. They
result from incomplete induction of the metanephric blastema into
mature renal parenchymal tissue by the ureteral bud. Isolated foci are
termed nephrogenic rests, whereas multiple or diffuse involvement is
referred to as nephroblastomatosis (77,78,79). Nephrogenic rests and nephroblastomatosis are not malignant tumors per se, but can be a precursor to Wilms tumor (80).
They have been found in nearly 100% of kidneys with bilateral Wilms
tumors and in approximately 25% of children with unilateral Wilms tumor
(31,32).
Table 9.1 National Wilms Tumor Study Group Staging System | |
|---|---|
|
 |
Figure 9.28.
Tumor recurrence. CT scan of a 15-month-old girl several months after
resection of a left Wilms tumor shows a soft tissue mass (arrow) in the left renal fossa, displacing the splenic vein anteriorly. |
Nephrogenic Rests
Nephrogenic rests are classified by their location into
two types: perilobar, which lies in the peripheral renal cortex or
columns of Bertin, and intralobar, which may be found anywhere within a
renal lobe. They are associated with Beckwith–Wiedemann syndrome,
hemihypertrophy, Perlman syndrome, and chromosomal abnormalities in the
11p15 locus. Intralobar rests are considerably less common than the
perilobar type but
have a higher association with Wilms tumor development. They are also associated with chromosomal abnormalities in the 11p13 locus, sporadic aniridia, and Drash syndrome.
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have a higher association with Wilms tumor development. They are also associated with chromosomal abnormalities in the 11p13 locus, sporadic aniridia, and Drash syndrome.
 |
Figure 9.29. Tumor recurrence. CT shows a soft tissue mass (arrow)
in the pelvis. The capsule of the kidney had ruptured at the time of
the original surgery, and the recurrence was thought to be a drop
metastasis. |
At CT, nephrogenic rests appear as ovoid or lenticular
peripheral nodules. On unenhanced CT, they appear homogeneous and
isodense or hyperdense to adjacent cortex. Following administration of
intravenous contrast medium, they become hypodense to adjacent enhanced
renal cortex (Fig. 9.30). Nephrogenic rests
that enlarge, appear heterogeneous, or have a spherical configuration
are of concern for malignant transformation.
Nephroblastomatosis
Two basic patterns of nephroblastomatosis have been described: diffuse and multifocal (81,82).
Diffuse nephroblastomatosis can be further subdivided into pancortical
(infantile) and superficial (late infantile) types. In the pancortical
form of diffuse nephroblastomatosis, the renal cortex is completely
replaced by immature renal tissue. Patients often die early in the
neonatal period because of impaired renal function. In the superficial
form of diffuse nephroblastomatosis, there is a subcapsular rind of
primitive tissue that surrounds normal renal cortex and medulla. This
form tends to affect infants toward the end of the first year of life
and is responsive to chemotherapy. Both forms of the diffuse disease
present as bilateral flank masses.
The more common multifocal nephroblastomatosis is
usually found in older infants and young children and may be detected
during a screening examination in patients with high risk factors for
developing Wilms tumor, during CT evaluation of a Wilms tumor, or at
operation. The multifocal form involves the subcapsular cortex and
columns of Bertin.
 |
Figure 9.30.
Nephrogenic rest. Contrast-enhanced CT in a patient with a prior left
nephrectomy shows a hypoattenuating ovoid mass in the cortex of the
right kidney (arrow). This appearance is indistinguishable from a metachronous Wilms tumor, and biopsy is needed for diagnosis. |
At CT, diffuse nephroblastomatosis is usually seen as
reniform enlargement with a thick peripheral rind of soft tissue that
may show striated enhancement (Fig. 9.31) (77,78,81,82). Multifocal disease appears as soft tissue nodules with poor enhancement relative to normal renal parenchyma (Fig. 9.32). It may deform the cortex, producing a lobulated appearance mimicking fetal lobulation (77). The management of nephrogenic rests is controversial. Arguments exist for and against the use of
chemotherapy (identical to that used to treat stage I Wilms tumor). Regardless of the treatment choice, close imaging follow-up is needed to exclude the development of Wilms tumor (78).
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chemotherapy (identical to that used to treat stage I Wilms tumor). Regardless of the treatment choice, close imaging follow-up is needed to exclude the development of Wilms tumor (78).
 |
Figure 9.31. Diffuse nephroblastomatosis. A:
Pancortical form. In this patient, with bilateral nephromegaly, the
renal cortex is completely replaced by soft tissue mass. The renal
medulla (M) is compressed. B: Superficial form. A subcapsular rind of soft tissue (arrows) compresses the enhancing renal cortex. |
 |
Figure 9.32. Multifocal nephroblastomatosis. Contrast-enhanced CT scan shows small, soft tissue–attenuation cortical masses (arrows) in both kidneys. These lesions were detected as part of a surveillance study for hemihypertrophy. |
Renal Cell Carcinoma
Renal cell carcinoma accounts for 2% to 6% of all pediatric malignant renal tumors (31,83).
Mean patient age at presentation is approximately 10 years. There is a
2:1 male predominance. Clinical findings are similar to those in adults
and include a palpable abdominal mass, abdominal or flank pain, and
gross painless hematuria. Hypertension, polycythemia, dysuria, and
fever may also be present. Renal cell carcinoma is associated with von
Hippel–Lindau syndrome, tuberous sclerosis, urogenital malformations,
and treated neuroblastoma; the mean time interval between treatment for
neuroblastoma and development of renal cell carcinoma is approximately
11 years (84,85).
Renal cell carcinoma arises from epithelial cells of the
renal tubule with the clear cell subtype being most common. At
pathologic examination, it often is surrounded by a rim of compressed
tissue (pseudocapsule) and commonly contains hemorrhage, necrosis, and
calcification. Ossification also may be seen (86). The tumor can invade the renal vein. Metastases to lung, liver, and bone are present in 8% to 30% of cases (83).
On CT, renal cell carcinoma appears as a nonspecific
solid or mixed solid-cystic, intrarenal mass with well-circumscribed or
ill-defined margins (Fig. 9.33). The cystic
changes represent necrosis or hemorrhage. Calcifications occur in about
25% of tumors. The tumor enhances but to a lesser degree than the
normal renal parenchyma. Mean diameter is 4 cm, which is significantly
smaller than Wilms tumor. Secondary findings include local spread into
the renal pelvis, retroperitoneum, adjacent organs, lymph nodes, and
renal vein or inferior vena cava. On the basis of CT alone, it is
difficult to distinguish renal cell carcinoma from Wilms tumor.
Although the relatively small tumor size and the age of the patient are
helpful in suggesting renal cell carcinoma, definitive diagnosis
requires tissue sampling. Treatment typically is by radical
nephrectomy. Nephron-sparing partial nephrectomy may be performed for
small tumors.
Lymphoma
Renal involvement is more often associated with non-Hodgkin lymphoma than with Hodgkin disease (87,88).
Since the kidneys do not contain lymphatic tissue, renal involvement by
lymphoma likely occurs either as a result of hematogenous spread or
direct extension of retroperitoneal tumor. Lymphoma usually affects
patients older than 5 years of age.
The most common CT appearance of renal lymphoma is
multiple parenchymal masses or nodules (70% of cases) that may distort
the renal contour and displace the collecting system (Fig. 9.34) (89,90,91,92,93). Less common presentations include a solitary intraparenchymal mass (Fig. 9.35), diffuse renal enlargement (Fig. 9.36),
and direct invasion from adjacent lymph nodes or retroperitoneal
masses. Diffuse renal enlargement may be a manifestation of tumor lysis
or diffuse parenchymal infiltration (94).
Secondary findings include renal fascial thickening and tumor
encasement of the renal pelvis and proximal ureter with obstructive
hydronephrosis. Perinephric involvement can arise from retroperitoneal
disease or transcapsular spread of parenchymal tumor. Lymphomatous
masses are usually homogeneous and hypoattenuating relative to normal
parenchyma. Heterogeneous areas of necrosis or hemorrhage may be seen
in larger lesions. The CT appearance of solitary lymphoma is similar to
that of other solid intrarenal neoplasms. Multiple renal lesions may
mimic nephroblastomatosis, leukemia, and metastatic disease. The
diagnosis of lymphoma can be suspected when there is coexisting
splenomegaly or widespread lymphadenopathy elsewhere.
Leukemia
Acute lymphoblastic leukemia is the most common
malignancy of childhood, usually occurring in children between 3 and 5
years of age. The kidneys can be involved by leukemia during the active
stages of disease or they may serve as a sanctuary for disease during
bone marrow remission. Renal infiltration by leukemia usually is
clinically occult, although it can result in enlarged palpable kidneys,
abdominal pain, hematuria, hypertension, and renal failure (95).
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 |
Figure 9.33. Renal cell carcinoma, spectrum of appearances. A: Contrast-enhanced CT scan in a 15-year-old girl demonstrates a cystic left renal mass (arrow)
with a focal enhancing nodule (Bosniak IV lesion). The nodule makes it
unlikely that this mass is a simple cyst. The cystic appearance
resulted from necrosis. B: CT in a
12-year-old boy shows a large, heterogeneous soft tissue tumor
extending exophytically from the kidney and invading the renal vein (arrow). C: CT in a 7-year-old boy shows a heterogeneous mass (M) replacing the upper pole of the left kidney, para-aortic adenopathy (white arrow), and a lytic bone metastasis (black arrow). |
 |
Figure 9.34.
Renal lymphoma. Contrast-enhanced CT shows bilateral renal masses. This
is the most common appearance of renal involvement by lymphoma. |
 |
Figure 9.35. Renal lymphoma. There is a solitary nodule (arrow) in the upper pole of the right kidney. |
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 |
Figure 9.36. Renal lymphoma. CT shows bilaterally enlarged, low-attenuation kidneys, representing diffuse infiltration by lymphoma. |
The CT patterns of renal infiltration by leukemia
include bilateral symmetric nephromegaly with loss of corticomedullary
differentiation and solitary or multiple masses (Fig. 9.37) (95).
Leukemic masses show minimal enhancement and appear hypodense to normal
parenchyma. The pelvicalyceal system may be dilated as a result of
ureteral obstruction by enlarged retroperitoneal lymph nodes.
Rarer Malignant Renal Tumors
Rhabdoid Tumor
Rhabdoid tumor is an uncommon, highly aggressive
malignancy arising in the renal medulla accounting for about 2% of
renal malignancies in young children (31,32,96).
It most often is found in young infants with mean age at diagnosis of
18 months. The usual clinical presentation is that of a palpable
abdominal mass, but hematuria, fever, hypertension, and hypercalcemia
are also seen (96,97,98,99).
It also is associated with synchronous or metachronous primary
intracranial tumors, most commonly primitive neuroectodermal tumor, and
brain metastases ((96,97). Gross examination shows a lobulated, solid tumor (98).
 |
Figure 9.37. Leukemia. Contrast-enhanced CT demonstrates a small hypodense mass (arrow) in the right kidney. This lesion is well seen in the nephrographic phase of contrast enhancement. |
 |
Figure 9.38.
Rhabdoid tumor. An irregular, poorly defined soft tissue mass (M)
infiltrates the parenchyma and renal pelvis of the left kidney. A
characteristic low-attenuation superficial fluid collection (white arrows),
representing an area of necrosis, is present in the periphery of the
left kidney. Note also a second tumor in the right kidney, which also
infiltrates the renal pelvis, and a hepatic metastasis (black arrow). |
At CT, it appears as a heterogeneous tumor with indistinct margins involving the renal hilum (Fig. 9.38). A peripheral, crescentic subcapsular fluid collection occurs in approximately 50% to 70% of case (96,97,98) (Fig. 9.38).
The subcapsular fluid represents necrosis or hemorrhage. The presence
of this fluid collection is characteristic but not pathognomonic of
rhabdoid tumor, and similar collections are occasionally seen with
Wilms tumor, mesoblastic nephroma, and clear cell sarcoma (98). The tumor may contain calcification and it may extend into the renal vein or inferior vena cava (96,97,98,99). Uncommonly, there may be bilateral renal involvement (96).
Rhabdoid tumor metastasizes to lymph nodes, liver, lung, bone, and
brain. These tumors have highly aggressive behavior, which is
associated with a poor prognosis.
Clear Cell Sarcoma
Clear cell sarcoma is another aggressive tumor that arises in the renal medulla. It accounts for about 4% to 5% or
primary renal tumors in childhood (31,100). The peak age incidence is 1 to 4 years of age. At gross examination, the tumor is a heterogeneous mass with areas of necrosis and hemorrhage (70% of cases) (98). At CT, it appears as a highly necrotic mass compressing surrounding normal parenchyma and distorting collecting structures (100) (Fig. 9.39). It may metastasize to bone, lymph nodes, brain, liver, and lungs, but generally it is not associated with vascular invasion (98).
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primary renal tumors in childhood (31,100). The peak age incidence is 1 to 4 years of age. At gross examination, the tumor is a heterogeneous mass with areas of necrosis and hemorrhage (70% of cases) (98). At CT, it appears as a highly necrotic mass compressing surrounding normal parenchyma and distorting collecting structures (100) (Fig. 9.39). It may metastasize to bone, lymph nodes, brain, liver, and lungs, but generally it is not associated with vascular invasion (98).
 |
Figure 9.39. Clear cell sarcoma. A, B:
Contrast-enhanced CT scans in two patients show large heterogeneous
tumors infiltrating and expanding the kidney. Areas of necrosis (arrows) are typical of clear cell sarcoma. Infiltration of the renal pelvis is noted in part B, consistent with the medullary origin of this tumor. |
Primitive Neuroectodermal Tumor
Primitive neuroectodermal tumor (PNET) is a rare
malignant renal tumor that has been associated with translocation of
tissue from chromosome 11 to 22 (101,102,103).
On histologic examination, the tumor contains round blue cells with
large areas of necrosis. CT shows a minimally enhancing, infiltrative
mass (101,102,103) (Fig. 9.40).
Calcifications and low-attenuation areas representing necrosis or
hemorrhage may be seen. Similar to Wilms tumor and renal cell
carcinoma, this tumor can extend into the renal vein and inferior vena
cava.
Desmoplastic Small Round Cell Tumor
Desmoplastic small round cell tumor is an uncommon
intra-abdominal malignant neoplasm that typically involves serosal
surfaces with rare renal involvement. Similar to primitive
neuroectodermal tumor, the desmoplastic tumor shows reciprocal
translocation involving chromosomes 11 and 22. However, in desmoplastic
tumor the short arm of chromosome 11 is affected, whereas in primitive
neuroectodermal tumor the long arm is involved (104,105). CT shows a hypovascular mass with punctate calcifications (Fig. 9.41).
 |
Figure 9.40.
Primitive neuroectodermal tumor. Coronal multiplanar reformation shows
a homogeneous mass (M) extending beyond the margins of the kidney.
(Case courtesy of Armed Forces Institute of Pathology.) |
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 |
Figure 9.41. Desmoplastic tumor. Contrast-enhanced CT shows a well-defined low-attenuation mass (arrow) containing several punctate calcifications in the midpolar region of the left kidney. (Reprinted from Egloff
AM, Lee EY, Dillon JE, et al. Desmoplastic small round cell tumor of
the kidney in a pediatric patient: sonographic and multiphase CT
findings. AJR Am J Roentgenol 2005;185:1347–1349, with permission. ) |
Renal Medullary Carcinoma
Renal medullary carcinoma is a highly aggressive
malignant tumor of epithelial origin that originates in the medulla and
almost always occurs in patients with sickle cell (SC) trait or
hemoglobin SC disease, but not with homozygous hemoglobin sickle cell
disease (31,106).
Patients are usually in the second or third decade of life and present
with flank or abdominal pain or gross hematuria and less commonly with
a palpable mass, weight loss, or fever. The tumor affects the right
kidney more than the left kidney.
On CT, renal medullary carcinoma is typically a
heterogeneous, hypovascular mass containing hemorrhage and extensive
necrosis. It typically is located deep in the parenchyma, invading and
encasing the renal pelvis and causing caliectasis (Fig. 9.42) (31,107).
Extrarenal spread occurs by direct extension into the perinephric fat,
regional lymph nodes, and retroperitoneal soft tissues and also by
invasion of the renal vein with propagation into the inferior vena
cava. Distant metastases are to lung and liver. The prognosis is
extremely poor, and most patients have advanced disease at time of
diagnosis.
Secondary Tumor Deposits
Renal metastases are uncommon, although they have been
reported in children with sarcomas or melanomas who have widespread
metastases elsewhere (108). At CT, renal
metastases may be small and non–contour deforming, but large, exophytic
lesions that infiltrate or replace most of the kidney have been
described.
 |
Figure 9.42.
Renal medullary carcinoma. CT done to evaluate hematuria in this
patient with sickle cell anemia shows an infiltrative soft tissue mass
(M) expanding the upper pole of the right kidney. The tumor has invaded
the renal pelvis and also extended into the inferior vena cava (arrow). |
Benign Renal Tumors
Angiomyolipoma
Angiomyolipoma, also called renal hamartoma, is a benign
renal neoplasm that contains varying amounts of mature adipose tissue,
smooth muscle, and blood vessels (109,110).
It is rare as an isolated lesion in the general pediatric population,
but it is present in as many as 80% of children with tuberous sclerosis
(cerebral, cutaneous, and visceral hamartomas). Angiomyolipomas are
also associated with neurofibromatosis and von Hippel– Lindau syndrome (110).
The tumors are usually asymptomatic and detected as an incidental
finding, but some patients present with an abdominal mass or abdominal
pain, anemia secondary to tumoral hemorrhage, or renal failure because
of parenchymal replacement by tumor. There appears to be a relationship
between the size of the angiomyolipoma and the risk of bleeding.
Angiomyolipomas >3.5 cm in diameter have a higher risk of hemorrhage
(111).
At CT, angiomyolipomas are typically small, multiple,
and bilateral. They range from being completely fatty to being nearly
all soft tissue attenuation (Fig. 9.43). A
specific diagnosis can be made in virtually all cases by CT when an
area measuring fat (<10 HU) is seen within a renal mass. Lesion
characterization is improved by the use of thinly collimated sections (109). In one series, the fat content of the tumors was <10% despite large tumor size (112).
Attenuation measurements should be made on precontrast CT scans, since
vessels within the fat elements may enhance after administration of
intravenous
contrast medium, thereby increasing the average attenuation value of the lesion into the water or soft tissue range. Coexistent cystic lesions are common in patients with tuberous sclerosis (40,110). Fatty tissue can also be present in other renal tumors, including Wilms tumor, lipoma, and teratoma. The clinical history and presence of concomitant cysts should suggest the diagnosis of angiomyolipoma.
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contrast medium, thereby increasing the average attenuation value of the lesion into the water or soft tissue range. Coexistent cystic lesions are common in patients with tuberous sclerosis (40,110). Fatty tissue can also be present in other renal tumors, including Wilms tumor, lipoma, and teratoma. The clinical history and presence of concomitant cysts should suggest the diagnosis of angiomyolipoma.
 |
Figure 9.43. Angiomyolipomas. A: Contrast-enhanced CT in a patient with tuberous sclerosis shows a small, fat attenuation mass (arrow). B: CT in another patient shows bilateral soft tissue masses without substantial fat content (arrows). |
Mesoblastic Nephroma
Mesoblastic nephroma, also termed fetal renal hamartoma,
leiomyomatous hamartoma, and mesenchymal hamartoma of infancy, is the
most common renal neoplasm in the first 3 months of life with nearly
all cases identified in the first year of life (31).
Gross pathologic sections show a solid, unencapsulated tumor, commonly
occurring near the renal hilum. Hemorrhage and necrosis are relatively
infrequent (98). Histologic sections show
bundles of spindle-shaped cells infiltrating between and entrapping
glomeruli and renal tubules. This tumor nearly always exhibits a benign
behavior, although there is a cellular variant that is associated with
local recurrence and metastases to lung, liver, and brain (113).The
benign form of this tumor has few mitoses. The cellular form
demonstrates densely packed cells with a high mitotic rate. Cytogenetic
abnormalities of chromosome 11 and translocations (t 14:15), (t12;15),
(p13;q25) have been reported (57). Mesoblastic
nephroma may be discovered incidentally on prenatal sonography, but
most affected patients present because of a palpable abdominal mass.
Hypertension is an occasional presenting feature (114).
On noncontrast CT, mesoblastic nephroma may be
isoattenuating or hypoattenuating relative to normal parechyma. On
contrast-enhanced CT, it most often appears as a fairly uniform,
hypoattenuating soft tissue mass, replacing a large part of the renal
parenchyma (Fig. 9.44A). Occasionally, it contains low-attenuation areas representing necrosis, hemorrhage, or cystic degeneration (Fig. 9.44B). Focal areas of intense enhancement may be seen, corresponding to entrapped nephrons or large vascular spaces (114,115).
Penetration of the renal capsule and local invasion of the perinephric
tissue, vascular pedicle, or renal pelvis can occur. The treatment of
choice is nephrectomy. Chemotherapy is reserved for those patients with
locally recurrent tumors or metastatic disease.
Rare Benign Renal Tumors
Metanephric Adenoma
Metanephric adenoma, also called embryonal adenoma or
metanephric (nephrogenic) adenofibroma, is part of a spectrum of benign
renal neoplasms with varying proportions of epithelial and stromal
components (116,117). It has been reported in infants and older adults (31).
Presenting clinical features include flank mass, pain, hematuria,
hypertension, hypercalcemia, and polycythemia. The latter is thought to
be the result of increased secretion of erythropoietin (118).
At gross pathology, the tumors are usually small, nonencapsulated,
round, and solid. On noncontrast CT, they may be isoattenuating or
hyperattenuating, related to the presence of psammomatous
calcifications. After contrast administration, they
enhance less than normal parenchyma, and they may contain low-attenuation foci related to necrosis or myxoid contents (Fig. 9.45) (31,118,119).
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enhance less than normal parenchyma, and they may contain low-attenuation foci related to necrosis or myxoid contents (Fig. 9.45) (31,118,119).
 |
Figure 9.44. Mesoblastic nephroma. A: Coronal reformatted CT shows a large mass (M) distorting and displacing the enhancing parenchyma (arrows) in the midpolar area of the right kidney. B: Axial CT in another infant shows a highly necrotic mass (M) replacing the right kidney. |
Ossifying Renal Tumor of Infancy
Ossifying renal tumor of infancy is a rare benign neoplasm of early infancy, usually occurring in the first year of age (120).
Most infants present with a palpable abdominal mass and hematuria. This
lesion arises from uroepithelium in the papillary region of the renal
pyramids and extends in a polypoid fashion into the collecting system.
It is usually <2 to 3 cm in diameter (31,120).
Histologically, the tumor contains osteoid, osteoblasts, and spindle
cells. At CT, ossifying renal tumor appears as a partially calcified
soft tissue mass, occupying part of the collecting system.
Hydronephrosis is common (Fig. 9.46) (121). Treatment is nephrectomy or heminephrectomy.
 |
Figure 9.45. Metanephric adenoma. Contrast-enhanced CT scan shows a soft tissue mass (black arrows) with a central area of necrosis or myxoid tissue (white arrow). (Reprinted from Navarro O, Conolly B, Taylor G, et al. Metanephric adenoma of the kidney: a case report. Pediatr Radiol 1999;29:100–103, with permission. ) |
Inflammatory Pseudotumor
Inflammatory pseudotumor, also known as inflammatory
myoblastic tumor, plasma cell granuloma, and pseudosarcomatous
fibromyxoid tumor, is a benign tumorlike condition of unknown cause (122,123).
It is characterized by an admixture of spindle-shaped cells and
inflammatory cells, including plasma cells, lymphocytes, and
histiocytes (122). Clinical features include
hematuria and abdominal pain. At CT, its appearance is nonspecific, appearing as a homogeneous or heterogeneous mass, with enhancement following contrast administration. It may arise in parenchyma or in the renal pelvis (123).
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hematuria and abdominal pain. At CT, its appearance is nonspecific, appearing as a homogeneous or heterogeneous mass, with enhancement following contrast administration. It may arise in parenchyma or in the renal pelvis (123).
 |
Figure 9.46. Ossifying renal tumor of infancy. Contrast-enhanced CT scan shows a calcified soft tissue mass (arrows)
arising in the left renal pelvis and dilated calyces (C). Because of
its location within the collecting system, this tumor commonly causes
hydronephrosis. |
Parenchymal Infections
Acute Infections
Infection is the most frequent disorder of the urinary
tract in children. In most cases, clinical signs, such as fever, flank
pain or tenderness, chills, and dysuria, and laboratory findings, such
as pyuria, bacteruria, and leukocytosis, indicate the presence of
urinary tract infection. Imaging is not needed to document the
diagnosis. In acute infection, the role of imaging is to identify
factors that predispose to infection, such as hydronephrosis and
vesicoureteral reflux. Sonography and voiding cystourethrography are
the initial imaging studies to identify these predisposing factors. If
response to treatment is poor or there are recurrent infections, CT can
be useful to detect potential complications, such as abscess or
pyonephrosis (124,125,126,127,128,129,130).
Although sonography can detect some abscesses and pyonephrosis, it is
not as reliable as CT in characterizing and defining the extent of
these abnormalities.
Acute Bacterial Pyelonephritis
Acute bacterial pyelonephritis is a nonsuppurative
bacterial inflammation of the kidney, regardless of extent or pattern
of distribution (125,126,130).
The term focal pyelonephritis is sometimes used to refer to involvement
of a focal area or one pole of the kidney with sparing of other
regions. Most pyelonephritis is a result of an ascending infection
associated with vesicoureteral reflux. The common inciting
microorganism is Escherichia coli.
Pyelonephritis may be uncomplicated or complicated; the latter term
indicates the presence of abscess formation or pyonephrosis.
Abnormalities in renal perfusion associated with acute
pyelonephritis are best seen during homogeneous enhancement of the
renal parenchyma in the late corticomedullary and the nephrographic
phases (127). CT scans may be normal in
patients with mild uncomplicated pyelonephritis. In moderate and severe
acute pyelonephritis, unenhanced CT may demonstrate enlargement of the
affected kidney and focal areas of hypoattenuation or hyperattenuation,
depending on the relative amounts of edema and hemorrhage,
respectively. The characteristic CT findings on contrast-enhanced scans
are round or wedge-shaped areas of diminished attenuation alternating
with areas of normal enhancing parenchyma, creating a striated
nephrogram (Fig. 9.47) (125,126,127,128,130). The cause of the low attenuation is thought to be vasospasm or edema caused by the infection (125).
Secondary findings include global or focal enlargement of the kidney,
thickening of the pelvicalyceal wall and renal fascia, and calyceal
obliteration (127). Global or polar atrophy may be seen as a sequela of severe parenchymal infection.
 |
Figure 9.47.
Acute pyelonephritis in a 4-year-old boy with fever and leukocytosis
despite appropriate antibiotic therapy. CT was performed to exclude
abscess. Nephrographic phase contrast-enhanced axial CT shows a patchy
striated nephrogram (alternating low- and high-attenuation
wedged-shaped areas) in the right kidney. The asymmetric involvement is
typical for infection. |
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 |
Figure 9.48. Focal pyelonephritis. Note a focal low-attenuation lesion (arrow) in the renal cortex of the right kidney. |
In focal pyelonephritis, there is a single masslike
region of low attenuation as a result of swelling owing to edema.
Striated or patchy enhancement may be limited to this area. (Fig. 9.48).
Complicated Pyelonephritis
Abscess
A renal abscess is a necrotic cavity filled with
purulent material. Renal abscesses are rare, and most are the result of
inadequately treated infection that ultimately liquefies. Less often
they are a complication of contiguous spread from other organs, trauma,
or surgery. Affected children typically present with fever, abdominal
or flank pain, and pyuria. Unenhanced scans show a focal
low-attenuation area of near-water attenuation (125,130,131,132).
The entire kidney may be enlarged, or there may be a focal mass that
bulges the renal margin. Contrast-enhanced CT findings of renal abscess
include a round shape, well-defined contours, nonenhancing fluid-filled
center, thin enhancing walls, and a peripheral rind of edema (Figs. 9.49 and 9.50). Septations may be present (131).
Thickening of the renal fascia is also common. Gas bubbles or gas–fluid
levels are pathognomonic of abscess but are uncommon. Although smaller
renal abscesses may respond to intravenous antibiotic treatment alone,
percutaneous or surgical aspiration often is needed for the management
of large renal abscesses. CT can be used to guide percutaneous drainage.
Perinephric abscess is usually the result of extension
of pre-existing renal parenchymal infection. The CT features are a
loculated fluid collection with an enhancing rim in the perinephric
space (133). It may be adjacent to a parenchymal abscess (Fig. 9.51). Thickening of the renal fascia and perinephric stranding are common.
 |
Figure 9.49. Renal abscess. Coronal multiplanar reformation shows a well-marginated cavity mass with a thick rim of edema (arrow) in the lower pole of the right kidney. Culture yielded Staphylococcus aureus. |
Pyonephrosis
Pyonephrosis results from infection of an obstructed
collecting system. The most common cause of obstruction is
ureteropelvic junction obstruction; distal ureteral calculi and
stricture are less frequent causes of obstruction
in children (130). CT findings of pyonephrosis are a dilated collecting system containing debris and/or gas, delayed or poor excretion of contrast, and parenchymal areas of low attenuation representing concomitant pyelonephritis (134). Thickening of the pelvic wall and renal fascia is common. CT can be used to guide subsequent aspiration and nephrostomy placement if sonography is not sufficient.
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in children (130). CT findings of pyonephrosis are a dilated collecting system containing debris and/or gas, delayed or poor excretion of contrast, and parenchymal areas of low attenuation representing concomitant pyelonephritis (134). Thickening of the pelvic wall and renal fascia is common. CT can be used to guide subsequent aspiration and nephrostomy placement if sonography is not sufficient.
 |
Figure 9.50. Multiple renal abscesses. On contrast-enhanced axial CT, there are several fluid collections (arrows),
which are surrounded by edema, in the upper pole of the right kidney.
Areas of diminished enhancement in the left kidney are consistent with
acute pyelonephritis. |
 |
Figure 9.51. Perinephric abscess. Contrast-enhanced CT shows a septated fluid collection (white arrows) with thin enhancing walls in the perinephric space. Note the adjacent parenchymal abscess (black arrow). |
Chronic Renal Infections
Chronic Pyelonephritis
Chronic pyelonephritis usually results from recurrent
episodes of vesicoureteral reflux associated with intrarenal reflux of
infected urine. CT findings include a small kidney with global or focal
cortical scarring overlying blunted calyces (Fig. 9.52). Compensatory hypertrophy of parenchyma adjacent to areas of renal scarring also may be seen.
The major differential diagnostic consideration for an
irregular renal contour is fetal lobulation. The cortical indentations
in fetal lobulation are interpolar in distribution; there is no
parenchymal loss, and the underlying calyces are normal. Cortical
scarring in chronic pyelonephritis has a polar distribution, and it
overlies a blunted calyx. Primary renal hypoplasia and atrophy
secondary to renal vein thrombosis, ischemia, obstruction, or
irradiation cause small, smooth kidneys with uniform parenchymal loss.
Xanthogranulomatous Pyelonephritis
Xanthogranulomatous pyelonephritis is an uncommon complication of the combination of renal obstruction and chronic infection (135,136,137,138).
Pathologically, there is destruction of renal parenchyma and
replacement by granulomatous infiltrate and lipid-laden macrophages
(xanthoma cells). In children, the disease is usually focal involving
the upper or lower poles. Rarely, the entire kidney is involved (135,136,137).
 |
Figure 9.52.
Reflux nephropathy and chronic atrophic pyelonephritis.
Contrast-enhanced CT scan shows a small right kidney with irregular
parenchymal thinning and compensatory enlargement of the left kidney. |
CT findings of xanthogranulomatous pyelonephritis
include enlargement of the entire kidney or a segment of the kidney,
multiple low-attenuation masses, parenchymal calcifications, and
calculi (Fig. 9.53) (135,136,137,138).
A large central (staghorn) calculus is characteristic of the diffuse
form of disease. The low-attenuation masses represent dilated calyces,
areas of tissue necrosis, or xanthoma collections. They do not enhance,
but they often demonstrate rim enhancement because of inflammatory
hypervascularity. Both focal and diffuse forms of the disease may
extend into the perinephric space, renal fascia, psoas muscles, soft
tissues of the flank, and adjacent viscera, such as the liver or bowel.
Nephrectomy is indicated for diffuse disease and partial nephrectomy
for the focal form.
Fungal Infection
Infants and children who have indwelling catheters for
hyperalimentation and those who are on prolonged antibiotic therapy or
immunocompromised (transplant recipients, AIDS patients, patients with
malignancies) are at increased risk for fungal infections (130,139). Most fungal infection is caused by Candida albicans
and is the result of hematogenous seeding. Fungi can cause
pyelonephrtitis and renal abscesses, mimicking the CT appearance of
bacterial pyelonephritis. CT findings most suggestive of fungal
infection are fungal balls or multiple microabscesses in the kidneys or
in the spleen or liver (Fig. 9.54). At CT,
fungal balls appear as poorly circumscribed, soft tissue masses in a dilated renal pelvis or calyces. Other CT findings that may be seen in fungal infections are diminished or absent contrast excretion, thickening of the perinephric soft tissues, urinary ascites, and contrast extravasation (139).
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fungal balls appear as poorly circumscribed, soft tissue masses in a dilated renal pelvis or calyces. Other CT findings that may be seen in fungal infections are diminished or absent contrast excretion, thickening of the perinephric soft tissues, urinary ascites, and contrast extravasation (139).
 |
Figure 9.53. Xanthogranulomatous pyelonephritis. A:
On a contrast-enhanced CT, the right kidney is enlarged and poorly
enhancing and contains multiple low-attenuation masses, representing
dilated calyces and xanthoma collections. Note surrounding rim
enhancement. B: Unenhanced CT scan through
the lower abdomen shows a large right ureteral calculus. (Case courtesy
of Armed Forces Institutes of Pathology.) |
Patients with AIDS are susceptible to various
infections, including bacterial, fungal, tuberculosis, and
oppor-tunistic infections. CT findings are similar to those of
bacterial pyelonephritis, abscess, and fungal infection. Opportunistic
infections, such as Pneumocystis carinii, Mycobacterium avium-intracellulare,
and cytomegalovirus can involve the kidney and can produce multiple
punctate calcifications in the kidneys, lymph nodes, and other
abdominal viscera (140).
 |
Figure 9.54. Renal candidiasis. Several, small low-attenuation lesions (arrowheads), representing microabscesses, are seen in the parenchyma of both kidneys. |
Noninflammatory Parenchymal Disease
In tyrosinemia, contrast excretion may be delayed and produce a prolonged cortical and/or medullary nephrogram (141).
Glycogen storage disease type I has been reported as a cause of
nephromegaly and increased cortical attenuation. The increased
attenuation is believed to be caused by excessive deposition of
glycogen in the cortex (142). Sarcoidosis is
associated with nephrocalcinosis, nephrolithiasis, and an interstitial
granulomatous nephritis. On CT, granulomatous renal involvement may
appear as heterogeneous enhancement or multiple hypoattenuating nodules
(143).
Renal Vascular Disease
Renal Artery Stenosis
Renovascular disease accounts for ≤10% of cases of pediatric hypertension (144).
Renal artery stenosis may be isolated or associated with various
vasculitides and syndromes, including Takayasu disease, moya-moya,
neurofibromatosis, midaortic syndrome, tuberous sclerosis, and Williams
syndrome (idiopathic infantile hypercalcemia) (144).
The advent of multidetector CT with near isotropic resolution has
enabled high-quality CT angiography with excellent visualization of the
main renal
arteries. The diagnosis of renal artery stenosis requires meticulous technique, using thin collimation, fast table speed, and postprocessing 3D and maximal-intensity projections (see Chapter 1 for details). Para-axial and paracoronal images are reconstructed along the axes of the renal arteries. Images are acquired in the arterial phase.
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arteries. The diagnosis of renal artery stenosis requires meticulous technique, using thin collimation, fast table speed, and postprocessing 3D and maximal-intensity projections (see Chapter 1 for details). Para-axial and paracoronal images are reconstructed along the axes of the renal arteries. Images are acquired in the arterial phase.
 |
Figure 9.55. Renal artery stenosis in a 2-year-old boy with hypertensive crisis. A: Axial CT scan in the arterial phase shows marked narrowing in the left renal artery (arrow)
with poststenotic dilatation. The origin of the right renal artery is
not well seen at this level. There are indirect signs of stenosis,
including a small kidney with smooth contours and thinned renal cortex.
B: Posterior coronal 3D volume-rendered
image demonstrates the left renal artery stenosis and also shows a
normal-caliber right renal artery (RRA). Fibromuscular dysplasia was
found at the time of surgical reimplantation of the left renal artery
into the aorta. (See color insert.) |
Direct CT findings of renal artery stenosis are vessel narrowing and poststenotic dilatation (Fig. 9.55) (145).
Indirect findings corroborating the diagnosis include a small
ipsilateral kidney with a smooth contour, cortical loss, and a delayed
and prolonged nephrogram. A negative CT angiogram does not exclude the
diagnosis of renal artery stenosis given the relatively high frequency
of peripheral stenoses in children. Conventional renal angiography is
the definitive study for detecting peripheral branch stenoses or
narrowing of small accessory renal arteries.
Renal Arterial Infarction
Global infarction is usually the result of renal artery
occlusion from blunt abdominal trauma. Contrast-enhanced CT findings of
global (total) renal infarction include preservation of the renal
outline and complete absence of renal parenchymal enhancement and
contrast media excretion (Fig. 9.56). In some
cases, there may be a thin peripheral rim of cortical enhancement
(i.e., cortical rim sign) or central medullary enhancement as a result
of perfusion by capsular and ureteral vessels, respectively. The
cortical rim sign is usually not seen in the first few hours after
infarction, but it is a reliable sign of subacute
infarction. This sign is not specific for renal artery occlusion, and it can be seen in other diseases affecting renal hemodynamics, including renal vein thrombosis and acute tubular necrosis. Associated CT findings in cases of trauma include retroperitoneal hematoma, abrupt cutoff of an enhanced renal artery (Fig. 9.57), and retrograde filling of the renal vein (146).
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infarction. This sign is not specific for renal artery occlusion, and it can be seen in other diseases affecting renal hemodynamics, including renal vein thrombosis and acute tubular necrosis. Associated CT findings in cases of trauma include retroperitoneal hematoma, abrupt cutoff of an enhanced renal artery (Fig. 9.57), and retrograde filling of the renal vein (146).
 |
Figure 9.56.
Renal infarction secondary to acute traumatic occlusion of the left
renal artery. Nephrogram-phase CT shows a low attenuation left kidney
with capsular (white arrows) and medullary (black arrow) enhancement, secondary to intact capsular and ureteral vessels. |
 |
Figure 9.57.
Global infarction secondary to traumatic occlusion of the left renal
artery. Arterial phase image shows cutoff of main left renal artery (arrow) and absent enhancement of the left kidney. |
Segmental infarction may result from blunt abdominal
trauma, vasculitis, or embolus from an indwelling arterial line or
cardiac valvular vegetation. It also has been associated with systemic
lupus erythematosus and other connective tissue disorders (147).
Patients usually present with acute flank pain and hematuria. CT
findings include a wedge-shaped area that shows poor parenchymal
enhancement and a high-attenuation rim peripheral to the lesion
(cortical rim sign). The base of the lesion is typically oriented
toward the renal capsule, and the apex is oriented toward the renal
hilum. Atrophy of the infarcted area may be seen on follow-up
examination.
Renal Vein Thrombosis
Renal vein thrombosis is predominantly a disease of the
newborn, but it can occur in any age group. In neonates, it is usually
a complication of severe dehydration and associated hemoconcentration
secondary to blood loss, diarrhea, or sepsis. In older children, renal
vein thrombosis may be a result of trauma, neoplastic invasion of the
renal vein, or dehydration, and it is common in nephrotic syndrome.
Affected patients often present with flank pain, a palpable flank mass,
hematuria, and proteinuria. Most renal vein thrombosis is unilateral,
but bilateral involvement does occur. Pathologic findings include edema
and hemorrhage in the acute phase, followed by cellular infiltration
and fibrosis.
 |
Figure 9.58.
Renal vein thrombosis in a 5-year-old boy with nephrotic syndrome.
Axial CT in the nephrographic phase of enhancement shows an enlarged
right kidney with delayed function and hypodense thrombus extending
into the inferior vena cava (arrow). |
In acute thrombosis, the affected kidney is enlarged
with a prolonged nephrogram owing to decreased glomerular filtration
and tubular compression by interstitial edema. The renal vein is
distended and filled with low-attenuation clot (Fig. 9.58). Perirenal collateral veins and thickening of Gerota fascia may be seen in subacute or chronic venous thrombosis.
The ultimate fate of the kidney depends on the extent of
venous occlusion and the formation of venous collateral channels or
venous recanalization. If there is adequate venous drainage, allowing
continued arterial perfusion, the outcome is favorable. Collateral
vessels develop more often with thrombosis of the left kidney, since
gonadal, inferior adrenal, and inferior phrenic veins serve as
alternate routes for venous drainage. Right renal vein thrombosis is
associated with a higher incidence of hemorrhagic infarction as the
right kidney lacks these collateral veins. Calcifications within the
renal parenchyma, renal vein, or inferior vena cava may be seen on
follow-up examinations (Fig. 9.59) (148).
Renal Transplantation
Renal transplant complications are most often evaluated
with radionuclide imaging and sonography. CT may be of value in
identifying complications, such as abscess and posttransplant
lymphoproliferative disorder (PTLD), and it may help in distinguishing
among various fluid collections, including urinomas, lymphoceles,
abscesses, and hematomas (149,150,151). PTLD of the
kidney tends to be unilateral and unifocal (152,153). A round, solitary, hypoattenuating lesion without renal enlargement is most common (Fig. 9.60). Diffuse infiltration by PTLD with nephromegaly is a less frequent manifestation.
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kidney tends to be unilateral and unifocal (152,153). A round, solitary, hypoattenuating lesion without renal enlargement is most common (Fig. 9.60). Diffuse infiltration by PTLD with nephromegaly is a less frequent manifestation.
 |
Figure 9.59.
Chronic renal vein thrombosis. Non–contrast enhanced CT scan
demonstrates a bullet-shaped calcification in the right renal vein (arrow). |
Lymphoceles and urinomas are sharply marginated
low-attenuation masses. Urinomas will opacify following administration
of intravenous contrast medium. There will be no contrast excretion in
a lymphocele. CT features of abscess are a low-attenuation mass with an
enhancing wall; gas bubbles or an air–fluid level may be present.
Unfortunately, it is sometimes difficult to distinguish between gas in
the surgical site and an abscess in the immediate postoperative period.
A fresh hematoma is seen as a high-attenuation mass. As the blood clots
and lyses, its attenuation value decreases, and the appearance of a
chronic hematoma can be similar to that of an abscess, lymphocele, or
urinoma. In such cases, percutaneous needle aspiration may be needed
for differentiation. CT angiography can be used to evaluate suspected
renal artery stenosis, venous thrombosis, pseudoaneurysm formation, and
renal graft torsion (149).
 |
Figure 9.60. Posttransplant lymphoproliferative disorder. Contrast-enhanced CT demonstrates a soft tissue mass (arrow) in the transplant kidney. |
Urinary Tract Calcifications
Nephrocalcinosis
Nephrocalcinosis refers to a pathologic deposition of
calcium in the renal parenchyma. Common causes of nephrocalcinosis in
neonates and infants are furosemide therapy and renal tubular acidosis.
Less frequent causes include ACTH treatment, Bartter syndrome, Williams
syndrome (idiopathic infantile hypercalcemia), and hypophosphatasia. In
older children and adolescents, common causes of nephrocalcinosis are
renal tubular acidosis and oxaluria. Less frequent causes include
hypercalcemic states such as hyperparathyroidism, sarcoidosis,
hypervitaminosis D, milk-alkali syndrome, malignancy, Cushing syndrome,
and hyperthyroidism; parenchymal renal diseases including chronic
glomerulonephritis, mycoses, and medullary sponge kidney; and vascular
conditions such as acute cortical or tubular necrosis.
Nephrocalcinosis is easily recognized on unenhanced helical CT scans (Fig. 9.61), appearing as areas of increased parenchymal attenuation (154,155,156,157). Occasionally, the pattern of distribution can suggest a specific diagnosis (158). Multiple medullary calcifications have been described in prolonged ACTH therapy and hypophosphatasia, whereas
cortical calcifications have an association with oxalosis, cortical necrosis, and chronic glomerulonephritis.
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cortical calcifications have an association with oxalosis, cortical necrosis, and chronic glomerulonephritis.
 |
Figure 9.61. Nephrocalcinosis. Type II hyperoxaluria. Unenhanced axial CT shows extensive bilateral medullary nephrocalcinosis. |
Increased density in the renal medulla is not specific
for calculi, and it can also be seen in dehydration states and acute
tubular dysfunction (159). Acute tubular
dysfunction, also known as stasis nephropathy, occurs when
glycoproteins (the principal one being the Tamm–Horsfall protein)
accumulate within the tubules, causing temporary tubular obstruction.
It usually affects neonates, is transient, and resolves within the
first week of life. Sonography generally suffices for diagnosis.
Calcifications may also occur in renal masses.
Ap-proximately 5% to 10% of Wilms tumors contain calcification.
Calcifications also occur in renal cell cancer, lymphoma, rhabdoid
tumor, primitive neuroectodermal tumor, desmoplastic round cell tumor,
and ossifying renal tumor of infancy. Inflammatory masses and hematomas
also may calcify. Calcifications are a feature of xanthogranulomatous
pyelonephritis, renal tuberculosis, schistosomiasis, and Pneumocystis carinii
infection. An important pitfall to recognize is that debris within the
collecting system can be a cause of increased attenuation in the
urinary tract (160). A factor in separating debris from calculi is recognizing that debris has attenuation lower than calcium.
Urolithiasis
Urolithiasis refers to the presence of calculi within
the calyces, renal pelvis, or ureter. In children, it often is a
complication of underlying urinary tract obstruction and infection.
Other causes include renal tubular syndromes, such as renal tubular
acidosis, cystinuria, and glycinuria; enzyme disorders, such as
hyperoxaluria and xanthinuria; uric acid lithiasis owing to hereditary
hyperuricosuria and myeloproliferative states; the hypercalcemic states
mentioned above as well as hypercalcemia following chemo-therapy and
furosemide therapy.
Calculi are easily identifiable on unenhanced CT, even
at low-dose techniques, appearing as areas of high attenuation in the
calyceal system, ureteral lumen, or bladder (155).
The secondary signs of obstruction include hydro-nephrosis, ureteral
dilatation, renal enlargement, ureteral thickening, and perinephric
stranding (156).
Perinephric Disease
Perinephric disease may represent tumor, fluid,
infection, or hemorrhage. In children, perirenal disease is most often
a complication of trauma, surgery, or inflammatory disease.
Occasionally, pancreatitis is a cause of fluid collections in the
perirenal space or thickening of the renal fascia (161).
Acute hemorrhagic fluid collections typically have high attenuation,
similar to that of circulating blood, whereas chronic hematomas have
attenuation similar to urinomas. Urinomas result from disruption of the
renal collecting system and are usually low-attenuation fluid
collections, with attenuation values between -10 and +20 HU on
noncontrast CT examinations (162). They may opacify following administration of intravenous contrast medium (Fig. 9.62).
Perirenal abscess and inflammatory fluid collections, such as those
secondary to pancreatitis, have attenuation values closer to those of
soft tissue. Thickening of the renal fascia and perinephric stranding
are common in all disease processes. On the basis of CT alone, it may
be difficult to differentiate among the various causes of perinephric
disease, but the CT findings in conjunction with the clinical history
should allow a specific diagnosis. In some cases, percutaneous or
surgical aspiration or biopsy may be needed for diagnosis (162).
 |
Figure 9.62. Perinephric urinoma. Nephrographic phase CT scan shows a low-attenuation fluid collection in the right perinephric space (arrows).
There is hydronephrosis of the collecting system, owing to
ureteropelvic junction obstruction. Aspiration of the fluid yielded
urine. |
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