Renal, Bladder, and Adrenal Ultrasound

Imaging Technique

Kidneys

A renal US examination typically includes sonography of both kidneys, the perirenal areas, the aorta, inferior vena cava (IVC), and the urinary bladder. The American Institute of Ultrasound in Medicine provides guidelines for a satisfactory examination [1]. A sector or curved array transducer using frequencies between 2.25 and 5.0 MHz is recommended. The right kidney is examined from an anterolateral or direct lateral approach with the patient supine or in left lateral decubitus position, using the right lobe of the liver as a sonographic window. The left kidney is often more difficult to visualize because the spleen provides a more limited sonographic window. The left kidney is often obscured by bowel when scanned from the anterior abdomen. Placing the patient in right lateral decubitus position provides access to a more lateral and posterior approach through the spleen and psoas muscle. Multiple images of both kidneys are documented in longitudinal and transverse planes including the upper pole, middle section, and lower pole. Maximum renal lengths are recorded. Renal volumes may be calculated by measuring transverse and anteroposterior (AP) diameters from a mid-kidney transverse image. The standard formula (volume = length × width × AP diameter × 0.52) is utilized. The bladder lumen, wall thickness, and mucosal surface are documented. The retroperitoneum is examined for ureteral dilatation, adenopathy, or other abnormality.

Color flow and spectral Doppler are frequently utilized to confirm patency of the renal artery and vein, parenchymal blood flow, and the vascularity of any lesion detected. Power Doppler allows the most sensitive demonstration of renal vascularity [2,3].

Bladder

For US examination, the bladder should be moderately distended to stretch the wall and to better visualize the mucosal surface and bladder lumen. Images are obtained in transverse and longitudinal planes. Attention should be directed to the trigone area, ureteral orifices,

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and prostate gland. Transvaginal scanning will improve evaluation of the bladder in women. Large cystic pelvic masses may be mistaken for the bladder. When this is suspected, the bladder should be emptied by voiding or Foley catheter and rescanned.

Adrenal Glands

Although small and tucked away in the retroperitoneum normal and abnormal adrenal glands can be visualized by US in most patients with a little effort and attention to anatomic landmarks. Normal adrenal glands are prominent and easily seen in the third-trimester fetus and the newborn, but require exacting technique to visualize in most adults. Adrenal abnormalities may be detected during routine renal sonography. Careful attention to the location of the adrenal glands is the key to recognizing them on US. The right adrenal gland is truly suprarenal and is best visualized by a posterolateral approach in transverse plane looking for the adrenal gland just above the right kidney, between the liver and right crus of the diaphragm posterior to the IVC as it enters the liver. The left adrenal gland is imaged by a posterolateral approach in coronal plane through the long axis of the left kidney. The left adrenal gland is seen between the upper pole of the left kidney and the aorta. High-resolution, real-time sonography allows visualization of normal adrenal glands in 71-92% of adults [4].

Anatomy

Kidneys

The normal adult kidney is bean-shaped with a smoothly convex, often lobulated, outer border (Fig. 3.1). The kidney is well defined by a thick fibrous capsule outlined by echogenic perirenal fat. This echogenic fat continues into the renal sinus, entering at the anteromedially oriented renal hilum and filling the middle of the kidney. The outer renal cortex is equal to, or slightly less than, the liver and spleen in echogenicity. Renal cortical echogenicity distinctly greater than liver parenchymal echogenicity is highly indicative of impaired renal function [5]. Liver parenchymal echogenicity distinctly greater than renal cortical echogenicity is highly indicative of diffuse hepatocellular fatty infiltration [6]. The cortex that extends centrally into the kidney is called septal cortex as it surrounds and separates the less echogenic medullary pyramids. Fusion of septal cortex from adjacent lobes produces a normal, but often bulbous, mass of cortex referred to as a column of Bertin (see Fig. 3.3) [7]. Distinct differentiation of cortical and medullary echogenicity is a sign of a

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normal kidney. In infants up to 24 months of age, the echogenicity of the cortex is significantly greater than the renal cortex in adults and older children (Fig. 3.2). Its echogenicity commonly exceeds liver parenchymal echogenicity. The medullary pyramids remain echolucent and prominent. This appearance has been mistaken for hydronephrosis.

Figure 3.1 Normal Adult Kidney. The renal cortex (short arrow) is equal in echogenicity to the liver parenchyma (l). The renal pyramids (long arrow) are slightly hypoechoic compared to the renal cortex. The septal cortex extends between the medullary pyramids. The central renal sinus (s) is invested with echogenic fat. The contour of the kidney is sharply defined by fat in the perirenal space. The length of the kidney is measured between cursors (+).

Figure 3.2 Normal Newborn Infant Kidney. Longitudinal view of the normal right kidney (between cursors, +, x) of a newborn infant demonstrates echogenicity of the cortex to be slightly greater than the echogenicity of the liver (L). The medulla (arrows) is significantly less echogenic.

Persistent fetal lobation is a common renal anatomic variant [8]. The normal kidney is made up of 12-18 separate lobes consisting of a medullary pyramid surrounded by subcapsular and septal cortex [9]. A single lobe drains into a simple calyx. When several lobes drain into a single calyx, the calyx is considered to be a compound calyx. The fetal lobes act as tiny independent kidneys early in fetal life but progressively fuse into a single kidney with maturation. Incomplete lobular fusion is common and results in V-shaped indentations on the renal surface (Fig. 3.3). A prominent indentation between the upper and lower portion of the kidney has been called the junctional defect [7]. These normal V-shaped defects should not be mistaken for parenchymal scars.

Calyces unite to form the renal pelvis, which exits the renal sinus at the hilum. The calyces and pelvis are usually collapsed and are not seen as discrete structures within the renal sinus. When patients are well hydrated, high urine output causes mild normal dilatation of the calyces and pelvis. The renal pelvis may also be seen as a prominent fluid-filled structure when it is “extrarenal,” that is, primarily outside of the renal sinus. Lower surrounding tissue pressure allows the pelvis to be chronically dilated. These normal variations must be differentiated from hydronephrosis.

The main renal arteries are solitary in 60% of individuals and multiple and smaller in the remainder. The renal arteries arise from the lateral aspects of the aorta approximately 1 cm below the origin of the superior mesenteric artery. The right renal artery passes behind the IVC causing a small but prominent indentation on the posterior wall of the IVC (see Fig. 2.11). The left renal artery has a short direct course to the left kidney. Renal arteries are more commonly multiple when the kidney is malpositioned or malrotated. Supplemental renal arteries may course directly into the polar regions of the kidney without coursing through the renal hilum. Renal veins are usually solitary. The right renal vein is anterior to the right renal artery and courses anterosuperiorly to enter the IVC usually somewhat above the level of the right renal hilum. The left renal vein courses transversely anterior to the aorta to enter the IVC. The left gonadal vein enters the left renal vein just outside the left renal hilum. The right gonadal vein enters the IVC directly just below the junction of right renal vein and IVC.

The Doppler spectrum of the normal renal artery shows continuous forward flow into the kidney with relatively high velocities maintained throughout diastole indicating low intrarenal vascular resistance. Maximum normal peak systolic velocity is 180 cm/sec. Normal resistive index (RI) is below 0.70. The Doppler spectrum of the renal vein shows continuous venous flow with slight respiratory undulation.

Doppler spectra can be obtained from tiny intrarenal arteries (interlobar and arcuate arteries), whether they are actually visualized or not, by placing a Doppler sample volume

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at the corticomedullary junction along the borders of the pyramids. The RI, calculated from the spectral display, has diagnostic value in a number of disease states. Like the main renal artery, RI of 0.70 is the upper limit of normal for intrarenal arteries. A number of representative readings should be averaged to determine a single representative value [10].

Figure 3.3 Normal Renal Lobes. Line drawing illustrates the basic anatomy of the renal lobes. The normal adult kidney is made up of approximately 14 lobes, which are the basic structural unit of the kidney. Each lobe resembles a kernel of corn and consists of subcapsular and septal cortex containing glomeruli and a central medulla (medullary pyramid) containing collecting tubules and portions of the loops of Henle. The collecting tubules drain urine into calyces. Lack of complete fusion of the renal lobes results in fetal lobulation with a V-shaped defect on the capsular surface marking the junction of the lobes. Fusion of the lobes results in a smooth capsular surface. A column of Bertin refers to fusion of the septal cortex of two adjacent lobes. A prominent column of Bertin may be mistaken for a renal mass. The junctional defect is a prominent V-shaped defect in the cortical surface that marks the junction of lobes from the upper pole with lobes of the lower pole. Renal parenchymal scarring, occurring as a result of infarction, reflux nephropathy, or renal infection, produces a U-shaped defect that overlies the calyx. The calyx underlying the parenchymal scar is normal in shape with infarction but is blunted as a result of reflux nephropathy or recurrent infection.

Characteristics of the normal kidney are summarized in Table 3.1.

Bladder

The exact shape and appearance of the bladder varies with the degree of distension. When empty or nearly empty, the bladder wall is thick and somewhat irregular due to contraction of the wall musculature and wrinkling of the mucosa. With filling, the wall thins and the mucosa flattens to a smooth, well-defined surface. The normal bladder wall does not exceed 4 mm in thickness when the bladder is distended. The trigone is defined by the slight protuberances of the ureteral orifices and the more inferior urethral opening. The ureteral orifices are most easily located by identifying ureteral jets. Periodic ureteral peristalsis (average rate, 6 waves per minute) squirts jets of urine into the bladder lumen. These jets are seen on gray-scale US as tiny streams of microbubbles, and on color flow US as flashes of color projecting into the bladder lumen (Fig. 3.4) [11]. The urethral orifice is seen as a slight V-shaped depression at the bladder base. Enlargement of the prostate elevates the bladder base. Postvoid bladder volume does not normally exceed 22 mL. Normal

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urine is anechoic. Reverberation artifact commonly projects into the bladder from the anterior bladder wall. Residual urine after voiding is quantified by the standard formula: volume = width × height × length × 0.52 (Table 3.2).

Table 3.1: US Characteristics of Normal Kidneys

Feature	Normal Characteristic
Size [100]	Length: Adult: 9-13 cm (decreases with age) Male: 11.4 cm median length Female: 10.9 cm median length Volume: (length × width × height × 0.52) Adult: Male: range: 109-194 mL 151 mL median volume Female: range: 91-151 mL 122 mL median volume Parenchymal thickness: Normal >10 mm
Echogenicity of cortex	Adult: renal parenchyma echogenicity equal to, or slightly less than, normal liver parenchyma Neonate: renal parenchyma echogenicity usually greater than normal liver parenchyma
Echogenicity of medulla	Adult: slightly less than renal cortex Neonate: much less than renal cortex
Surface	Smooth, well-defined, slightly lobulated with V-shaped notches between lobes
Peak systolic velocity in main renal artery	Normal <180 cm/sec
Renal/aortic velocity ratio	Normal <3.5
Resistive index–intrarenal arteries and main renal artery	Adult: Normal <0.70 Child <5 years: Normal commonly >0.70
Systolic rise time (time to early systolic peak) in main renal artery

Adrenal glands

Adrenal glands are composed of cortex and medulla, which have different embryologic origin, function, and US appearance. The cortex secretes the steroid hormones cortisol, androgens, and aldosterone, whereas the medulla secretes catecholamines. The cortex is hypoechoic to liver parenchyma, whereas the medulla is near isoechoic with fat (Fig. 3.5).

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Adrenal glands are relatively larger in the fetus and newborn because of the presence of the prominent fetal cortex that atrophies by 1 of year of age.

Figure 3.4 Normal Ureteral Jet. Ureteral peristalsis produces a flash of color as urine squirts into the bladder lumen (see Color Figure 3.4).

Table 3.2: US Characteristics of Normal Bladder

Feature	Normal Characteristic
Size (bladder volume)	Post-void volume
Measure length, width, and height. Use formula L × W × H × 0.523 = Volume.	Adult: <22 mL
	Child: <10 mL
Thickness of bladder wall	Adult: <4 mm when distended
	Child: <4 mm when distended
Appearance of bladder wall	Smooth, thin, well defined when distended
	Slightly irregular and thickened when contracted

Kidneys

Congenital Anomalies

Horseshoe Kidney

Horseshoe kidney describes the appearance of congenital fusion of the lower poles of both kidneys [12]. This is the most common renal fusion anomaly with a prevalence of 1:400

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individuals. One-third of affected patients have additional congenital anomalies. Horseshoe kidneys are prone to urinary stasis, infection, calculus formation, hydronephrosis, vesicoureteral reflux, anomalous blood supply, and have increased susceptibility to traumatic injury.

Figure 3.5 Normal Adrenal Glands. US images show the normal adrenal glands (long arrows) in the fetus at 35 weeks (A), the newborn (B), and the adult (C). The cortex is hypoechoic and the medulla is echogenic. The short arrows indicate the inferior vena cava. l, liver; S, fetal spine.

Figure 3.6 Horseshoe Kidney in an Infant. Transverse image shows the fusion (arrows) of the two kidneys (RT, LT) anterior to the spine (S).

The key to US diagnosis is demonstration of the isthmus connecting the kidneys across the midline (Figs. 3.6, 3.7) [12]. The isthmus crosses the midline anterior to the IVC and aorta just below the origin of the inferior mesenteric artery. The isthmus may be functioning renal parenchyma with echogenicity identical to the kidney or it may be thinner and more echogenic fibrous tissue. In 15% of cases, the isthmus may not be demonstrable by US.
The kidneys are low in position because the isthmus encounters the inferior mesenteric artery stopping the normal ascent of the kidneys. A definitive sign of low position is the left kidney lying caudal to the inferior tip of the spleen.
The long axes of the kidneys are reversed with the lower poles positioned closer together than the upper poles. The kidneys appear curved or bent and the lower poles are ill defined, narrowed, and elongated (Fig. 3.7). The lower poles of the kidneys are not defined on routine longitudinal images. The orientation of the renal pelvis is anterior rather than anteromedial.

Figure 3.7 Horseshoe Kidney in an Adult. A. Longitudinal image of the left kidney shows elongation of the lower pole (arrows) without visualization of its lower margin. B. Transverse image over the spine shows the connection of the lower poles (arrow) of both kidneys.

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Collecting System Duplication

Duplication of the collecting system is the most common congenital anomaly of the urinary tract. Duplication is complete when two separate ureters drain separate portions of one kidney. This anomaly is associated with ureteroceles, obstruction, and reflux. Incomplete duplication ranges from a bifid renal pelvis to duplex ureters that join before entering the bladder through a single orifice. Because non-dilated ureters are seldom demonstrated by US, precise classification is not often possible by US alone.

Two central echogenic sinuses separated by a band of parenchyma suggest some degree of collecting system duplication, statistically most often a bifid pelvis without ureteral duplication.
With complete duplication, the ureter draining the lower pole collecting system inserts in the normal location at the bladder trigone. The ureter draining the upper pole collecting system always inserts lower and medial to the orifice of the lower pole system. This ectopic location, sometimes outside of the bladder in the prostate or vagina, often results in ureteral obstruction and formation of an ectopic ureterocele. The ectopic ureterocele may mechanically disrupt the valve mechanism of the lower pole ureteral insertion and result in vesicoureteral reflux (VUR).

Stones and Obstruction

Renal Stone Disease

Urolithiasis has its highest prevalence in men aged 20-40 years. Approximately 12% of men and 5% of women experience renal colic caused by stone disease at least once in their lifetimes. Most renal stone disease is idiopathic.

Both radiopaque and radiolucent calculi produce highly echogenic foci with acoustic shadowing (Fig. 3.8).
US reliably demonstrates stones >5-mm size, but smaller stones are commonly not detected [13]. Up to 40% of the small stones present may be missed [14].
US is inaccurate in measuring stone size.
Calcifications in renal arteries or within tumors must not be mistaken for renal stones.
Obstructing stones in the ureter are detected by following the dilated ureter to the point of obstruction (Figs. 3.9, 3.10). Transvaginal or transrectal US are useful adjunctive techniques in the demonstration of distal ureteral calculi [15].

Figure 3.8 Renal Calculi. A. Numerous stones are seen within dilated calyces as echogenic foci (closed arrows) with acoustic shadowing (open arrows). B. Solitary stone produces a bright echogenic focus (arrow) in the renal sinus and casts an acoustic shadow.

Figure 3.9 Acute Obstruction with Impacted Distal Ureteral Stone. A. Acute obstruction produces minimal dilatation of the renal calyces, although the patient experienced severe pain. B. Longitudinal image of the bladder reveals a swollen uterovesical junction (arrow) with a small impacted stone that shadows.

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A color Doppler “twinkling sign” has been described within or just distal to urinary tract calculi [16]. This appears as a comet tail of alternating bands of red and blue colors. The artifact is useful in identification of calculi and must not be mistaken for blood flow. The artifact is accentuated by increasing Doppler power.

Figure 3.10 Moderate Hydronephrosis. A. Rounded calyces filled with urine (arrows) connect to the fluid distended pelvis (P). Cursors (+) mark the poles of the kidney. B. Hydronephrosis terminates abruptly at a calculus (arrow) impacted at the ureteropelvic junction. Note the acoustic shadow (arrowhead) emanating from the stone.

Figure 3.11 Marked Hydronephrosis. The renal collecting system is markedly dilated, and the renal parenchyma is thinned (arrow), indicating long-standing hydronephrosis. The cause of hydronephrosis in this case was diabetes insipidus. Cursors (+) mark the poles of the kidney.

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Hydronephrosis and Obstruction

US demonstration of hydronephrosis is not, by itself, diagnostic of urinary obstruction. Hydronephrosis is an anatomic finding, not a functional one, and is caused by acute and chronic urinary obstruction, VUR, pregnancy, high urine output states (diabetes insipidus), and congenital dilatation of the collecting system (prune belly syndrome). Hydronephrosis may be absent or minimal when obstruction is acute or incomplete (Fig. 3.9), and hydronephrosis may persist for months after obstruction is relieved. Confirmation of functional urinary obstruction must be provided by Doppler US findings, or by additional imaging (intravenous urography, radionuclide studies).

Dilatation of the calyces, pelvis, and ureter constitutes the anatomic finding of hydronephrosis (Fig. 3.10). Calyces appear rounded and cystic and communicate with the renal pelvis. Well-hydrated normal patients may show mild pelvicalyectasis that is accentuated when the bladder is full. Re-imaging after emptying the bladder shows resolution of this normal dilatation.
Pelvicalyceal dilatation is most severe when obstruction is long-standing (Fig. 3.11). Chronic obstruction is often associated with diffuse parenchymal atrophy. Proximal obstruction causes greater dilatation than distal obstruction. Acute obstruction, even when complete, often causes only mild hydronephrosis (Fig. 3.9).
Physiological hydronephrosis is seen in the third trimester of 90% of pregnancies with the right side being more commonly and more severely affected [17].
Parapelvic cysts mimic the US appearance of hydronephrosis (Fig. 3.12). US differentiation is difficult. The correct diagnosis is confirmed most easily by referring to previous imaging studies that show the presence of renal sinus cysts causing compression and attenuation of the collecting system. Clues to US diagnosis include non-uniform size and appearance of the cysts, the presence of uninvolved areas of the renal sinus, and the observation that the parapelvic cyst does not abut the tip of the medullary pyramid.
Extrarenal location of the renal pelvis often results in dilatation of the pelvis without associated dilatation of the calyces or ureter. This is a normal variant that should not be mistaken for pathologic hydronephrosis.
Demonstration of ureteral jets caused by periodic ureteral peristalsis confirms patency of the ureter [11]. Gray scale US shows a stream of low-level echoes extending from the ureteral orifice into the bladder lumen. Color Doppler accentuates detection of this fluid jet (Fig. 3.4).
Absence of a ureteral jet on the affected side during several minutes of observation confirms complete obstruction [11]. This finding is unreliable in pregnancy [18].
Intrarenal artery RI >0.70 is highly suggestive of obstruction, provided (a) technique is adequate and waveform is large enough to be clearly measured; (b) the patient is older than 4-5 years (RI is normally >0.70 in children under 5 years); and (c) significant
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medical renal disease is not present. Elevated RI is a more reliable sign of obstruction when the opposite kidney has a normal RI. Obstruction may elevate the intrarenal RI before significant hydronephrosis is present. RI values return to normal after obstruction is relieved, even though pelvicalyectasis may still be present [19].
Pregnancy-induced hydronephrosis does not typically elevate the intrarenal artery RI. RI >0.70 is highly suggestive of obstructing calculus in a symptomatic pregnant patient [20].
Urinary obstruction in the newborn may be overlooked on US examinations performed immediately after birth because of dehydration and limited renal function. Infants with antenatal demonstration of fetal pyelectasis are best evaluated at 4-7 days with the examination repeated at 6 weeks [21].

Figure 3.12 Parapelvic Cysts Mimic Hydronephrosis. A. Longitudinal US image shows fluid-filled structures (c) in the renal sinus that mimic dilated calyces and pelvis. Note that the dilated “calyx” is separated from the renal parenchyma by a layer of echogenic fat (arrow). Compare to the images in Figure 3.10. True dilated calyces directly abut the tip of the medullary pyramid. Cursor (+) marks the upper pole of the kidney. B. CT scan shows the parapelvic cysts (c), which compress the contrast-filled collecting system (arrows).

Vesicoureteral Reflux and Reflux Nephropathy

VUR is a common problem of childhood associated with frequent urinary tract infections and progressive renal damage if untreated. VUR is seen in adults with neurogenic bladders and bladder outlet obstruction.

VCUG (voiding cystourethrography) is the imaging method of choice for demonstration of VUR. A normal renal US does not exclude VUR [22].
VUR is a common cause of fetal and neonatal hydronephrosis. Intermittent, waxing and waning hydronephrosis seen over several minutes of observation suggests VUR [23]. The condition may be unilateral or bilateral.
Findings of reflux nephropathy include focal renal parenchymal scarring, usually most prominent at the upper pole with associated dilatation of the underlying calyx (see Fig. 3.40). The renal pelvis is spared. Chronic infection progressively scars the kidney and impairs renal growth.
Serial renal length measurement is a sensitive method of monitoring renal growth in children with VUR [24].

Figure 3.13 Echogenic End-Stage Kidney. The kidney (between cursors, +) is significantly more echogenic than the adjacent liver parenchyma (l). Differentiation of cortex from medulla, and even from the renal sinus, is lost. The kidney is small, measuring only 7 cm, indicating it is end stage and unlikely to respond to any form of therapy. The patient has chronic renal failure.

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Diffuse Renal Parenchymal Disease

Renal Failure

In the clinical setting of impaired renal function, US is used to demonstrate the size and appearance of the kidneys and to detect the rare occurrence of bilateral obstruction presenting with renal failure. US diagnosis of a specific cause of renal failure is exceedingly rare [25].

Diffuse increased echogenicity of the parenchyma of both kidneys is the US hallmark of diffuse renal parenchymal disease (Fig. 3.13). Corticomedullary differentiation is usually absent.
End stage kidneys are small and echogenic (Fig. 3.13).
US is commonly used to guide renal biopsy to provide a specific diagnosis and identify a hopefully treatable cause of renal failure. Kidneys smaller than 9 cm in length in adults are usually end-stage kidneys unresponsive to treatment [25,26]. Biopsy is seldom beneficial to these patients.
An extracapsular rim of perirenal lucency (“kidney sweat”) has been described in 14% of patients with renal failure [27]. The significance of this finding is unknown.

Diabetic Nephropathy

Diabetes mellitus is the most common cause of chronic renal failure in the United States. Patients develop proteinuria, hypertension, and progressive renal failure over the course of their disease.

Bilateral renal enlargement (>13 cm length) with normal parenchymal echogenicity is seen early in the course of disease [28].
With time the kidneys shrink, become diffusely echogenic, and show high (>0.70) intrarenal artery RI.

Human Immunodeficiency Virus-Associated Nephropathy

Nephropathy associated with human immunodeficiency virus (HIV) infection is an important cause of AIDS morbidity. Patients present with rapid deterioration of renal function and proteinuria [29].

Enlarged kidneys with increased cortical echogenicity are characteristic findings (Fig. 3.14) [30].
Additional findings include a globular appearance to the kidney, decreased renal sinus fat, and heterogeneous parenchyma with echogenic striations [29].

Figure 3.14 HIV-Associated Nephropathy. The renal parenchyma (between cursors, +) is distinctly more echogenic than the liver parenchyma (l). The renal sinus (s) lacks echogenic fat. Both kidneys measured large (15 cm). These findings are characteristic of HIV nephropathy.

Echogenic Renal Pyramids

Increased echogenicity of the medullary pyramids is usually a non-specific finding of metabolic disease. Nephrocalcinosis is the most common cause, but numerous other diseases may cause this finding (Table 3.3) [31].

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Echogenicity of the renal pyramids exceeds the echogenicity of the renal cortex (Fig. 3.15). The condition is bilateral. Acoustic shadowing is usually absent. Renal cortical echogenicity is normal.

Renal Tumors

Renal Cell Carcinoma

Renal cell carcinoma (RCC) accounts for 90% of solid renal tumors. When a solid renal mass is encountered, the US examination should be extended to examine the retroperitoneum for nodal metastases and should utilize Doppler to look for extension of tumor into the renal vein or IVC. The tumor is often clinically silent until it becomes large. Small “incidental” RCC may be discovered by routine renal US [32].

Table 3.3: Causes of Increased Echogenicity of the Renal Pyramids

Infants and Children	Adults
Medullary nephrocalcinosisA	Medullary nephrocalcinosis
Furosemide therapy (for bronchopulmonary dysplasia)	Medullary sponge kidney
Vitamin D therapy (for rickets or hypophosphatemia)	Hyperparathyroidism
Renal tubular acidosis	Renal tubular acidosis
Idiopathic hypercalcemia	Hypercalcemia
Absorptive hypercalciuria	Hypercalciuria
Williams syndrome	Vascular congestion
Protein deposition	Sickle hemoglobinopathies
Newborn dehydration	“Urate deposition
Vascular congestion	Gout
Sickle cell disease	Hyperuricemia
Infection
Candida
Cytomegalovirus
Urate deposition
Lesch-Nyhan syndrome
Metabolic diseases
Glycogen storage disease, type 1
Fanconi syndrome
Renal dysplasia

Figure 3.15 Echogenic Renal Pyramids. The renal pyramids (white arrows) are markedly echogenic (instead of echolucent). Acoustic shadows (black arrows) emanate from some of the pyramids in this case of medullary nephrocalcinosis. Cursors (+) mark upper and lower poles of the kidney.

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Most RCC are solid tumors that may be hyperechoic, isoechoic, or hypoechoic compared to renal parenchyma (Fig. 3.16). Tumors commonly have a slightly more heterogeneous echotexture than parenchyma. They cause a focal bulge that distorts the margin of the kidney or impinges on the renal sinus.
Necrosis, hemorrhage, and cystic degeneration cause intratumoral cystic spaces (Fig. 3.17).
Calcification is common (up to 18%) and variable in appearance: punctate, coarse, central, peripheral, or curvilinear (Fig. 3.17).
Cystic forms of RCC most often have thick walls and internal debris [33]. RCC arising within simple cysts are rare and appear as cysts with a mural nodule.
Multicystic form of RCC has thick walls (>2 mm) and thick septations (Fig. 3.18).

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Doppler shows prominent vascularity with high velocity flow in most tumors. Absence of hypervascularity does not exclude malignancy, because some RCC are hypovascular.
Metastatic lymphadenopathy is visualized as hypoechoic solid nodules near the renal vessels and around and between the aorta and IVC.
Tumor thrombus within the renal vein or IVC appears as solid tissue enlarging the vein (Fig. 3.19) [34]. Color flow US may show venous blood flow diverting around the tumor thrombus and, sometimes, arterial flow within the tumor thrombus. Venous flow within the vein is absent if the vein is completely occluded.

Figure 3.16 Echogenic Renal Cell Carcinoma. A. Initial US shows a small, solid echogenic mass (arrow) in the renal parenchyma. The lesion resembles angiomyolipoma; however, CT failed to demonstrate intratumoral fat. B. US scan 6 months later shows enlargement of the tumor (arrow, between cursors, +). Surgical excision confirmed renal cell carcinoma. The gallbladder (G) is seen anterior to the kidney in both images.

Figure 3.17 Renal Cell Carcinoma with Hemorrhage and Calcification. This tumor (between fat arrows) expands from the upper pole of the kidney (K) and has central low density representing necrosis and hemorrhage. Punctate calcification (long arrow) is also present within the tumor.

Angiomyolipoma

Angiomyolipoma (AML) is a common benign renal tumor that contains variable amounts of blood vessels (angio), smooth muscle (myo), and fat (lipoma) [35]. AML is multiple and bilateral in patients with tuberous sclerosis, but is more commonly an isolated lesion discovered incidentally by US. Most tumors are asymptomatic, but large tumors may bleed, especially during pregnancy, or cause flank pain or a palpable mass.

Tumor appearance depends upon the proportion and distribution of the tumor elements (Fig. 3.20) [36].
A well-defined, homogeneous hyperechoic lesion is the classic appearance of an AML that is predominantly fat (Fig. 3.21).
Lesions with minimal fat are typically isoechoic to renal parenchyma [37].

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Tumors may be markedly heterogeneous with a mixture of fat, smooth muscle, and blood vessels (Fig. 3.22).
Doppler demonstrates internal tumor vascularity in large tumors but often not in small ones. Spectral Doppler shows no specific findings.
AML is difficult to differentiate from RCC when the renal tumors are small (<3 cm) and echogenic (Fig. 3.21) [38]. Signs that favor RCC over AML include the presence of intratumoral cystic spaces, a peripheral hypoechoic rim, or intratumoral calcification [39,40]. These findings are all rare in AML. Acoustic shadowing is sometimes seen with AML, but not with RCC [39].
CT confirmation is recommended for lesions discovered on US that are believed to be AML [35,36].
AML show significant growth when followed by US over time [41].

Figure 3.18 Multicystic Renal Cell Carcinoma. A multicystic mass (arrows) with prominent solid components extends exophytically from the kidney (K). Acoustic enhancement is seen deep to the mass.

Figure 3.19 Tumor Invasion of Renal Vein and IVC. Transverse image shows tumor (T) extending from the right kidney and expanding into the renal vein (arrows) and inferior vena cava (IVC). a, aorta; s, spine.

Figure 3.20 Angiomyolipoma. This predominantly fatty tumor (arrows) extends from the upper pole of the kidney (k) where it becomes indistinguishable from the perirenal fat.

Figure 3.21 Small Angiomyolipoma. This tumor was shown by CT to consist almost entirely of fat. US shows a small echogenic mass (arrow). Note the similarity to the echogenic renal cell carcinoma shown in Figure 3.16. Arrowheads mark the upper and lower poles of the kidney.

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Transitional Cell Carcinoma

Transitional cell carcinoma (TCC) arises from the transitional epithelium that lines the renal collecting system, ureter, and bladder [42]. TCC of the renal pelvis and ureter is much less common than TCC of the bladder. TCC may be papillary (85%) with a frondlike growth pattern or infiltrating with plaque-like lesions, wall thickening, and stricture.

TCC appears as a central hypoechoic or isoechoic mass that replaces the echogenic renal sinus fat [42].
Obstruction by the tumor results in focal calyceal or renal pelvis dilatation.
Infiltrating tumors cause focal thickening of the wall of the collecting system.
Whereas most tumors are hypovascular, larger and high-grade tumors may show visible vascularity on color Doppler [43].
Small lesions are easily overlooked with US unless some degree of obstruction is present.
TCC occasionally have coarse punctate calcifications [44].
TCC of the ureter appears as intraluminal hypoechoic soft tissue with a variable degree of proximal hydronephrosis [45].

Renal Lymphoma

The kidney contains no lymphoid tissue, so nearly all cases of renal lymphoma occur by hematogenous dissemination or direct extension in patients with systemic lymphoma. The

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kidneys are one of the most common sites of extranodal lymphoma. Renal involvement is particularly common in immunocompromised patients [46]. Non-Hodgkin’s lymphoma is most common. Most patients have no urinary symptoms.

Figure 3.22 Heterogeneous Angiomyolipoma. US shows a markedly heterogeneous mass (between arrows) reflecting the mixture of tissue elements in this angiomyolipoma.

Renal lymphoma is typically hypoechoic, homogeneous, and bilateral (75%) [47]. Calcification is extremely rare. Cystic change is also very rare and is seen only in patients with tumor necrosis induced by chemotherapy [46].
Multiple, small (1-3 cm), bilateral, solid, hypoechoic tumors are most common (60% of cases) [46]. Rarely, the multiple renal lymphomatous masses may be unilateral.
Direct renal invasion (25-30%) into the renal sinus from contiguous retroperitoneal lymphoma is typically nodular, homogeneous, and hypoechoic. Bulky retroperitoneal adenopathy typically envelops the renal artery and vein, IVC, and aorta. The blood vessels remain patent despite encasement, a finding that is typical of lymphoma.
Solitary homogeneous hypovascular solid tumor (10-20%) may be indistinguishable from RCC. Solitary lymphoma masses can reach 15 cm in size. A heterogeneous hypervascular lesion with cystic necrosis or calcification favors RCC.
Disease may invade the perirenal space and surround the kidney with or without directly involving the kidney. This results in a hypoechoic tumor halo partially or completely surrounding the kidney. This pattern of involvement is virtually pathognomonic of lymphoma, but is uncommon.
Diffuse infiltration of the renal interstitium globally enlarges the kidney with minimal or no alteration of shape or echotexture [47].
Enlarged retroperitoneal lymph nodes are seen in only 50% of cases.

Renal Leukemia

More than 50% of children and 65% of adults who die of leukemia have renal involvement at autopsy [47]. Acute lymphoblastic leukemia is the most common form to involve the kidney.

Bilateral, global renal enlargement caused by diffuse, interstitial leukemic infiltration is most common [47]. Corticomedullary differentiation is usually lost.
Discrete renal masses resemble lymphoma but are uncommon with leukemia.

Metastases to the Kidney

Metastases to the kidney are usually asymptomatic. They are nearly always discovered in patients with a diagnosed malignancy that is already metastatic elsewhere. Lung, breast, and gastrointestinal carcinomas are the most common primary neoplasms [47].

Metastases to the kidney resemble lymphoma on US (Fig. 3.23) [47].
Multiple bilateral circumscribed solid renal masses in a patient with associated metastases in other organs are most common [48].
Solitary renal mass in a patient with a history of non-renal malignancy, but without known metastases, will usually be an RCC. However, metastases to the kidney from colon cancer will often be solitary, large, and cannot be differentiated from RCC without biopsy.

Oncocytoma

Oncocytoma is an uncommon benign solid renal tumor that arises from the proximal tubules. It occurs most often in men in their 60s.

Well-defined solid mass is the usual appearance. A stellate central scar is characteristic but not pathognomonic. No imaging finding reliably distinguishes this tumor from RCC [49]. Diagnosis is made by surgical excision or biopsy (Fig. 3.24).

Figure 3.23 Metastasis to the Kidney. A subtle mass (arrows) causes a focal bulge in the contour of the kidney and disruption of the parenchymal echotexture. This solitary mass proved to be a metastasis from lung carcinoma.

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Wilms Tumor

Wilms tumor (also called nephroblastoma) is a malignant tumor of childhood that arises from embryonal nephrogenic tissue [50]. Mean age of diagnosis is 3 years. It is the most common solid malignant abdominal tumor found in children. Metastases to lung and liver are most frequent [47].

The tumor is expansile, replaces renal parenchyma, and forms a pseudocapsule of fibrous tissue and compressed renal parenchyma at its border [47]. Tumors are bilateral in 4-13% of cases [51].
The tumor is primarily solid (Fig. 3.25) but is typically heterogeneous with hypoechoic and anechoic areas of necrosis and cyst formation [51].

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Tumor invasion of the renal vein and IVC may occur with findings similar to RCC.
Calcification is present in 9% of Wilms tumors.
Echogenic fat is present in some tumors and is not a sign of a benign AML in children as it is in adults [51].

Figure 3.24 Oncocytoma. Extending from the kidney (k) is a solid mass (arrows) with central echogenicity. It is indistinguishable from a renal cell carcinoma. Surgical excision confirmed benign oncocytoma.

Figure 3.25 Wilms Tumor. A well-defined solid mass (between arrows) arises from the kidney (k) of a 4-year-old boy.

Nephroblastomatosis

Nephroblastomatosis refers to the presence of fetal renal tissue (mesoblastic blastema) in the renal parenchyma of infants and children. Most Wilms tumors and most multilocular cystic nephromas arise from these abnormal rests of benign tissue [52]. Nephroblastomatosis is a common feature of Beckwith-Wiedemann syndrome. The nephrogenic rests may be microscopic, multinodular, or diffusely infiltrating [51,52].

Enlarged kidneys with loss of corticomedullary differentiation are characteristic of diffusely infiltrating nephroblastomatosis. Renal echogenicity may be normal or increased. Cysts of varying size may be present.
Multiple homogeneous hypoechoic small masses are a less common appearance. Some nodules may appear hyperechoic.
Children with documented nephroblastomatosis are followed at regular intervals for progressive enlargement or other signs of developing Wilms tumor [52].

Mesoblastic Nephroma

Mesoblastic nephroma is a benign tumor of infancy, most commonly diagnosed at 2 months of age and rare after 6 months of age [47]. The tumor is infiltrating with benign spindle cells growing between nephrons.

The tumor is predominantly solid and unencapsulated with indistinct margins. Tumor replaces most of the renal parenchyma.
Homogeneous solid hypoechoic mass is the most common appearance [47]. Concentric rings of alternating echogenicity have been reported as a characteristic appearance.
Although necrosis is rare, some tumors develop cystic areas and appear quite heterogeneous.

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Renal Pseudotumors

Islands of normal parenchyma may resemble renal tumors.

Pseudotumors are identical in echogenicity to normal renal parenchyma. Contrast-enhanced CT is definitive in the diagnosis of normal parenchyma when the suspected tumor nodule enhances identical to renal parenchyma.
Renal cortex may be bulbous at the hilum, so-called “hilar lips.”
Hypertrophied intrarenal cortex extending along the septal columns form prominent islands of tissue between the medullary pyramids [40]. These masses of normal tissue have been called junctional parenchyma, hypertrophied columns of Bertin, and cloisons.

Renal Cystic Disease

Simple Renal Cyst

Simple renal cysts are by far the most common renal mass lesions. One-half of all adults older than age 50 have simple renal cysts. Although the diagnosis is straightforward and confident when cysts are large, small cysts (<3 cm) sometimes cause difficulty because of volume averaging and when US resolution is poor.

Simple cysts are definitively diagnosed by US when they have the following features: well-defined thin wall; sharp demarcation with renal parenchyma; anechoic fluid; and accentuated through-transmission (Fig. 3.26).
These features are more difficult to demonstrate when cysts are small (<3 cm). Excellent US technique is mandatory. When suspected cysts are not clearly demonstrated, consider improving technique by (1) increasing transducer frequency (to improve resolution of the lesion and to improve demonstration of accentuated through-transmission), (2) adjusting the focal (transmit) zone to the level of the lesion, (3) carefully centering the lesion in the US beam (to limit volume-averaging image degradation), (4) adjusting gain to limit false internal echoes, (5) scanning the lesions from different orientation to completely evaluate all aspects of the wall.
Multiple and bilateral simple cysts occur commonly and must be differentiated from the various forms of polycystic kidney disease. Patients with multiple simple cysts are usually
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older (>50 years), and have a countable number, rather than innumerable, renal cysts. Cysts are generally not found in other organs as they are with autosomal dominant polycystic disease. Multiple simple cysts do not affect renal function.

Simple cysts are much less common in children than in adults. However, when a firm US diagnosis of simple cyst is made in a child, no further evaluation or intervention is necessary [53].

Figure 3.26 Simple Renal Cyst. Anechoic internal fluid, sharp interface with the renal parenchyma, thin wall, and accentuated through-transmission are features of a simple renal cyst (arrow).

Figure 3.27 Multilocular Cyst. The multilocular cyst is indicated by the cursors (+, x). A moderately thick septum (arrow) separates two of the locules. Blood flow within this septum would favor this lesion being a tumor.

Atypical Renal Cysts

Renal cystic lesions that fail to meet the strict criteria for simple renal cyst are considered to be atypical renal cysts [54]. Many of these more complex lesions can still be accurately classified as benign [55,56]. Many are simple cysts that were complicated by hemorrhage or infection (i.e., complicated cysts).

Septations. Thin, smooth, regular, non-vascular internal septations within a cyst are benign [54]. Thick, nodular septations containing blood vessels are potentially neoplastic (Fig. 3.27).
Thick wall. Wall thickening may occur when a simple cyst becomes infected or develops internal hemorrhage. Thick walls are also found in abscesses and in cystic renal tumors. These lesions are indeterminate and require further evaluation, usually surgical biopsy [54].
Calcifications. Thin calcification in the wall of a cyst is benign, provided that all other US criteria for simple cyst are met [54]. Calcification is otherwise a non-specific finding. Thick wall or associated soft tissue mass indicates possible neoplasm.
Echogenic fluid. Simple cysts have anechoic fluid. Complicated cysts commonly contain echogenic particulate matter resulting from hemorrhage or infection. The echogenic material may be diffusely dispersed within the cyst or show dependent layering (Fig. 3.28). These cysts can be considered benign if the wall is thin and the cyst remains well defined with no solid component.

Multilocular Cystic Nephroma

Multilocular cystic nephroma is an uncommon benign tumor that arises from the same nephrogenic rests that predispose to Wilms tumor [47]. The tumor occurs most commonly in boys younger than age 4 and in women aged 40-60 years [57].

Figure 3.28 Fluid Layering in Renal Cyst. Several cysts arise off this kidney. The largest (large arrow, between cursors, +) contains fluid with echogenic particulate matter. A smaller cyst shows a fluid-fluid layer (open arrow). Both these cysts are simple cysts complicated by hemorrhage.

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The tumors are multicystic with thick walls and septa (Fig. 3.29) [47,58]. Small curvilinear calcifications are occasionally seen in the septa [57]. The tumors are well demarcated from the renal parenchyma.
Most lesions are 8-10 cm in size but range up to 30 cm.

Autosomal Dominant Polycystic Kidney Disease

The primary anatomic defect of autosomal dominant polycystic kidney disease (ADPKD) is cystic dilatation of the nephrons as well as the collecting tubules. Islands of normal parenchyma are interspersed between cysts. Affected patients develop progressive renal failure and hypertension in middle age. The presence of cerebral aneurysms in 10% of patients results in subarachnoid hemorrhage as a common cause of death.

The kidneys are progressively replaced and are markedly enlarged by diffuse parenchymal cysts of varying size (Fig. 3.30). The cysts do not communicate with each other or with the calyceal system or pelvis. The condition is always bilateral but may be asymmetric especially in younger patients with less advanced disease.

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Hepatic and pancreatic cysts are common and their presence confirms ADPKD.
Hemorrhage within the cysts is common, causing wall thickening and echogenic internal fluid in affected cysts. Hemorrhage commonly causes flank pain.
Calcification commonly occurs in cyst walls as a result of hemorrhage. Renal stones are common in this disorder [59].
In the fetus and young child, the presence of multiple renal cysts confirms the presence of the disease when a parent is known to be affected. The kidneys may be enlarged and echogenic. However, presentation is quite variable and a normal appearance of the kidneys does not exclude the disease.

Figure 3.29 Multilocular Cystic Nephroma. This renal mass consists of cysts of varying size separated by thick septa and defined by thick walls.

Figure 3.30 Autosomal Dominant Polycystic Kidney Disease. A. When the disease is advanced, the renal parenchyma is replaced by numerous non-communicating cysts of varying size (arrows). B. When the disease is early, the kidneys are of normal size and only a few cysts (arrows) are present.

Autosomal Recessive Polycystic Kidney Disease

Autosomal recessive polycystic kidney disease usually presents in the neonate and is detectable in the fetus. The condition covers a spectrum of abnormality from poor renal function at birth (infantile polycystic kidney disease) to progressive renal failure and hepatic fibrosis in childhood (juvenile polycystic kidney disease) [60]. The primary defect is diffuse tubular and saccular dilatation of the renal collecting tubules. Prognosis depends upon the number of abnormal nephrons present.

The kidneys are markedly enlarged and strikingly echogenic (Fig. 3.31A) [60]. The marked echogenicity is caused by the numerous sonographic interfaces created by dilatation of the collecting tubules. The peripheral cortex has no collecting tubules and is compressed but otherwise uninvolved, resulting in a characteristic peripheral sonolucent rim [61]. Reniform shape is maintained. Corticomedullary differentiation is absent.
High-resolution US may visualize tiny cysts and dilated tubules within the renal parenchyma.
Older children have predominant hepatic fibrosis and less severe renal impairment. The kidneys are less enlarged and show a coarse, more heterogeneous pattern of increased echogenicity (Fig. 3.31B) [62]. Punctate renal parenchymal calcifications are common [63]. The liver shows features of portal hypertension as the hepatic fibrosis progresses.

Figure 3.31 Autosomal Recessive Polycystic Kidney Disease (ARPKD). A. Longitudinal image of a kidney in a newborn infant reveals massive enlargement with marked increase in central echogenicity. The peripheral sonolucent rim (arrow) of compressed cortex is characteristic. B. The kidney of a 5-year-old boy with ARPKD is mildly enlarged and heterogeneous with visible small cysts. The child had moderately severe liver disease.

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Acquired Renal Cystic Disease Associated with Hemodialysis

Patients with end-stage renal disease on chronic hemodialysis are prone to develop multiple renal cysts and RCC in their native kidneys [64]. The disease is progressive and increases in prevalence with length of time on hemodialysis [65]. It occurs in 10-20% of patients on hemodialysis for 1-3 years and in up to 90% of patients treated with hemodialysis for longer than 10 years. RCC develops in approximately 5% of patients [65]. After renal transplantation the cysts reduce in size and number but the risk of malignancy persists [66]. Affected patients lack a history of polycystic kidney disease.

The kidneys are initially small and echogenic reflecting end-stage renal disease.
As the time on hemodialysis treatment lengthens, cysts form primarily in the cortex and vary in size up to 2-3 cm [65]. As cyst formation progresses, the kidneys enlarge.
The cysts are fragile and may develop internal or perirenal hemorrhage [64].
Calcifications within cyst walls and in the renal parenchyma are common [66].
The presence or development of a solid tumor is highly suggestive of RCC.

Von Hippel-Lindau Disease

Von Hippel-Lindau disease (VHL) is an uncommon, autosomal-dominant, neurocutaneous disorder characterized by cerebellar hemangioblastomas, retinal angiomas, multiple visceral cysts, RCC, and pheochromocytoma [67]. Because RCC develops in 24-45% of patients with VHL, periodic surveillance of the kidneys is often recommended [68]. RCC may develop as early as age 15. Renal cysts are found in 59-85% of patients. Central nervous system and eye manifestations are usually evident at the time of discovery of renal disease.

Renal cysts in VHL show a continuum of appearance from simple cyst to thick-walled cyst to cystic tumor with papillary projections and small solid nodules [67]. Simple cysts grow slowly (5 mm/year) and may involute [68]. Extensive renal cystic disease mimics ADPKD and may progress to renal failure. End-stage kidneys should be removed because of risk of RCC.
Most RCC arise de novo as a solid renal tumor that grows rapidly (up to 2.2 cm/year) [68]. Some RCC have a cystic appearance. Any distinct solid element within a cystic lesion in a patient with VHL is likely to be RCC [67].
Adrenal pheochromocytoma is found in 7-18% of patients.

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Cysts in the pancreas are a feature of VHL found in high prevalence (93%) in some families and absent in others [67]. Pancreatic cysts vary in size from 1-2 mm up to 10 cm and may completely replace the pancreas.

Figure 3.32 Tuberous Sclerosis. The renal parenchyma contains numerous small cysts (black arrows) and numerous echogenic nodules (white arrows) representing fat in multiple angiomyolipomas.

Tuberous Sclerosis

Tuberous sclerosis is another uncommon, autosomal-dominant, neurocutaneous disorder with renal manifestations. Clinical features include adenoma sebaceum, mental handicap, epilepsy, retinal hamartomas, cortical tubers, and subependymal nodules. Renal lesions consist of multiple bilateral renal cysts and AMLs [69]. The renal lesions have no malignant potential.

Cysts are bilateral and vary in size and number (Fig. 3.32) [69].
AMLs are characteristically bilateral and infiltrative [69]. They vary in size from 1-2 mm up to several cm. The fatty component of the tumors causes foci of high echogenicity and a markedly heterogeneous echotexture to both kidneys (Fig. 3.32). Tumors may enlarge and bleed during pregnancy.

Multicystic Dysplastic Kidney

Classic multicystic dysplastic kidney (MCDK) results from complete ureteral obstruction in early fetal life [60]. Complete obstruction in classic MCDK results from atresia of the upper third of the ureter [70]. The pelvis and calyces never form. The affected kidney does not function and renal parenchyma is completely replaced by cysts. When in utero obstruction is incomplete, hydronephrosis develops, cystic dysplastic change is less severe, and residual renal function is present. This condition is not heritable. When bilateral, it is fatal at birth.

Classic MCDK appears as multiple non-communicating cysts of varying size completely replacing all parenchyma (Fig. 3.33A) [60]. No renal pelvis or calyces are present [70]. The kidney is markedly enlarged at birth but will progressively shrink to a small nubbin that commonly calcifies [71,72]. No renal function is present on radionuclide imaging.
In the hydronephrotic form of MCDK, dilated renal pelvis and calyces are identifiable (Fig. 3.33B). Multiple cysts of varying size replace most, but not all, of the renal parenchyma. Islands of heterogeneous dysplastic solid renal tissue are also seen. Radionuclide studies show limited renal function.
Atypical forms of MCDK include a single or few large cysts replacing the kidney (Fig. 3.33C).

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The opposite kidney commonly (30-41%) shows a developmental anomaly, more often congenital ureteropelvic (UPJ) obstruction.

Figure 3.33 Multicystic Dysplastic Kidney. A. The classic multicystic dysplastic kidney consists of cysts of varying size replacing all of the renal parenchyma. This kidney showed no function on radionuclide scan. B. Transverse image shows the hydronephrotic form consisting of advanced hydronephrosis with a recognizable renal pelvis (P) and extensive cystic dysplasia of the parenchyma. Radionuclide imaging showed very limited renal function . C. The variant form of multicystic dysplastic kidney consists of a few large cysts replacing all of the renal parenchyma (between cursors, +).

Renal Dysplasia

Renal dysplasia describes the presence of primitive mesenchymal tissue, cartilage, and cysts of varying size in the parenchyma of a kidney obstructed early in fetal life [73]. Dysplastic tissue is functionless tissue. Overall renal function is determined by the number of normal nephrons present relative to the amount of dysplastic tissue present. The timing and severity of renal obstruction in fetal life determine the severity of renal dysplasia. Dyplasia may develop as a result of any cause of fetal renal obstruction including such entities as congenital ureteropelvic or uterovesical junction (UVJ) obstruction, posterior urethral valves, or ectopic ureterocele.

Cysts are a primary feature of renal dysplasia seen in the newborn. Cysts vary in number from one to many and in size from 1 mm up to 3 cm or larger [73]. The more proximal and severe the obstruction, the greater the number and size of the cysts.
Solid renal dysplasia decreases the volume of renal parenchyma and increases its echogenicity. Globally dysplastic, functionless kidneys are tiny and echogenic. Segmental areas of dysplasia show limited echogenic solid tissue and cysts. Renal dysplasia may produce a solid renal mass (Fig. 3.34).
MCDK is on the most severe end of the spectrum of renal dysplasia.

Figure 3.34 Solid Renal Dysplasia. A focus of renal dysplasia produced a solid mass (arrows) in the kidney (k) of a child. l, liver.

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Renal Infection

Acute Pyelonephritis

In adults, the diagnosis of acute renal infection is usually based on clinical and laboratory findings and imaging is utilized primarily to detect complications. In children, the clinical diagnosis is commonly equivocal and imaging is used to confirm the diagnosis. Acute pyelonephritis is most common in young women, aged 15-35 years. Patients who respond to therapy require no imaging.

Renal US is commonly normal in uncomplicated acute pyelonephritis.
Renal involvement by infection may be focal, multifocal, or diffuse. The kidney becomes diffusely or focally swollen. Corticomedullary differentiation is lost. The margin of the kidney becomes indistinct.
Affected areas are usually hypoechoic because of edema fluid (Fig. 3.35A). If interstitial hemorrhage occurs, affected areas become hyperechoic (Fig. 3.35B).
Inflammation and edema constrict renal arterioles in affected areas and result in segments of reduced perfusion. Color or power Doppler flow imaging shows single or multiple foci of decreased or absent blood flow, often in a wedge-shaped pattern [74]. These areas of decreased perfusion correspond to areas of decreased enhancement seen on CT. Power Doppler is more sensitive than color Doppler in showing subtle areas of abnormality.

Figure 3.35 Acute Pyelonephritis. A. Acute renal infection produces hypoechoic, focal, edematous swelling of the renal parenchyma (arrows). B. Acute renal infection with interstitial hemorrhage produces hyperechoic focal swelling of the renal parenchyma (arrows).

Figure 3.36 Pyonephrosis. Pus produces fluid layers (arrows) within the dilated collecting system of a 5-year-old boy with infection complicating congenital, ureteropelvic junction obstruction. c, dilated calyces; P, dilated renal pelvis. Cursors (+) measure size of the kidney.

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Pyonephrosis

Pyonephrosis describes the presence of purulent material within an obstructed collecting system [75]. Most patients are acutely symptomatic, although an indolent presentation is prevalent (15%). Relief of obstruction and treatment of infection are critical to prevention of septic shock and rapidly progressive renal parenchymal destruction.

The collecting system is dilated and contains layering echogenic debris, and, sometimes, calculi or gas (Fig. 3.36).
The wall of the collecting system is often thickened.
The renal parenchyma may show any of the signs of acute pyelonephritis or abscess.
An echogenic, nonshadowing, mobile mass within the collecting system suggests a fungus ball (a mycetoma) (Fig. 3.37), caused by chronic fungal infection [76].

Renal and Perirenal Abscess

Abscess results from areas of pyelonephritis that progress to parenchymal necrosis, or from infection of cysts. Most renal abscesses extend into the perirenal space. Rupture of pyonephrosis may also result in perirenal abscess.

Poorly marginated, thick-walled, hypoechoic mass with internal debris and acoustic enhancement is characteristic (Fig. 3.38A) [75]. The mass may appear echogenic and solid depending on the nature of its contents. Abscesses may be solitary, multiple, or small (microabscesses) with a tendency to coalesce into a single cavity.
Stones or gas may be present within or near the abscess (Fig. 3.38B).

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Extrarenal extension is suggested by a hypoechoic perirenal mass (Fig. 3.39).
US is commonly used to guide aspiration for culture and catheter drainage.

Figure 3.37 Fungus Ball. Transverse image of the kidney of a 2-month-old premature infant with systemic Candida albicans infection shows dilated pelvis (p) and calyces (c) that contain echogenic urine and a discrete mobile fungus ball (arrow). The fungus ball caused partial urinary obstruction. Fungus balls consist of fungal hyphae mixed with inflammatory cells and debris.

Figure 3.38 Renal Abscess. A. An intrarenal abscess produces a thick-walled mass (straight arrows) containing echogenic fluid within the kidney. The perirenal space contains mostly normal echogenic fat (arrowhead) and an area of inflammatory infiltration (curved arrow) but no distinct fluid collection. B. This renal abscess contains a large pocket of air (white arrow) that produces characteristic intense reverberation artifact (black arrow).

Emphysematous Pyelonephritis

Emphysematous pyelonephritis is a rare and serious complication of urinary tract infection with extensive necrosis and gas formation in the renal parenchyma. Most patients (90%) have diabetes mellitus and 20% have associated urinary tract obstruction [77,78]. Patients are acutely ill with fever and flank pain. Escherichia coli is the most common causative organism. Gas formation results from fermentation of glucose in the urine by the infecting bacteria.

High-amplitude echoes with reverberation or comet tail echoes characteristic of air (Fig. 3.39) emanate from the renal parenchyma or perirenal space [78]. Extensive emphysema may completely obscure the affected kidney.
Plain film radiographs or CT confirm the presence of air in the renal parenchyma. Gas confined to the collecting system or within a discrete abscess is a less ominous finding than diffuse gas in the renal parenchyma [79].

Chronic Pyelonephritis/Reflux Nephropathy

Chronic pyelonephritis may be the end stage of reflux nephropathy or occur as the result of recurring infection associated with calculi and chronic obstruction [76]. Patients at risk include those with neurogenic bladders, ileal conduits, and recurrent renal stone disease.

Focal parenchymal scars with an underlying blunted calyx are the hallmark finding (Fig. 3.40). The polar regions are most often affected.

The affected kidney is often reduced in size and is lobulated in contour with focal parenchymal thinning, usually most pronounced at the poles.
Compensatory hypertrophy in uninfected areas may result in bulbous islands of normal tissue that resemble tumors.

Xanthogranulomatous Pyelonephritis

Xanthogranulomatous pyelonephritis is a rare form of chronic renal infection with progressive destruction of renal tissue and replacement by a cellular infiltrate of lipid-laden macrophages

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[76]. Most patients are middle-aged women who present with recurrent flank pain and fever.

Figure 3.39 Perirenal Abscess. A. The kidney (K) shows inflammatory changes that extend into the perirenal space (open arrows). A discrete perirenal abscess (white arrow) spread to the liver by tracking along the retroperitoneum to the bare area, forming a hepatic abscess (black arrows). L, liver. B. In another patient a perirenal abscess (white arrows) extended into the muscles and soft tissues of the back (black arrows). K, left kidney.

The process is unilateral and may be diffuse, focal, or segmental (Fig. 3.41).
The kidney enlarges but maintains its reniform shape.
An obstructing calculus is commonly present (70%) [47].
Multiple hypoechoic areas represent purulent cavities in the affected areas of the kidney.

Figure 3.40 Chronic Pyelonephritis. Longitudinal image of the kidney (K) demonstrates a focal parenchymal scar (curved arrow) with an underlying dilated calyx (open arrow).

Figure 3.41 Xanthogranulomatous Pyelonephritis (XGP). Longitudinal image of the kidney (between cursors, +) in a patient with chronic urinary tract infection shows an obstructing calculus (open arrow) with acoustic shadow (black arrow) and a low density complex hypoechoic mass (curved white arrow). The kidney had minimal function on a radionuclide scan and was surgically removed, resolving the chronic infection. Pathology confirmed XGP.

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Renal Tuberculosis

Renal tuberculosis is a delayed complication of pulmonary tuberculosis, occurring as long as 10-15 years after the initial infection [76]. Patients present with hematuria or sterile pyuria. The pathologic effects of tuberculous infection include granuloma formation, parenchymal destruction, fibrosis, stricture, and calcification.

Hypoechoic parenchymal masses are granulomas or chronic abscess cavities.
Parenchymal scarring and calcification are typical findings.
Calyceal clubbing and hydronephrosis result from papillary necrosis and obstruction caused by strictures in the collecting system.
The kidney can become a functionless hydronephrotic sac (Fig. 3.42) or a shrunken calcified mass.

Figure 3.42 Renal Tuberculosis. Chronic renal tuberculosis with ureteral stricture has resulted in an end-stage, minimally functioning kidney with marked hydronephrosis (H) and thinned renal parenchyma (arrow).

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Renal Hydatid Disease

The kidneys are affected in only 3% of patients with hydatid disease [80]. Renal lesions are usually asymptomatic, although they may cause hematuria or pain. The disease may be suspected in patients living in or traveling to endemic cattle and sheep raising areas of northern and eastern Africa, Asia, New Zealand, Australia, South America, and the Mediterranean coast. Complications include secondary infection and rupture of the cyst into the perinephric space or collecting system. Diagnosis is confirmed by immunoelectrophoresis.

Multilocular cysts with curvilinear internal septa and floating internal echoes are characteristic [80]. The internal echoes are produced by “hydatid sand,” which consists of parasite parts and debris. Septa are produced by the walls of daughter cysts. Most cysts are located at the upper or lower poles.
Cyst walls and septa become thickened and commonly calcify. Hydatid sand may completely fill the cyst and mimic a solid lesion.

Vascular Abnormalities

Renal Vein Thrombosis

Thrombosis of the renal vein may be primary, caused by intrinsic renal disease (glomerulonephritis, pyelonephritis, lupus nephritis) or, more commonly, is secondary to other diseases (RCC invasion of the renal vein, pancreatitis, systemic hypercoagulable states, acute dehydration, extension of IVC thrombosis) [81]. Clinical findings include hematuria, proteinuria, and flank pain. The condition may be clinically silent. US findings depend upon whether the thrombosis is acute or gradual, complete or partial [81,82].

Echogenic clot is visualized in an enlarged renal vein (Fig. 3.19). In acute stage the clot may be isoechoic with flowing blood on gray scale US.
Color flow shows absent venous flow with complete occlusion, or flow around the clot with partial occlusion.
Acute complete thrombosis causes marked renal edema seen as renal enlargement with decreased parenchymal echogenicity.
With partial occlusion, renal swelling is less prominent.
Venous collateral formation and enlargement begin at 24 hours and peak at 2 weeks following thrombosis.
Left renal vein collaterals are more prominent and include enlarged ureteral, gonadal, adrenal, and inferior phrenic veins.
Right renal vein collaterals are limited to the ureteral vein.
Lumbar, azygos, perivesical, and portal vein collaterals may become enlarged via ureteral vein connections.
Intrarenal artery Doppler resistance index is commonly, but not always, elevated (>0.70). Absent or reversed diastolic flow may be seen with renal vein thrombosis (40% of cases) [82].

Renal Artery Stenosis

When a complete examination is possible, Doppler US is highly accurate in the diagnosis of renal artery stenosis. Unfortunately, complete diagnostic evaluation with US is difficult because of problems with patient body habitus, breath holding, and overlying bowel gas. Technically satisfactory examinations are reportedly performed in 0-75% of cases [2]. In any case, the examination is time-consuming and highly operator dependent. Breath-hold, gadolinium-enhanced, magnetic resonance angiography is superior to US in detection of significant stenosis and in the demonstration of accessory renal arteries [83]. A variety of criteria have been utilized for US diagnosis of significant stenosis.

Thickening and calcification of the wall of the renal artery indicate the presence of atherosclerotic plaque, but not necessarily significant stenosis [2].

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The beaded appearance characteristic of fibromuscular dysplasia may be visualized on gray-scale US of the main renal artery [2].
Early systolic acceleration <3 m/sec2 indicates significant stenosis.
Renal:aortic ratio >3.5 is 75% sensitive for 75% stenosis. The renal:aortic ratio is calculated by dividing the highest renal artery velocity by the highest aortic velocity obtained at the level of the renal arteries.
Peak systolic velocity >200 cm/sec in the renal artery indicates significant stenosis.
Turbulent flow with spectral broadening and flow reversal is present downstream from the stenosis.
Tardus-parvus spectral waveform is present in the distal renal artery with high-grade (>80%) proximal stenosis (Fig. 3.43). The rise to peak systolic velocity is slow (tardus) and the peak systolic velocity is decreased (parvus).

Figure 3.43 Renal Artery Stenosis. Doppler spectrum obtained from an intrarenal artery shows a tardus-parvus waveform. The peak systolic velocity (arrowhead) is late and reduced in velocity. The curved arrow shows the position of the Doppler sample volume.

Renal Artery Occlusion

Occlusion of the renal artery occurs with embolus, thrombosis, trauma, or surgical error. Occlusion of the main renal artery results in global infarction whereas occlusion of an accessory or branch renal artery results in focal or segmental infarction.

With acute global infarction, the appearance of the kidney remains normal on gray-scale US.
Color Doppler shows the occluded stump of the renal artery with no blood flow (~60%) [2].
Intrarenal arteries may show no detectable Doppler signals (~80%) or a severe tardus-parvus spectrum (~20%) [2].
Focal or segmental arterial occlusion results in a wedge-shaped area of decreased or increased echogenicity indistinguishable from acute pyelonephritis.
Power Doppler imaging is the most sensitive for demonstration of the corresponding area of hypoperfusion [84].

Arteriovenous Fistula

Most often, intrarenal arteriovenous fistulas (AVF) occur as a complication of renal biopsy or other penetrating trauma.

Color flow US shows a bright focus of high-velocity blood flow. Tissue vibration artifact may be prominent [2].
The draining vein is enlarged, particularly if the AVF is long-standing.
High-velocity, highly turbulent flow is present at the site of the AVF.
The supplying artery shows a very low resistance spectral pattern (RI <0.40).
The draining vein spectrum shows arterial pulsations.

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Bladder

Thickening of the Bladder Wall

The bladder wall is thickened when it exceeds 4 mm in diameter with the bladder distended. Thickening is commonly the result of hypertrophy of the detrusor muscle that causes marked irregularity (trabeculation) of the luminal surface of the bladder wall (Fig. 3.44) (Box 3.1).

Neurogenic bladder is a cause of bladder wall thickening, trabeculation, incomplete bladder emptying, ureteral dilatation, and stone formation. A “Christmas tree” appearance of the bladder with several areas of focal constriction of the bladder lumen is characteristic of long-standing neurogenic bladder.
Bladder outlet obstruction caused by prostatic enlargement is a common cause of bladder wall thickening. The enlarged prostate is evident. Other causes of outlet obstruction include posterior urethral valves, urethral stricture, and ectopic ureterocele.
Cystitis is caused by infection, radiation, and chemotherapy. The bladder may appear normal, or show focal or diffuse wall thickening. Floating debris is commonly present in the bladder lumen.
Bladder augmentation procedures are performed to prevent progressive renal damage in patients with small capacity bladders and high intravesical pressures. A bowel loop is opened and transposed to the bladder dome to increase bladder capacity. The bowel wall is commonly irregular in thickness and shape and may show peristalsis. Secreted mucus mixes with urine to produce echogenic particles and debris in the bladder lumen.

Figure 3.44 Thickened Bladder Wall. Two patients with neurogenic bladders have thickened bladder walls. A. The bladder wall is thickened to 11 mm (between cursors, +). Thickening of the bands of the detrusor muscle causes the irregularity of the mucosa surface of the bladder. B. Mucosal herniation through the hypertrophied muscle bands (white arrow) causes the formation of numerous saccules (black arrow) in the thickened bladder wall. The curved arrow indicates an enlarged prostate.

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Emphysematous Cystitis

In patients with diabetes, chronic bladder outlet obstruction, or chronic infection, bacterial infection may produce air in the bladder wall or lumen. E. coli and Enterobacter aerogenes are the most common causative organisms.

The bladder wall is diffusely thickened and markedly echogenic [79]. Reverberation and comet tail artifacts are produced by focal collections of air.
CT and plain film radiography confirm the presence of air in the bladder wall and bladder lumen.

Bladder Diverticuli

Bladder diverticuli are congenital or acquired herniations of bladder mucosa through the muscle of the bladder wall [85].

Fluid-filled perivesical masses communicate with the bladder lumen through a small orifice (Fig. 3.45).
If the orifice is not clearly seen, compression of the bladder during color Doppler examination shows a jet of urine flow into the diverticulum.
Stasis of urine within the diverticulum may result in echogenic urine and stones within the diverticulum. TCC may arise within a bladder diverticulum.

Intraluminal Objects

A variety of iatrogenic and pathologic structures may be seen within the bladder lumen.

Figure 3.45 Bladder Diverticuli. Transverse image of the bladder (B) demonstrates bilateral diverticuli (d) that communicate with the parent bladder via small openings. When the bladder empties, the neck of the diverticulum may close, resulting in the diverticulum remaining filled with urine.

Figure 3.46 Bladder Calculus. Transverse image of the bladder shows an echogenic focus (large arrow) with acoustic shadowing (small arrow) lying on the dependent bladder wall. The stone was observed to move when the patient rolled into the decubitus position. Enlargement of the prostate (P) resulted in urinary stasis within the bladder, predisposing to stone formation.

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Bladder calculi appear as mobile hyperechoic foci with acoustic shadowing (Fig. 3.46).
Blood clots appear as moderately echogenic nodules that commonly adhere to the bladder wall (Fig. 3.47). Absence of blood flow on color flow US distinguishes clots from tumors. Fluid-fluid levels from layering blood and urine are commonly present. Most patients have gross hematuria.
Foley catheter balloons will be seen even when the bladder is empty. Air within the Foley balloon produces a bright interface with shadowing.
Ureteral stents are identified as coiled hyperechoic tubes. The walls of the stent produce parallel curving echogenic lines.
Foreign bodies are of any shape and may be mobile or adherent to the bladder wall.

Figure 3.47 Blood Clots in the Bladder. Blood clots appear as moderately echogenic masses (arrows) within the bladder in a patient with gross hematuria caused by renal trauma. Documenting free movement of these masses with changes in patient position confirms blood clots. When blood clots are adherent to the bladder wall, showing a lack of blood flow by use of color Doppler aids in differentiation from tumors.

Figure 3.48 Simple Ureterocele. Longitudinal image of a distended bladder (B) shows the cystic protrusion (arrow) of a dilated distal ureter (u) into the bladder lumen. The wall of the ureterocele includes the wall of the ureter and the mucosa of the bladder. The ureterocele changes in size and appearance with ureteral peristalsis.

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Ureterocele

Ureteroceles are balloon-like dilatations of the terminal ureter caused by obstruction of the ureteral orifice. Urinary stasis increases the risk of infection and stone formation [86].

Simple ureteroceles occur at the normal location of the ureteral orifice and are seen as thin-walled cystic masses (Fig. 3.48). Ureteral peristalsis causes the ureteroceles to periodically distend and collapse. The degree of obstruction is usually mild with dilatation confined to the terminal ureter. More severe obstruction causes dilatation of the proximal ureter and occasionally pelvicalyectasis.
Ectopic ureteroceles occur with complete duplication of the collecting system at the ectopic location of the upper pole ureter insertion. Large ectopic ureteroceles may obstruct the contralateral ureter or the urethral orifice. Ectopic ureteroceles are more varied in appearance (Fig. 3.49). Some contain anechoic urine whereas others are intensely echogenic due to urine precipitates and complications of obstruction.

Bladder Transitional Cell Carcinoma

Bladder TCC is the most common neoplasm of the urinary tract [42]. Most (90%) bladder tumors are TCC. Papillary bladder TCC are often multiple (30%) and usually (80%) superficial and low stage. Invasive TCC is solitary and high grade. Synchronous tumors are present in the upper tracts in 2-3% of patients with bladder TCC.

Figure 3.49 Ectopic Ureteroceles. Transverse image of the bladder (B) of an infant reveals bilateral ectopic ureteroceles (E). Both kidneys showed complete duplication of the collecting system with hydronephrotic upper pole moieties that terminated in these ectopic ureteroceles.

Figure 3.50 Polypoid Transitional Cell Carcinoma. Longitudinal image of the bladder shows a broad-based polypoid projection (arrow) from the otherwise smooth bladder mucosa. Color flow (not shown) revealed blood flow within the polypoid mass. Transurethral resection confirms a superficial transitional cell carcinoma.

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Smooth or papillary hypoechoic soft tissue mass projects into the bladder lumen (Fig. 3.50) [42].
Focal or diffuse thickening of the wall occurs with infiltrating tumors (Fig. 3.51).
Whereas most tumors are hypovascular, larger and high-grade tumors may show visible vascularity on color Doppler [43].
Blood clots may be present in the bladder lumen. Hydronephrosis and hydroureter result from involvement of the ureteral orifice.

Urachal Anomalies

The urachus is a vestigial remnant of the embryonic allantois. The normal urachus is a fibrous cord (also called the median umbilical ligament) that extends anterior to the peritoneum along the midline anterior abdominal wall from the umbilicus to the apex of the bladder [87]. Failure of complete closure of the urachus results in cystic and tubular masses. Infection may complicate any of the urachal anomalies.

Figure 3.51 Diffusely Infiltrating Transitional Cell Carcinoma. Longitudinal image shows marked circumferential thickening (arrows) of the bladder wall with a markedly contracted bladder lumen (b). Biopsy revealed an aggressive, diffusely infiltrative transitional cell carcinoma. A portion of the prostate (P) is visible.

Figure 3.52 Urachal Cyst. Longitudinal images (A, B) show an anechoic, fluid-filled tubular structure (U) in the midline intimately applied to the inner surface of the anterior abdominal wall (arrow) between the bladder and the umbilicus. f, subcutaneous fat.

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Patent urachus is vesicocutaneous fistula that extends from the dome of the bladder to the umbilicus. US shows a small diameter tubular structure in the midline anterior abdominal wall.
Vesicourachal diverticulum is a closed sac that extends from the anterior bladder dome to the anterior abdominal wall.
Urachal cysts are found closely applied to the midline anterior abdominal wall between the umbilicus and the bladder. Cyst contents are usually anechoic and may be spherical or tubular in shape (Fig. 3.52).
Urachal sinus is a tubular tract that extends caudally from the umbilicus and ends blindly on the midline anterior abdominal wall.

Adrenal Glands

Adrenal Adenoma

Benign, nonhyperfunctioning adrenal adenomas are common incidental findings on imaging studies. Hyperfunctioning adenomas produce endocrine syndromes (Cushing’s disease, Conn’s syndrome). Lesions can be accurately characterized as benign or potentially malignant by non-contrast CT or chemical-shift MR but not reliably by US [88].

Most adrenal adenomas are homogeneous, solid, well defined, and less than 5 cm in size (Fig. 3.53). Adenomas are bilateral in up to 10% of patients.
Hemorrhage, necrosis, and calcification may occur in benign adenomas, but these findings are more characteristic of carcinoma [89].

Adrenal Carcinoma

Carcinoma of the adrenal cortex is a rare but aggressive lesion. Approximately one-half of the tumors secrete hormone, most commonly producing Cushing’s syndrome. Metastases go to bone, liver, lung, and lymph nodes.

Figure 3.53 Adrenal Adenoma. A. Transverse image shows a well-defined, small focal bulge (curved arrow) in the right adrenal gland. In an asymptomatic patient, this finding is most indicative of benign adrenal adenoma. Note the anatomic landmarks used for identification of the right adrenal gland. i, inferior vena cava; L, right lobe of the liver; straight arrow, right crus of the diaphragm. B. Longitudinal image obtained from a patient with Cushing’s disease shows a homogeneous solid mass (arrows) above the right kidney (k). L, liver.

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Tumors are usually large (>5 cm) and necrotic at presentation. Calcifications are common (30%) [90]. Up to 10% are bilateral [91].
The tumor may invade the renal vein or IVC producing findings similar to those found with RCC.

Adrenal Metastases

Metastases to the adrenal gland arise most commonly from lung, breast, colon and renal cancer, or melanoma.

Lesions smaller than 3 cm are homogeneous, solid, round, and indistinguishable by US from benign adenoma.
Lesions larger than 3 cm are typically heterogeneous with necrosis, hemorrhage, calcification, and poorly defined borders (Fig. 3.54).

Pheochromocytoma

Pheochromocytoma secretes catecholamines and typically presents with paroxysmal hypertension. However, atypical presentation is common and the tumor may not be suspected clinically. Approximately 10% of lesions are malignant and 10% are extra-adrenal. Pheochromocytoma is found in 7-18% of patients with VHL [67]. Tumors in VHL are often multiple, bilateral (50-80%), and extra-adrenal. Pheochromocytoma shows a broad spectrum of US findings [92].

Most lesions (two-thirds) are purely solid with either homogeneous (~50%) or heterogeneous (~50%) echogenicity [92]. Compared to renal parenchyma, tumors may be isoechoic, hypoechoic, or hyperechoic (Fig. 3.55).
One-third of lesions are partially or near completely cystic [92]. Cystic lesions contain echogenic fluid and have thick walls and visible solid components.
US is unable to differentiate benign from malignant pheochromocytomas [92].

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Percutaneous biopsy of pheochromocytoma may result in hypertensive or hypotensive crisis [93].

Figure 3.54 Metastasis to Adrenal Gland. A large, heterogeneous, solid mass (between cursors, +) arises from the right adrenal area, displacing the liver anteriorly. This was a metastasis from malignant melanoma to the adrenal gland.

Adrenal Hemorrhage

Adrenal hemorrhage occurs in stressed newborns, patients on anticoagulant therapy, and following blunt trauma, surgery, childbirth, myocardial infarction, liver transplantation, sepsis, or burns [94]. Hemorrhage may be unilateral or bilateral.

Oval heterogeneous mass replaces the adrenal gland. Size varies up to 4-6 cm.
The mass shows the evolution characteristic of hematoma on serial follow-up. Acutely the mass is echogenic. With time the mass becomes heterogeneous, hypoechoic and cystic, and shrinks (Fig. 3.56).

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Adrenal hemorrhage following blunt trauma has a strong predilection for the right side [95].

Figure 3.55 Pheochromocytoma. A. Longitudinal image through the spleen (S) and left kidney (K) of a patient with von Hippel-Lindau syndrome reveals a homogeneous, hypoechoic, solid left adrenal mass (arrows). B. Longitudinal image through the liver (L) and right kidney (K) of a patient with severe hypertension reveals a heterogeneous, hyperechoic, solid right adrenal mass (arrows. Both lesions were confirmed to be pheochromocytomas.

Figure 3.56 Adrenal Hemorrhage. A. Longitudinal image in a 30-week-gestation, premature infant shows acute hemorrhage into the right adrenal gland (curved arrow). The right kidney (arrowhead) is compressed by the hemorrhage. B. Transverse image of the adrenal obtained for follow-up of adrenal hemorrhage in another infant shows the lucency that characteristically develops within adrenal hemorrhage in 2-3 weeks.

Adrenal Cysts

Four types of adrenal cysts are encountered [96]. Approximately equally common are endothelial cysts (45%) and post-hemorrhage pseudocysts (39%). True epithelial cysts and parasitic cysts are rare. Cysts may hemorrhage internally or become secondarily infected [97].

Cysts are well marginated with anechoic contents unless hemorrhage or infection has occurred [90].
Most adrenal cysts have a visible wall 3 mm or less in thickness [98].
Avascular internal septations are characteristic of post-hemorrhage pseudocysts. Calcification in the wall of old pseudocysts is common.
Distinct, vascularized solid components suggest a malignant lesion (carcinoma or metastasis).

Adrenal Myelolipomas

Myelolipomas are rare benign tumors containing mature fat and bone-marrow elements. Hemorrhage into the tumor may occur [99].

Tumors are typically intensely echogenic because of their fat content (Fig. 3.57). Hypoechoic regions represent myeloid content. They are easily overlooked on US because they blend in with retroperitoneal fat. CT confirmation of fat content is diagnostic [99].

Neuroblastoma

Neuroblastoma is the most common extracranial malignancy in infants.

Figure 3.57 Adrenal Myelolipoma. Longitudinal image demonstrates the high echogenicity of this tumor (between black and white arrows) containing mostly fat. Because they blend in with retroperitoneal fat, these lesions are easily missed during US examination. K, right kidney; L, liver.

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Lesions are large, solid, poorly encapsulated, and commonly cross the midline (Fig. 3.58).
Calcifications are found in 50% of tumors.
The tumor commonly encases blood vessels and may extend into the spinal canal.

Adrenal Hyperplasia

Bilateral adrenal hyperplasia accounts for approximately 20% of adrenal endocrine syndromes.

Hyperplasia diffusely enlarges the adrenal glands without a discrete mass. The limbs exceed 1-cm diameter and are elongated [91].

Figure 3.58 Neuroblastoma. Transverse image shows a large solid mass (arrows) arising from the right adrenal and compressing the liver (l) and inferior vena cava (i). a, aorta.

Figure 3.59 Varix Mimics an Adrenal Mass. This patient was referred for biopsy of a left adrenal mass seen on a CT of the abdomen performed without contrast because the patient had impaired renal function. A. US revealed a homogeneous, hypoechoic, left suprarenal mass (arrow). K, left kidney; S, spleen. B. Color Doppler confirmed the “mass” was a varix (arrow) formed because of the patient’s portal hypertension (see Color Figure 3.59).

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Adrenal Calcification

The adrenal gland may become completely or partially calcified as a result of previous adrenal hemorrhage, or late in adrenal involvement by tuberculosis or histoplasmosis. Destruction of 90% or more of the adrenal cortex by these infections may result in adrenal insufficiency (Addison’s disease) [91].

Coarse or punctate calcifications produce bright echodensities with acoustic shadowing. No adrenal parenchyma may be evident.
Wolman’s disease is a rare lipid storage disorder characterized by large adrenal glands with punctate calcification. Marked hepatosplenomegaly is usually present.

Pitfalls in Adrenal Imaging

Because the adrenal glands are small and surrounded by numerous other structures, non-adrenal structures are commonly mistaken for adrenal masses (Fig. 3.59). Tortuous splenic vessels, portosystemic collateral vessels, renal, splenic, and pancreatic masses, adenopathy, gastric diverticuli, and portions of the stomach may all mimic adrenal masses.

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Neurogenic bladder	Cystitis (infectious, inflammatory)
Chronic bladder outflow obstruction	Chronic/recurrent bacterial cystitis
Prostate enlargement	Tuberculous cystitis
Urethral stricture	Schistosomiasis
Diffuse infiltrating neoplasm	Cyclophosphamide cystitis
Transitional cell carcinoma	Radiation therapy
Squamous cell carcinoma	Bladder augmentation procedures

	Core Curriculum, The: Ultrasound 1st Edition
	© 2001 Lippincott Williams & Wilkins

Core Curriculum, The: Ultrasound1st Edition

Core Curriculum, The: Ultrasound
1st Edition