The characteristic appearance of a malignant renal tumor is that of a circumscribed hypoechoic mass. Renal cell carcinoma (RCC) appears as a sharply circumscribed bulge in the renal outline, while urothelial carcinoma forms a hypoechoic mass in the central sinus echo. With extensive tumor infiltration, the kidney appears substantially enlarged and broadened. Its structure is markedly nonhomogeneous owing to intrarenal pyelectasis and the presence of calcifications (Fig. 9.32).

Fig. 9.32 Greatly enlarged kidney completely permeated by tumor. The kidney shows a heterogeneous, predominantly hypoechoic structure. Histological diagnosis: highgrade non-Hodgkin lymphoma.

As a solitary functioning kidney, the renal allograft is enlarged owing to adaptive hypertrophy. Additional enlargement occurs in association with allograft rejection. Enlargement is not a dependable sign of rejection, however. A more definitive sign is occlusive vasculopathy, which can be demonstrated with Doppler ultrasound.

Complications consist of renal artery stenosis, renal vein thrombosis, and arteriovenous fistulas. The RI in these cases is greater than 0.9 and the pulsatility index (PI) is greater than 1.6. Published values of sensitivity and specificity range from 14% to 98% (Fig. 9.33).

Fig. 9.33 Renal transplant. The allograft is enlarged to 13.0 cm, with accentuated renal columns (C) and prominent hypoechoic medullary pyramids (arrows).

Small Kidneys

Hypoplasia

Renal Artery Stenosis, Embolism

Arteriosclerosis, Arteriolosclerosis (Ischemic Nephropathy)

Chronic Pyelonephritis

Analgesic Nephropathy

Chronic Glomerulonephritis

Diabetic Nephropathy

While arteriolosclerosis leads to a decrease in renal size with thinning of the cortex, arteriosclerosis causes an irregular surface with areas of parenchymal thinning, but an overall normal renal size. The echogenicity is normal or slightly hyperechoic (due to sclerosis) and the parenchyma is frequently narrowed. The surface appears smooth when arteriolosclerosis is predominant; in arteriosclerosis the surface appears coarse, with a scarred contour, and thickened segmental arteries showing bright double echoes with a central, narrow echofree band can be seen in the renal sinus.

Similar changes are seen as a result of multiple infarcts in panarteritis nodosa (Fig. 9.35).

Fig. 9.35

a Retraction of the kidney surface and parenchymal scars and rarefaction by arteriosclerosis.10

Chronic pyelonephritis is a chronic interstitial (bacterial), episodic inflammatory process characterized by the scarring and destruction of renal parenchyma. In bilateral cases that have progressed to a stage requiring dialysis, the kidneys are significantly smaller than normal, especially in their longitudinal dimension.5 Additional features are focal changes such as stones (33%) and cysts (31%) and changes in cortical structure with a significant increase in echogenicity (9.2 g). In interstitial renal diseases, a correlation exists between the echogenicity of the renal cortex and histological changes such as sclerosis, tubular atrophy, hyaline casts, and focal leukocyte infiltration.6

A small or atrophic kidney in pyelonephritis is more commonly unilateral than bilateral, and it can be difficult in these cases to establish a cause. In the advanced stage of renal atrophy when the longitudinal size of the kidney has dwindled to approximately 6–7 cm, ultrasound is generally no longer helpful in diagnosing the cause. In addition to these changes, abscesses may form in the renal pelvis, appearing as hypoechoic masses. This is especially common in diabetics with an acute infection (Fig. 9.36,

Fig. 9.61, 9.5 d).

The term analgesic nephropathy refers to a chronic, noninfective, interstitial, bilateral nephritis that is incited by the use of analgesic medication. The histological features are a lu- men-occluding capillary sclerosis, tubular and papillary necrosis, and papillary necrosis with calcification of the papillary tips.

The sonographic features reflect the histological changes in the form of decreased renal size, increased echogenicity, wavy contours, and fine calcifications at the tips of the medullary pyramids. Some cases present with secondary microcysts, usually resulting from the cystic degeneration of medullary pyramids, or with tubular retention cysts (detectable in 50% of cases) (Fig. 9.37).7

Fig. 9.37 Analgesic nephropathy (N). Marked parenchymal rarefaction with a hazy structure and fine calcifications projected over the papillary tips (arrows). Secondary cyst (Z). Patient had a 30-year history of daily analgesic use and known pyelonephritis. Creatinine 4.8 mmol/L. Harmonic imaging.

Chronic glomerulonephritis and diabetic nephropathy (glomerulosclerosis) are both characterized by a decrease in renal size that does not occur until an advanced stage. In both diseases, the longitudinal diameter of the kidney is within normal limits in patients who have reached the dialysis stage.7 The authors found cystic lesions in 14% of cases.

Sonographically, the kidney shows markedly increased echogenicity due to glomerular hyalinization and tubular atrophy. The medullary pyramids may still be appreciated as hypoechoic areas, but in most cases they disappear owing to histologically demonstrable tubular atrophy. In advanced stages the renal structural changes may no longer be helpful in identifying the cause of the disease (Figs. 9.38, 9.41, 9.42).

Fig. 9.38 Small, hyperechoic right kidney (N) due to an unknown cause. Left-sided hydronephrosis (following ureteral ligation). Renal failure with creatinine of 5.6 mg/dL. L = liver; A = ascites.

In our own observations of diabetics with nephropathy, we found that the renal volumes in diabetic nephropathy patients with stage I–IV disease2 (Table 9.3) were consistently above normal, with volumes in excess of 200 mL. In stage V disease, the kidneys return to either a normal or slightly decreased size, and small kidneys are not seen until the later dialysis stage.

Ultrasound at that stage demonstrates rarefied areas in the cortex and increased echogenicity. Microcysts are also found, consisting mainly of medullary pyramids that have undergone cystic degeneration. The end stage is marked by atrophic kidneys with complete parenchymal destruction, and the genesis of the disease can no longer be determined by sonographic findings (Fig. 9.39).

Kidneys

Anomalies, Malformations

Diffuse Changes

Large Kidneys

Small Kidneys

Hypoechoic Structure

Hyperechoic Structure

Irregular Structure

Circumscribed Changes

Acute Renal Failure

Acute Nephritis

Right Ventricular Failure

Renal Vein Thrombosis