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9

Kidneys

Hyperechoic Structure

Kidneys

Anomalies, Malformations

 

 

 

 

 

 

Diffuse Changes

 

 

 

 

 

 

 

Large Kidneys

 

 

 

 

Small Kidneys

 

 

 

 

Hypoechoic Structure

 

 

 

 

Hyperechoic Structure

 

 

 

 

 

 

 

 

Irregular Structure

 

 

 

Circumscribed Changes

 

 

 

Hypoxemic Renal Shock

Diabetic Nephropathy

Acute and Chronic Glomerulonephritis Chronic Pyelonephritis

Analgesic Nephropathy

Septic–Toxic Kidneys Severe Metabolic Disorders

Light-chain Deposition Disease, Waldenström Macroglobulinemia Amyloidosis

Infiltration by Lymphoma Atrophic Kidneys

An increase in echogenicity is to be found in

renal function: increased echogenicity is corre-

many acute and chronic renal diseases. It indi-

lated with the change in renal function (Table

cates no special nephropathy, but it is an im-

9.2).

portant sonographic sign indicating disturbed

 

Table 9.2 Hyperechoic transformation of the renal parenchyma in kidney diseases

Acute renal diseases

Chronic renal diseases

Metabolic disease (diabetes, paraproteinemia)

Amyloidisis

Hypoxemic renal shock

Diabetic nephropathy

Nephrotic syndrome

Chronic glomerulonephritis

Acute glomerulonephritis

Chronic interstitial nephritis

Acute pyelonephritis (focal abscess)

Analgesic nephropathy

Hydronephrosis

Nephrosclerosis: hyperechoic vascular wall thickness, only some

Interstitial nephritis

vascular spots; increased RI

After furosemide

 

Acute nephritis

 

Hypoxemic Renal Shock

A septic–toxic illness or hypoxemia can cause severe kidney damage with renal failure, leading to subtle but definite changes consisting of a diffuse increase in cortical echogenicity and very echopenic medullary pyramids. These changes are caused by diffuse tubular damage and necrosis, and also by decreased vascularization in cases with severe hypoxemia, so that hypovascular or avascular areas are found in color Doppler scanning (Fig. 9.40).

 

 

 

Fig. 9.40 Hypoxemic renal shock in the setting of acute

b Color Doppler shows scant color signals, reflecting the

 

 

 

cardiac and renal failure. The patient was resuscitated for

marked decrease in vascularity.

 

 

 

ventricular fibrillation (after sniffing butane gas, with a

 

 

 

 

fatal outcome).

 

 

 

 

a The parenchyma is broadened and hyperechoic, result-

 

 

 

 

ing in a narrow sinus echo complex. Prominent hypo-

 

 

 

 

echoic medullary pyramids.

 

Diabetic Nephropathy

 

 

Today, diabetic nephropathy has become the

drome), shows increased cortical echogenicity

the medullary pyramids stands in sharp con-

most frequent indication for hemodialysis. Re-

due to histopathological changes in basement

trast to the very echogenic cortex ( 9.1; Table

nal ultrasound examination in glomerular dis-

membrane collagenization, glomerular en-

9.3, Table 9.4).

eases,

including

diabetic glomerulosclerosis

largement, mesangial cell proliferation, and

 

(also

known as

Kimmelstiel–Wilson syn-

subsequent glomerulosclerosis. The lucency of

 

338

Table 9.3 Sonographic changes seen in different stages of diabetic nephropathy

Early stage

Advanced stage

Renal enlargement (volume increase)

Normal renal size with rarefied parenchyma

Increased cortical echogenicity

Increased cortical echogenicity

Markedly hypoechoic medullary pyramids

Cystic transformation or disappearance of

 

medullary pyramids

 

Wavy contours

9.1 Diabetic Nephropathy3

Stages I and II

Hyperperfusion with a volume increase

Stage III

Incipient nephropathy with microalbumi-

 

nuria (hyperperfusion with a volume

 

increase)

Stage IV

Overt nephropathy (proteinuria)

Stage V

Renal failure (nephrotic syndrome)

Stage V with dialysis

End stage

Small kidneys

Intensely hyperechoic parenchyma

Disappearance of medullary pyramids

Secondary cysts, calcifications

a Large kidneys, normal structure.

b Enlarged kidneys (N), normal width, incipient hyperechoic cortex, prominent hypoechoic medullary pyramids (arrows). L = liver.

c Normal-size kidneys (N), parenchymal thickness still normal, increased cortical echogenicity; broadened, hypoechoic medullary pyramids.

d Renal size still normal, rarefied cortex, markedly hypoechoic “cystic” pyramids with echogenic demarcation.

e and f Small kidneys (N) (8.7 cm), rarefied cortex, degeneration or disappearance of the medullary pyramids (MP), parenchymal destruction (possible secondary cysts, calcifications). Spotty, deformed vascular segments. L = liver.

9

Diffuse Changes

339

9

Kidneys

Acute and Chronic Glomerulonephritis

Both acute and chronic (bilateral) glomerulo-

glomerulonephritis, normal-sized in chronic

The usually pronounced increase in echoge-

nephritis are associated with increased cortical

glomerulonephritis, and smaller in later stages.

nicity is caused by histological changes. It has

echogenicity, which is more distinct than in

The medullary pyramids are prominent,

been shown that cortical echogenicity corre-

diabetic nephropathy.7 Again, the medullary

whereas in later stages the surface becomes

lates with histological criteria such as sclerosis,

pyramids appear markedly hypoechoic relative

undulated. In the dialysis stage, secondary

tubular atrophy, hyaline casts, and focal leuko-

to the cortex. The kidney is enlarged in acute

cysts are frequent (Fig. 9.41, Fig. 9.42).

cytic infiltration (Table 9.4).8

Fig. 9.41 Acute glomerulonephritis: enlarged kidneys (N)

Fig. 9.42

with markedly increased cortical echogenicity and very

a Chronic glomerulonephritis (prior history of rheumatic

prominent, hypoechoic medullary pyramids (arrows).

fever) and chronic renal failure: small kidney (N), hyper-

 

echoic cortex, disappearance of the medullary pyramids,

 

shallow notches due to scarring (arrows). L = liver.

Chronic Pyelonephritis

Chronic pyelonephritis is also associated with

tory conditions listed above, and scarring leads

increased echogenicity. The kidney is generally

to areas of parenchymal thinning (Fig. 9.43,

small, however, compared with the inflamma-

Table 9.4).

b Membranous glomerulonephritis due to chronic hepatitis C. Markedly increased echogenicity of the renal cortex compared to the liver structure, normal size (cursors). LE = liver; N = kidney.

Table 9.4 Histopathology of chronic diabetic, glomerular and interstitial nephropathy

Diabetic nephropathy

Early stage

 

Glomerular enlargement, mesangial cell proliferation

 

Basement membrane collagenization

 

Late stage

 

Glomerulosclerosis

 

Broadened mesangium with deposits

 

Arteriosclerosis

 

Glycogen storage in tubules

 

Papillary tip necrosis

Chronic glomerulonephritis

Mesangial cell proliferation

 

Glomerular enlargement

 

Basement membrane thickening

 

Mesangial, capillary, tubular deposits

 

Cellular infiltrates

Chronic pyelonephritis

Interstitial scarring

 

Lymphoplasmocytic infiltrates

 

Tubular atrophy

 

Tubular protein deposits

 

Scarring of the pyelocaliceal system

Analgesic nephropathy

Papillary necrosis

 

Broadening of the capillary basement membrane in the

 

renal medulla (capillary sclerosis)

 

Lipofuscin deposits in tubules

 

Lymphoplasmohistiocytic infiltrate with fibrosis, sclerosis

Fig. 9.43 Old chronic pyelonephritis: small kidney with multiple echogenic sites of parenchymal retraction due to scarring.

340

Severe septic–toxic disease states are characterized by a markedly hyperechoic, swollen renal cortex. These changes are usually associated with renal enlargement. Direct septic– toxic tissue effects such as necrosis, lympho-

leukocytic infiltration, or ischemic vascular changes can occur. Similar changes are found in acute tubular obstruction by urates in the chemotherapy of malignant lymphoma, also in acute renal failure, lupus erythematosus, he-

Fig. 9.44 Analgesic nephropathy: nonhomogeneous, hyperechoic parenchyma with ill-defined contours. Note the hyperechoic areas at the tips of the medullary pyramids (calcifying papillary necrosis, acoustic shadows S).

molytic–uremic syndrome, and acute glomerular renal diseases. After the systemic manifestations have subsided, the diffuse structural changes also regress (Fig. 9.45, Fig. 9.46).

9

Diffuse Changes

Fig. 9.45 Septic–toxic abdomen: normal-size kidney with increased cortical echogenicity and prominent hypoechoic medullary pyramids.

Fig. 9.46 Septic–toxic renal failure.

a The kidney (N) shows greatly increased echogenicity relative to the liver (L). Note the prominent, hypoechoic medullary pyramids.

b Enlarged view shows massive swelling and decreased echogenicity of the medullary pyramids (MP).

Severe Metabolic Disorders

Severe metabolic disorders such as untreated diabetes mellitus, with or without diabetic coma, are occasionally associated with pronounced renal structural changes. Possible causes are severe dehydration, tubular glycogen storage or other storage disorders, as well as glomerular/tubular changes that do not always have a discernible cause, especially if the case cannot be evaluated histologically (Fig. 9.47, Fig. 9.48).

Fig. 9.47 Neglected case of type I diabetes mellitus: massive parenchymal swelling, increased echogenicity (relative to the spleen, M), prominent hypoechoic pyramids (arrows). Lateral flank scan displays the aortic band at the bottom of the image. N = kidney.

Fig. 9.48 Toxic renal failure secondary to extensive thrombosis of the portal venous system: large, echogenic kidney (N), prominent hypoechoic pyramids, perirenal ascites.

341

9

Kidneys

Light-chainDeposition Disease, Waldenström Macroglobulinemia

Light-chain deposition disease is a nonspecific condition that leads to renal failure based on the precipitation of light-chain paraproteins in the distal tubules, a hypercalcemic tubulopathy in hypercalcemia syndrome, and/or an accompanying deposition of amyloid. Similar changes are encountered in Waldenström macroglobulinemia and amyloid kidney.

Ultrasound may demonstrate renal enlargement and increased cortical echogenicity. Often there is only mild enlargement with an indistinct parenchymal texture (Fig. 9.49).

Fig. 9.49 Light-chain deposition disease, hypercalcemic crisis, renal failure.

a Right kidney (N): parenchyma has a somewhat indistinct structure and appears slightly hyperechoic to the liver (L). Prominent medullary pyramids.

b Acute renal failure requiring dialysis in a patient with paraproteinemia (and initial hypercalcemia) and a plasmacytoma. The kidneys are still of normal size (N, cursors). The parenchyma shows markedly increased echogenicity with enlarged, hypoechoic to anechoic medullary pyramids (arrows).

Amyloidosis

Amyloidosis is also associated with an increase in cortical echogenicity and prominent hypoechoic pyramids. We see, then, that these diffuse structural changes occur in a variety of diseases and cannot be considered specific sonographic features; indeed, they are very nonspecific. Only if the underlying disease is known can the echogenicity changes be referred to a specific renal complication. In the beginning the kidneys are normal in size and markedly hyperechoic. In later stages they become smaller and even diminutive at the dialysis stage (Fig. 9.50).

Fig. 9.50 Presumed renal amyloidosis: echogenic renal cortex with increased parenchymal volume causing slight narrowing of the sinus echo complex. Hypoechoic, illdefined medullary pyramids (rheumatoid arthritis, renal failure with nephrotic syndrome). L = liver; N = kidney.

Infiltrationby Lymphoma

The infiltrating lymphomatous tissue leads to renal enlargement (see above). Increased echogenicity may be seen, but the bulges in the renal outline (frequently heterogeneous in structure) and irregular tumor vascularity serve to distinguish this disease from those listed above (Fig. 9.32, Fig. 9.79).

Atrophic Kidneys

Generally the detection of renal atrophy does not point to a specific cause (Fig. 9.51), although bilateral atrophic kidneys are more likely to have a diabetic etiology (only in the late dialysis stage) or a glomerular cause, or may result from analgesic nephropathy.

Unilateral renal atrophy, or bilateral atrophy that differs in severity between the sides, usually has a different cause such as pyelonephritis or vasopathy (Fig. 9.52).

As the name implies, the kidneys appear small in ultrasound. The parenchyma is thinned, and the renal outlines are smooth (glomerular, diabetic) or wavy (pyelonephritis

Fig. 9.51 Small, hyperechoic right kidney (N, arrows) due to an unknown cause. Slight structural irregularity. L = liver.

Fig. 9.52 Renal atrophy (85 mm) due to arteriosclerosis and arteriolosclerosis: irregular, rarefied, slightly hyperechoic parenchyma (cursors) with a correspondingly broadened sinus echo.

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