Материал: Advanced Imaging of the Abdomen - Jovitas Skucas

KIDNEYS AND URETERS

setting of acute renal failure. Newer methods of estimating glomerular filtration rate include plasma clearance of small amounts of iohexol, a nonionic contrast agent. A correlation exists between renal clearance of inulin and iohexol in patients with moderate to severe renal failure. Doppler US appears useful in following acute renal failure; recovery of renal function is associated with a progressive drop in resistive index.

The normal postintravenous contrast pyelocaliceal phase MR signal intensity decrease is lacking in renal insufficiency patients; this change is due to the reduced renal concentrating ability in these patients.

Vascular Causes

A common cause of acute prerenal failure is hypoperfusion due to either cardiac failure or hypovolemia; the latter condition is detected with a fluid-load challenge. Bilateral renal artery or vein occlusion, although rare, also leads to renal hypoperfusion, with a lack of response to a fluid load. Vascular occlusion in a solitary kidney is perhaps a more common cause of acute failure than bilateral vascular involvement; US should exclude this finding.

Atherosclerotic vascular disease or small vessel disease such as cholesterol crystal embolization have led to acute renal failure. Drug-induced vasomotor disorders also play a role. Bilateral vasculitis leading to renal artery obstruction and small vessel disease are less common causes of acute renal failure.

Hypertensive nephropathy and related renal artery stenosis are common causes of chronic renal failure. The latter is discussed in Chapter 17.

Acute Tubular Necrosis

Acute tubular necrosis is a common cause of acute renal failure and associated high morbidity and mortality. The causes of acute tubular necrosis include nephrotoxic, ischemic, hypotensive, and other factors. It occurs after bilateral ureteral obstruction due to any cause. The evidence suggests that it is induced by tubular damage and tubular obstruction, although a role for renin is also suggested. Included among nephrotoxic agents are the following:

1.Iodinated radiographic contrast agents. The risk of nephrotoxicity is increased in a setting of impaired renal function.

2.Viper venom is mainly hemotoxic and causes coagulation abnormalities, but about one third of patients after systemic envenomation have renal involvement; renal biopsy in those with severe renal dysfunction reveals acute tubular necrosis.

3.Overexposure to aliphatic hydrocarbons present in diesel fuels and solvents.

4.A nephropathy due to Amanita phalloides exposure.

Clinically, acute tubular necrosis is mimicked by bilateral renal artery occlusion or severe stenosis, and these conditions should be excluded. Ultrasonography identifies normal kidneys in a setting of acute tubular necrosis. Doppler US, however, reveals an increased RI in most of these patients. Scintigraphy with Tc- 99m-DTPA or Tc-99m-MAG3 is useful in these patients to confirm the presence of acute tubular necrosis and exclude renal vascular occlusion; parenchymal activity without excretion suggests acute tubular necrosis.

Intravenous contrast in patients with acute tubular necrosis shows a dense, persisting nephrogram with little or no excretion of contrast from enlarged kidneys. Contrast can persist in renal parenchyma for a prolonged time.

Acute Cortical Necrosis

The etiology of acute cortical necrosis is usually multifactorial. Prior to 1980, obstetrical causes were common; since then sepsis, dehydration, drugs (discussed in the next section), and, in India, snake bite predominate. Shock and transfusion reaction have been implicated. Urinary obstruction is occasionally implicated. Chronic pyelonephritis, diabetes, and hypotension probably also play a role in this condition.

The underlying abnormality is cortical ischemia with relative sparing of medulla. Peripheral cortical regions remain viable due to intact capsular vessels. Initially involved kidneys enlarge but on a chronic basis shrink in size.

Acute cortical necrosis can be unilateral or bilateral. The papillae cavitate, and communi-

cate with an adjacent calyx, and the sloughing of papillae leads to calyceal clubbing. In time, linear cortical calcifications develop.

A diagnosis of acute cortical necrosis is most often suggested by IV urography or postcontrast CT. It can be detected by renal arteriography; the renal cortex does not enhance after contrast injection while the medulla enhances. No contrast excretion is evident from abnormal papillae. Magnetic resonance reveals a hypointense cortex on T2-weighted images.

Drug Induced

Renal toxicity is ascribed to numerous drugs, with some being anecdotal reports with little proof. An increased risk of nephrotoxicity due to long-term analgesic exposure is suggested by a number of studies. Yet one review concluded that although excessive use of phenacetincontaining analgesics probably does cause renal papillary necrosis and interstitial nephritis, no convincing epidemiologic evidence exists that non–phenacetin-containing analgesics (such as acetaminophen and aspirin) or nonsteroidal antiinflammatory drugs (NSAIDs) cause renal damage (124). Nevertheless, the literature contains numerous reports of an increased risk of nephrotoxicity from NSAIDs due to dehydration, hypotension and resultant renal hypoperfusion, congestive heart failure, and underlying renal failure. The NSAIDs appear to inhibit renal synthesis of prostaglandins. Normally in low perfusion states the vasodilator prostaglandins help prevent vasoconstriction and maintain renal blood flow, and in this setting the inhibition of prostaglandin production leads to renal failure and fluid retention.

Other believed associations with NSAIDs include acute tubulointerstitial nephritis, papillary necrosis, and nephrotic syndrome.

Patients with analgesic nephropathy lose renal volume bilaterally, and the kidneys develop an irregular outline. Papillary calcifications are common. Even in the early stages of analgesic nephropathy, CT detects papillary calcifications with a high sensitivity, and CT is superior in detecting calcifications to US and conventional radiography.

Even mannitol has led to acute anuric renal failure in a setting of chronic renal failure due to diabetic nephropathy.

ADVANCED IMAGING OF THE ABDOMEN

Acute Interstitial Nephritis

Acute interstitial nephritis is believed to represent an acute hypersensitivity reaction, most often secondary to drugs, including NSAIDs. Abnormal leakage from glomerular capillaries and an interstitial infiltrate lead to nephrotic syndrome and eventual renal failure. In general, renal failure resolves after withdrawal of the offending agent, although deaths are reported.

Prolonged renal failure developed in an adult with Henoch-Schönlein purpura after an episode of macroscopic hematuria (125); histology revealed findings of tubulointerstitial nephritis. Some infections are associated with acute interstitial nephritis.

The kidneys enlarge during the acute phase. Delayed postcontrast CT reveals corticomedullary contrast enhancement due to vascular and tubular stasis. Ultrasonography detects diffusely hyperechoic cortices. The kidneys gradually decrease in size as the condition clears.

Chronic Tubular Dysfunction

Disorders

Damage to renal tubules often also involves adjacent interstitial tissue and vice versa. The major factor in renal failure, however, is tubular damage. From a prognostic viewpoint, tubular injury progressing to tubular atrophy leads to a permanent loss of renal function.

Renal Tubular Acidosis

The term renal tubular acidosis describes several tubular transport disorders. Traditionally, it is subdivided into proximal and distal types based on which nephron segment is involved, although such an approach is an oversimplification of the underlying pathophysiology:

Type I: defect in hydrogen ion secretion (distal renal tubular acidosis)

Type II: defect involving bicarbonate reabsorption (proximal renal tubular acidosis)

Type III: defects in both distal and proximal renal tubules

KIDNEYS AND URETERS

Type IV: aldosterone deficiency and resistance to aldosterone result in a hyperkalemic renal tubular acidosis

In general, renal tubular acidosis in childhood has a congenital etiology, while in adults acidosis tends to be secondary to another condition. The prevalence of renal cysts appears increased in type I renal tubular acidosis.

Some children with vesicoureteral reflux also have renal tubular acidosis; growth failure in these children probably is due to the renal tubular acidosis.

Patients with type I disease develop nephrocalcinosis. Aside from detecting nephrolithiasis and nephrocalcinosis and excluding other conditions, imaging has a limited role in these disorders.

Renal tubular acidosis and decreased renal function result in decreased renal accumulation of Tc-99m-DMSA and increased background activity. Such a renal pattern should lead to a search for an underlying defect.

Cystinosis

Nephropathic cystinosis results in renal tubular acidosis.

The importance of detecting nephropathic cystinosis lies in that effective therapy exists for cystine accumulation.

Tubulointerstitial Nephritis

Medullary cystic disease, a type of tubulointerstitial nephritis, was discussed earlier (see Congenital Abnormalities).

Etiology of renal tubulointerstitial fibrosis is unknown, although two peptides— transforming growth factor-b (TGF-b) and angiotensin II—appear to play a role. Also, both interstitial fibroblasts and renal tubular epithelium are involved in formation of an extracellular matrix. Initially affected patients tend to be asymptomatic, and the condition is often discovered only when advanced.

Infection

Among unusual infections, Legionnaire’s disease has led to acute renal failure. Rocky Mountain spotted fever, due to infection with Rickettsia rickettsii, is associated with acute

renal failure; infected patients developing acute renal failure have a high mortality. Severe leptospirosis and severe malaria have led to acute renal failure.

Reversible acute oliguric renal failure is a rare complication of nonfulminant hepatitis A infection in some patients.

Rhabdomyolysis

Rhabdomyolysis typically develops secondary to muscle compression, epilepsy, infection, ischemia, heat stroke, or trauma, and results in acute renal failure. Occasionally nontraumatic rhabdomyolysis develops in a setting of diabetic ketoacidosis. Presumably increased myoglobin levels are responsible for renal damage in this condition; myoglobin is a nephrotoxin.

In Pregnancy

Septic abortion used to be the main cause of renal failure in pregnancy; currently preeclampsia and eclampsia are more common factors. In some women renal failure is multifactorial; thus chronic hypertension or acute pyelonephritis in a setting of preeclampsia should be considered. Occasionally idiopathic postpartum renal failure develops. Chronic renal failure ensues in some patients.

A rare complication is HELLP syndrome (hemolysis, elevated liver enzymes, and low platelets) occurring during both pregnancy and puerperium. A major complication of this syndrome is acute renal failure. In a pregnancyrelated acute renal failure study, HELLP syndrome accounted for 36%, postpartum hemorrhage for 26%, preeclampsia/eclampsia for 15%, and abruptio placenta for 10% (126).

Hemolytic-uremic syndrome is a rare complication developing in pregnancy and postpartum.

Diabetic Nephropathy

The most common cause of chronic renal failure is diabetes mellitus. One should keep in mind, however, that diabetic patients also develop renal stones, reflux, and infections, and in these patients voiding cystourethrography, urodynamic studies, and at times retrograde pyelography are indicated to exclude related conditions.

Initially the kidneys enlarge, but with time shrink in size. A glomerulosclerosis ensues and eventually nephrotic syndrome and end-stage renal failure develop.

Preand postcontrast helical CT in type 2 diabetic patients reveal that both axial renal diameters and arterial-phase cortical density are less in those with a nephropathy than in nonnephropathic diabetics and controls (127); these changes are related to the duration of disease.

Once nephropathy is well established, US identifies hyperechoic cortices. In patients with insulin-dependent diabetes mellitus but normal creatinine and blood urea nitrogen levels, Doppler US–derived renal interlobar artery RI is not sensitive enough in screening for glomerular hyperfiltration.

Glomerulonephritis

The subtypes of glomerulonephritis include membranous, immunoglobulin A (IgA)-related, vasculitis, and idiopathic. Systemic diseases associated with glomerulonephritis include a number of infections, polyarteritis nodosa, systemic lupus erythematosus, and Wegener’s granulomatosis.A minority of cirrhotic patients have glomerulonephritis ranging from membranoproliferative to focal segmental and membranous. An infected ventriculoatrial shunt can lead to glomerulonephritis, a condition known as shunt nephritis. Even an occasional patient with inflammatory bowel disease develops proteinuria due to membranous glomerulonephritis. Glomerulonephritis and nephrotic syndrome are associated with solid neoplasm paraneoplastic syndromes. Histopathology typically reveals membranous glomerulonephritis. Proteinuria generally clears after tumor resection.

Renal enlargement is common in acute glomerulonephritis. Renal echogenicity varies, but often is greater than in the adjacent liver. Echogenicity decreases with clinical improvement.

Chronic glomerulonephritis leads to a gradual loss of renal parenchyma. Only a faint but persisting nephrogram is identified post–contrast injection. Eventually the kidneys become small, smooth, and hyperechoic, similar to other end-stage renal disease.

Color Doppler US is helpful in distinguishing glomerular nephropathy and disorders of vas-

ADVANCED IMAGING OF THE ABDOMEN

cular origin. The resistive index is related more to the site of disease than to the degree of renal failure. A normal RI is found in most patients with glomerulonephrosis, while patients with tubulointerstitial or vascular nephrosis have an increased resistive index.

Absent parenchymal uptake during scintigraphy with Tc-99m-MAG3 suggests acute glomerulonephritis.

Patients with newly discovered glomerulonephritis probably should undergo chest radiography not only to detect evidence of cardiac failure and effusions but also to establish a baseline appearance.

Focal Segmental Glomerulosclerosis

Focal segmental glomerulosclerosis is a syndrome resulting in chronic, progressive renal fibrosis. It is a common cause of renal disease. Histology reveals sclerosis of some but not all glomeruli (hence the name). It does not appear to be an immune response. Most authors subdivide it into a primary form, with no discernible cause, and a secondary form associated with a number of diseases, including diabetes, analgesic abuse, reflux nephropathy, a rejection phenomenon, HIV-associated nephropathy, and, in some patients, renovascular hypertension. Collapsing glomerulopathy is a variant of focal segmental glomerulosclerosis manifesting by the collapse of glomerular capillaries, marked podocyte enlargement, and associated tubulointerstitial disease.

Clinically this entity manifests as nephrotic syndrome and leads to progressive renal failure. It develops both in children and adults.

Imaging plays a role mostly in detecting damage due to secondary causes.A hypertensive patient developed unilateral focal segmental glomerulosclerosis associated with contralateral renal artery stenosis (128); the contralateral kidney presumably was spared glomerulosclerosis by the renal artery stenosis. The patient’s renal insufficiency resolved after renal artery stenosis repair, suggesting renovascular hypertension as the primary cause for focal segmental glomerulosclerosis.

Therapy of any underlying condition is generally instituted. Corticosteroids are often used to treat patients with idiopathic focal segmental glomerulosclerosis, despite a lack of evidence for such therapy. The eventual therapy is renal