Diagnosing Vascular Causes of Renal Failure

  1. Gary J. Abuelo, MD
  1. From Rhode Island Hospital and Brown University School of Medicine, Providence, Rhode Island. For the current author address, see end of text. Acknowledgments: The author thanks Douglas Shemin, MD, Thomas Wachtel, MD, Lance Dworkin, MD, and Dianne Abuelo, MD, for comments on the manuscript; Alfredo Esparza, MD, for the photomicrographs; and Charlene McGloin for secretarial assistance. Requests for Reprints: J. Gary Abuelo, MD, Division of Renal Diseases, Rhode Island Hospital, 593 Eddy Street, Providence, RI 02903.
     
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    Abstract

    The incidence of renal failure due to vascular diseases is increasing. Two reasons for this are the epidemic of atherosclerotic vascular disease in the aging population and the widespread use of vasoactive drugs that can adversely affect renal function. These vascular causes of renal failure include vasomotor disorders such as that associated with nonsteroidal anti-inflammatory drugs, small-vessel diseases such as cholesterol crystal embolization, and large-vessel diseases such as renal artery stenosis. These causes of azotemia are less familiar to physicians than more classic causes, such as acute tubular necrosis, and are less likely to be recognized in their early stages. This article describes the various vascular diseases that impair renal function and outlines the steps necessary to identify them. Although some of these conditions, such as renal artery stenosis, can gradually impair function, the vascular causes of acute renal failure are emphasized in this article. Because the vasculitides primarily cause renal failure through secondary glomerulonephritis, they are mentioned only briefly. Extensive testing is rarely necessary because the cause is usually suspected through syndrome recognition. The diagnosis can then be confirmed by the results of one or two additional tests or by improved renal function after treatment.

    Vascular disorders have long been recognized as potential causes of azotemia [1]. In the past, these conditions were responsible for fewer than 10% of cases of acute renal failure [2, 3], and thus they may not be familiar to all practicing physicians. However, recent developments have increased their incidence. First, elderly persons, an increasing segment of our population, have more atheromatous renal emboli and atherosclerosis of the renal arteries. Second, radiocontrast agents, nonsteroidal anti-inflammatory drugs, and angiotensin-converting enzyme inhibitors, which are now used more frequently, can cause vasomotor renal failure [4]. In addition, thrombotic thrombocytopenic purpura and the hemolytic-uremic syndrome are being diagnosed more frequently [5-7]. Thus, vascular disorders now merit greater consideration when acute renal failure is evaluated. This article reviews these vascular disorders and their diagnosis. Treatment is not discussed.

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    Vasomotor Disorders

    Causes and Pathophysiologic Features

    Vasomotor causes of renal failure (Table 1) impair glomerular filtration by reducing glomerular capillary pressure. Because they do not usually damage renal tissue, kidney function recovers promptly when these causes are eliminated. Intraglomerular pressure decreases when afferent glomerular arterioles are constricted as a result of the hepatorenal syndrome [14]; hypercalcemia [15]; sepsis [16, 17]; or the use of nonsteroidal anti-inflammatory drugs [18-21], cyclosporine [22-24], or, possibly, radiocontrast agents [25-28]. Dilation of efferent glomerular arterioles by angiotensin-converting enzyme inhibitors also reduces intraglomerular pressure [29, 30].

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    Table 1. Vasomotor Disorders and Mechanisms of Reduced Glomerular Capillary Pressure*

    Some of these causes also decrease arterial fullness [31]. For example, hypercalcemia causes renal salt wasting [15]; the hepatorenal syndrome [14, 32-35], sepsis [36], and converting enzyme inhibitors reduce vascular resistance; and sepsis impairs cardiac function [36]. Decreased arterial fullness reduces renal perfusion pressure, which further lowers intraglomerular pressure.

    Any low-perfusion state, such as heart failure or fluid loss, may act synergistically with vasomotor disorders to impair renal function (Figure 1) [18-2133, 34, 37-40]. For example, nonsteroidal anti-inflammatory drugs and converting enzyme inhibitors normally have little effect on the kidneys. When renal perfusion is low, however, dilation of the afferent glomerular arterioles by prostaglandins [18, 20] and constriction of the efferent glomerular arterioles by angiotensin II [29, 30] maintain intraglomerular pressures adequate for filtration. Glomerular filtration is impaired by the inhibition of prostaglandin synthesis by nonsteroidal anti-inflammatory drugs and of angiotensin II synthesis by converting enzyme inhibitors (Figure 2). Thus, nonsteroidal anti-inflammatory drugs cause azotemia in persons with hypovolemia, heart failure, or the nephrotic syndrome [18-21]; and converting enzyme inhibitors cause azotemia in those with hypovolemia [38], heart failure [37, 39], and bilateral renal artery stenosis (or renal artery stenosis in one kidney) [41]. Added risk factors for renal failure induced by converting enzyme inhibitors in patients with heart failure are hypotension, hyponatremia, and azotemia [37, 39, 42, 43], which can reflect excessive diuretic use. In persons with heart failure, converting enzyme inhibitors often improve cardiac output sufficiently to offset renal vasomotor effects, and renal function remains stable or improves [37, 42].

    Figure 1. Low-perfusion states (shaded areas) such as renal artery stenosis and decreased arterial filling interact with vasomotor disturbances (white areas), and certain vasomotor disturbances interact with each other. Ca equals calcium; CEI equals converting enzyme inhibitors; NSAID equals nonsteroidal anti-inflammatory drugs; HR equals hepatorenal.
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    Figure 1. Low-perfusion states (shaded areas) such as renal artery stenosis and decreased arterial filling interact with vasomotor disturbances (white areas), and certain vasomotor disturbances interact with each other. Ca equals calcium; CEI equals converting enzyme inhibitors; NSAID equals nonsteroidal anti-inflammatory drugs; HR equals hepatorenal. Synergism in the production of renal failure by vasomotor disturbances.
    Figure 2. + = vasoconstriction, − = vasodilatation. A. Normal conditions. B. Perfusion pressure reduced within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilation and efferent vasoconstriction. C. Reduced perfusion plus nonsteroidal anti-inflammatory drugs (NSAIDs). Loss of vasodilatory prostaglandins increases afferent resistance. This causes glomerular capillary pressure to decrease to less than normal and GFR to decrease. D. Reduced perfusion plus converting enzyme inhibitor (CEI). Loss of angiotensin II reduces efferent resistance. This causes the glomerular capillary pressure to decrease to less than normal and GFR to decrease.
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    Figure 2. + = vasoconstriction, − = vasodilatation. A. Normal conditions. B. Perfusion pressure reduced within the autoregulatory range. Normal glomerular capillary pressure is maintained by afferent vasodilation and efferent vasoconstriction. C. Reduced perfusion plus nonsteroidal anti-inflammatory drugs (NSAIDs). Loss of vasodilatory prostaglandins increases afferent resistance. This causes glomerular capillary pressure to decrease to less than normal and GFR to decrease. D. Reduced perfusion plus converting enzyme inhibitor (CEI). Loss of angiotensin II reduces efferent resistance. This causes the glomerular capillary pressure to decrease to less than normal and GFR to decrease. Simplified diagram of intrarenal mechanisms for glomerular filtration rate (GFR) maintenance under reduced perfusion pressure, and GFR reduction by drugs.

    Chronic renal insufficiency also increases the risk for vasomotor renal impairment by converting enzyme inhibitors [39, 44, 45], nonsteroidal anti-inflammatory drugs [19, 46], and radiocontrast media [26, 28, 29, 47-51].

    Clinical Features

    Patients with vasomotor renal failure usually have liver failure, hypercalcemia, or sepsis or were exposed to a radiocontrast agent or drug (Table 1). Because these disorders are synergistic (Figure 1), several may be present, often combined with low-perfusion or chronic renal failure [33, 52-58]. After contrast media or vasoactive drugs are administered, the creatinine level increases within 1 or 2 days. Alternatively, the vasomotor disorder may already be present, but azotemia occurs with superimposition of arterial underfilling.

    Patients with the hepatorenal syndrome have hepatic failure with jaundice, ascites, cachexia, and often encephalopathy [32, 33, 57, 58]. The most common causes are alcoholic cirrhosis and other chronic liver diseases [58, 59]. Alternatively, some patients have fulminant acute liver failure, often due to viral hepatitis [32, 33, 59]. Blood pressure levels are low to normal due to reduced vascular resistance, and daily urine output is less than 1000 mL. Renal failure commonly begins in the hospital and is often precipitated by the use of diuretics, laxatives, or therapeutic paracentesis or by other forms of volume loss [57, 58, 60]. Except for rare patients with reversible acute liver failure, most patients die of complications of hepatic disease within weeks or months [32, 58, 61].

    Nephrotoxic radiocontrast reactions are usually seen after intravenous pyelography, angiography, or computed tomography in patients older than 40 years who have chronic azotemia [8, 47-52, 62]. The risk increases with diabetes mellitus [48, 49, 63-66], low cardiac output [40], higher contrast doses [28, 40], and probably ionic rather than newer, nonionic agents [63, 67]. Azotemia begins with or without oliguria within 1 day of the procedure, peaks within 3 to 5 days, and resolves by 2 to 3 weeks [8, 47-51, 62]. Dialysis is rarely needed.

    Urine Tests

    Urine from patients with vasomotor renal failure typically has no protein, no sediment, and little salt content (sodium and chloride concentrations less than 20 mmol/L; fractional excretions of sodium and chloride less than 1%) [21, 24, 68-71]. Low urine salt content indicates intact renal tubules and, in many cases, arterial underfilling. In patients with normal arterial filling, unknown intrarenal mechanisms produce the salt avidity. In patients with sepsis and the hepatorenal syndrome, arterial underfilling stimulates vasopressin, which increases urine-specific gravity to 1.015 or more.

    Three exceptions to these generalizations are recognized: Patients with preexisting kidney disease may show proteinuria and abnormal urinary sediment; hypercalcemia impairs urinary concentration and salt reabsorption (despite hypovolemia, urine-specific gravity is 1.010 or less, and sodium and chloride content is high [15]); and renal ischemia associated with the hepatorenal syndrome [60] or sepsis may induce acute tubular necrosis, increasing the urinary salt content and producing isotonic specific gravity (approximate 1.010) despite arterial underfilling.

    Diagnosis

    Patients usually have one or more obvious vasomotor causes. A characteristic urinalysis; contributory factors, such as hypovolemia; and the absence of another cause are further evidence. Low salt content in urine is almost sine qua non evidence in the hepatorenal syndrome and, if present, supports the diagnosis of other vasomotor causes. Therefore, after measuring urinary creatinine, sodium, and chloride concentrations, the physician should calculate the fractional excretions of sodium [UNa × Pcr/(PNa × Ucr) × 100%] and chloride [UCl × Pcr/(PCl × Ucr) × 100%]. In patients excreting nonreabsorbable urinary anions (such as β-lactams or ketoacids), urinary chloride reflects renal salt avidity better than sodium does. Although nonreabsorbable anions increase sodium excretion, the level of chloride excretion remains low. Ideally, the physician should wait 12 to 24 hours after administration of a diuretic before obtaining the urine sample.

    The diagnosis is confirmed if renal function recovers a few days after the patient has received radiocontrast media or has stopped using vasomotor drugs. However, with renal artery stenosis [30] or congestive heart failure [42], the physician may wish to continue therapy with converting enzyme inhibitors; if hypovolemia is present, volume repletion alone may improve renal function.

    Because low to normal blood pressure, salt-poor urine, and volume loss are common in the hepatorenal syndrome, prerenal azotemia is often suspected. If volume replacement is tried, prerenal azotemia will rapidly improve, but the hepatorenal syndrome will show no effect or a slight transient increase in urine output and renal function [34, 72]. Unfortunately, this transient increase can prompt vigorous volume administration, which only worsens ascites and edema. Hemodynamic measurements made through a Swan-Ganz catheter may also distinguish the hepatorenal syndrome from prerenal azotemia. The hepatorenal syndrome should not be confused with cirrhotic glomerulonephritis [73], urinary obstruction or acute tubular necrosis in a person with cirrhosis, or conditions that damage both the liver and kidneys [33], such as acetaminophen overdose [74]. Renal ultrasonography can exclude obstruction. Salt-poor urine, clinical features, and the absence of hematuria, proteinuria, and renal failure rule out these other conditions.

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    Small-Vessel Diseases

    Atheroemboli and other diseases of the small arteries and arterioles cause renal failure by blocking blood flow to the glomeruli (Table 2). Hypertensive nephrosclerosis causes chronic renal failure and is not considered here.

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    Table 2. Small-Vessel Diseases That Cause Acute Renal-Failure

    Atheroembolic Renal Disease

    In atheroembolic renal disease, cholesterol crystals embolize from atherosclerotic aortic plaques to small vessels of the kidneys and other organs (Figure 3). Atheroemboli may occur spontaneously, but manifestations usually appear 1 day to 7 weeks after arterial manipulation, such as angiography, vascular surgery, angioplasty, or intra-aortic balloon-pump placement [75-78]. A temporal (and causal) relation may also exist with anticoagulant or thrombolytic therapy [75, 79-81].

    Figure 3. Renal biopsy specimen showing an arteriole occluded by atheromatous emboli. The cholesterol crystals are surrounded by fibrin, a few histiocytes, and degenerating leukocytes. (Hematoxylin and eosin stain; original magnification, × 400.) Renal biopsy specimen from a patient with scleroderma renal crisis showing severe intimal proliferation with myxoid matrix and luminal narrowing of interlobular arterioles. The glomerulus on the left side shows chronic ischemic changes. (Hematoxylin and eosin stain; original magnification, × 250.) Glomerulus in an autopsy specimen from a patient who had the hemolytic-uremic syndrome. The capillaries are distended and filled with fibrin thrombi or stagnant erythrocytes. (Hematoxylin and eosin stain; original magnification, × 400.).
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    Figure 3. Renal biopsy specimen showing an arteriole occluded by atheromatous emboli. The cholesterol crystals are surrounded by fibrin, a few histiocytes, and degenerating leukocytes. (Hematoxylin and eosin stain; original magnification, × 400.) Renal biopsy specimen from a patient with scleroderma renal crisis showing severe intimal proliferation with myxoid matrix and luminal narrowing of interlobular arterioles. The glomerulus on the left side shows chronic ischemic changes. (Hematoxylin and eosin stain; original magnification, × 250.) Glomerulus in an autopsy specimen from a patient who had the hemolytic-uremic syndrome. The capillaries are distended and filled with fibrin thrombi or stagnant erythrocytes. (Hematoxylin and eosin stain; original magnification, × 400.). Top.Middle.Bottom.

    Affected patients are typically white men who smoke cigarettes, are older than 60 years, and have cerebral, coronary, aortic, or peripheral vascular disease [75, 76, 82]. The most common manifestation of atheroemboli is ischemia of the feet, which causes livedo reticularis or purple, blue, or gangrenous toes. Lower extremity pulses are usually normal [75]. The involvement of other organs can cause transient ischemic attacks, retinal ischemia, pancreatitis, ischemic colitis, polyneuritis, myalgias, and claudication [75, 76, 78, 83-86]. Rarely, patients have infarction of the bowel, spleen, adrenal glands, or spinal cord [76]. In addition, some persons have constitutional symptoms including fever, malaise, and weight loss [75, 76]. Morbidity and mortality rates are high because of strokes, myocardial infarctions, amputations, and general debility [75, 76].

    Azotemia usually progresses over weeks or months to end-stage renal failure, probably because of ongoing embolization, although partial recovery may occur [76, 78, 83, 86]. Patients often have sustained or episodic hypertension and sometimes flank or back pain [76].

    Erythrocyte sedimentation rates are usually elevated, and eosinophilia with or without leukocytosis is often present [75, 76, 78, 87]. The results of urinalysis are sometimes normal, but one half of patients have proteinuria [75], sometimes in the nephrotic range [86, 88], and one third show hematuria [75] that is sometimes gross [76] or accompanied by erythrocyte casts [86]. Low urine sodium content may be seen [89]. Thrombocytopenia or low serum concentrations of C3 and C4 can occur [87, 90]. The plasma renin level is often elevated [78]. Gastrointestinal embolization sometimes causes blood in the stool, and embolization to the pancreas, muscle, and liver increases amylase, creatine kinase, and aspartate aminotransferase levels, respectively [75, 76].

    Atheroembolic renal disease is classically diagnosed by finding intra-arterial cholesterol crystal clefts on renal biopsy. Alternatively, skin, calf muscle, and bone marrow biopsies are safer than renal biopsies and can also show intra-arterial clefts [85]. However, in typical cases, the physician may make a diagnosis on the basis of clinical evidence. Such a patient might have atherosclerosis, painful ischemic skin changes in the feet, intact pedal pulses, eosinophilia, a recent vascular procedure, and no other cause for renal failure. Ultrasonography is necessary to exclude urinary obstruction.

    When ischemic skin changes and eosinophilia are absent, atheroembolic renal disease may be misdiagnosed as hypertensive nephrosclerosis (if the azotemia has stabilized), as malignant hypertension (if hypertension is severe), or as a primary glomerulopathy (if hematuria and proteinuria are present). Constitutional symptoms, the involvement of multiple organs, and a high erythrocyte sedimentation rate may falsely suggest vasculitis [76, 89]. Worsening azotemia should prompt the physician to order a renal biopsy, which will reveal the cholesterol emboli. Conversely, rare patients with vasculitis, systemic lupus erythematosus, or other conditions may show typical pedal ischemic changes, and atheroemboli may be erroneously diagnosed [91].

    Scleroderma

    Scleroderma or systemic sclerosis is an idiopathic connective tissue disease that is more prevalent in women than in men. It causes fibrosis and narrowing of the arterioles and small arteries in the gut, lungs, heart, kidneys, and skin (Figure 3). It results in Raynaud phenomenon, skin tightness, joint stiffness, dysphagia, and dyspnea. Although most patients with scleroderma have renal vascular lesions [92, 93], only about 10% of patients with scleroderma develop kidney failure [92]. This scleroderma renal crisis usually affects middle-aged women within 7 years after the onset of scleroderma, but it can occur in men and in adolescents and adults of any age [94-97]. Typically, patients have sudden oliguric renal failure, hypertension, and grade 3 or 4 hypertensive retinopathy [94, 95]. Twenty-five percent have hypertensive encephalopathy or heart failure [95].

    Patients with scleroderma usually have antinuclear antibodies with a speckled or nucleolar immunofluorescence pattern [98, 99]. Certain antinuclear antibodies, anticentromere and anti-Scl-70 antibodies, are specific for scleroderma but not sensitive [99, 100]. Capillary loss and enlargement on nail-fold capillaroscopy done with an ophthalmoscope is specific and sensitive [100]. In scleroderma renal crisis, the urine sediment is often normal [95, 97] and proteinuria is moderate or absent [94, 95, 97]. Most patients have hyperreninemia [95, 101] and microangiopathic hemolytic anemia [94], often with thrombocytopenia [102].

    Scleroderma renal crisis is usually diagnosed clinically in patients with scleroderma who have new azotemia and severe hypertension with no other cause. Renal ultrasonography should be done to exclude obstruction. Microangiopathic anemia and thrombocytopenia support the diagnosis but could falsely suggest the hemolytic-uremic syndrome or thrombotic thrombocytopenic purpura. Rheumatologic evaluation is indicated if the diagnosis of scleroderma is in question.

    A renal biopsy should be done in atypical cases, such as in patients with scleroderma sine scleroderma, which has the clinical features of scleroderma without the dermatologic changes [103, 104], or perhaps in patients with scleroderma renal crisis but with normal blood pressure levels [95, 105].

    Malignant Hypertension

    A syndrome of acute vascular damage to the kidneys, retina, and brain, malignant hypertension is caused by severe hypertension. Fibrinoid necrosis and intimal thickening of the small arteries and arterioles occur diffusely but are particularly prominent in the target organs. The cause is renal disease in one half of patients, essential hypertension in one third of patients, and renovascular disease in most others [106, 107]. The malignant form of essential hypertension has become less common, perhaps because of better detection and treatment of new cases [107]. Although some patients have normal blood pressure levels days or weeks before presentation [108, 109], most have preexisting hypertension [106, 110]. Patient noncompliance with antihypertensive medication may be a precipitating factor [111].

    Typically, malignant hypertension is accompanied by a diastolic blood pressure greater than 130 mm Hg, throbbing headache, and blurred vision associated with retinal hemorrhages, exudates, or papilledema, or with cerebral ischemia. Generalized weakness, heart failure, nausea, vomiting, weight loss, oliguria, and encephalopathy with dizziness, altered mental status, or seizures are common [106, 109-113]. Transient ischemic attacks and cerebrovascular accidents may produce hemiparesis, paresthesias, and other focal signs [106, 113]. Rarely, malignant hypertension occurs without severe retinal changes [114-116] or with a diastolic blood pressure as low as 100 to 110 mm Hg [107].

    Renal function can vary from normal to oliguric kidney failure [106, 108-110]. Most patients have mild to moderate proteinuria, but heavy proteinuria and the nephrotic syndrome can occur, especially with underlying glomerulopathies [106, 117]. One third of patients have microscopic or gross hematuria [106], sometimes with erythrocyte casts [108]. Thrombocytopenia and microangiopathic hemolytic anemia are not uncommon [108, 109, 117, 118]. Hypokalemic metabolic alkalosis may occur, reflecting high renin production by ischemic glomeruli and secondary hyperaldosteronism [117, 119].

    Good blood pressure control alleviates visual and encephalopathic symptoms [113] but usually aggravates azotemia, possibly because of reduced perfusion pressure. Then, as vascular lesions heal, renal failure improves to a variable extent, even in patients who need dialysis [109, 112, 120]. This improvement typically occurs after 2 weeks of blood pressure control but can take place immediately or after months or years. However, some patients have permanent renal impairment [106, 107, 109, 112].

    Renal failure caused by malignant hypertension is usually diagnosed clinically on the basis of diastolic blood pressure greater than 130 mm Hg, grade 3 or 4 hypertensive retinopathy, and azotemia that is ameliorated within 3 weeks after hypertension is controlled. A renal sonogram with Doppler visualization of the renal arteries should be done to exclude urinary obstruction, determine kidney size, and look for renovascular disease. If the azotemia does not improve within a few weeks, the patient may have renal artery stenosis or a renal disease other than malignant nephrosclerosis [107]. Renal arteriography and a renal biopsy should be considered.

    Investigation of the cause of the malignant hypertension should depend on clinical clues. It may entail arteriography for renal artery stenosis in patients with atherosclerosis, abdominal or flank bruits, or asymmetrical kidney size, and biochemical studies for primary aldosteronism or pheochromocytoma in patients with unexplained hypokalemia or paroxysmal hypertension, respectively. Such studies are often unnecessary in black persons, in whom malignant hypertension is caused less often by renal artery stenosis and more often by essential hypertension compared with white patients [110, 111, 117, 121].

    The Hemolytic-Uremic Syndrome

    This condition is characterized pathologically by glomerular and arterial thrombotic microangiopathy (Figure 3) [122, 123]. Clinical manifestations of the hemolytic-uremic syndrome are hemolytic anemia, thrombocytopenia, and acute renal failure [122-125].

    The hemolytic-uremic syndrome has many causes (Table 3). The classic form occurs before the age of 4 years and begins with diarrhea, often with abdominal pain and bloody stools [122, 124, 125, 137, 138, 169-171]. Of the various bacterial and viral causes, enterohemorrhagic Escherichia coli, principally serotype 0157:H7, is the most important and in some areas is found in one half of cases [137, 138, 140, 171]. Alternatively, some children have a prodromal upper respiratory infection or no prodrome [122, 124, 125, 137, 138, 141, 169, 170].

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    Table 3. Causes of the Hemolytic-Uremic Syndrome

    The hemolytic-uremic syndrome is the most common cause of acute renal failure in children [172-174]. In contrast, in adults, it is rare, etiologically more heterogenous, and commonly associated with the postpartum period [146-149, 180] and the use of mitomycin C [126-128] rather than with gastroenteritis [140, 175-179].

    This condition is typically accompanied by hemolytic symptoms (weakness, pallor, or jaundice), renal symptoms (hematuria, oligoanuria, edema, or hypertension), thrombocytopenic symptoms (purpura or bleeding), and fever [122, 124, 125, 170, 171, 180-182]. Cerebral involvement may cause mental changes or seizures [125, 138, 170, 182-185]. Pulmonary, myocardial, pancreatic, and colonic damage sometimes occurs in children [124, 138, 185, 186]. When induced by chemotherapy, the hemolytic-uremic syndrome can manifest as noncardiogenic pulmonary edema [187].

    Typical laboratory findings include thrombocytopenia and microangiopathic hemolytic anemia (anemia, reticulocytosis, elevated indirect serum bilirubin and lactic dehydrogenase concentrations, reduced haptoglobin levels, and fragmented and nucleated erythrocytes on peripheral blood smear) [170, 171, 177, 180, 186]. Stool cultures from patients with diarrhea may show E. coli 0157:H7 [137-140171, 175, 176]. Many patients have leukocytosis [170, 171, 177, 188] or depressed serum C3 and CH50[189]. Although fibrin degradation products may be increased, disseminated intravascular coagulation is not present [122, 123, 125, 180, 188]. Proteinuria and hematuria are common [170, 171, 177, 188]. Erythrocyte casts [169, 177] and the nephrotic syndrome have been observed [181, 188].

    The diagnosis is made clinically on the basis of typical setting (such as postpartum state, mitomycin C therapy, or prodromal diarrhea) and the hematologic hallmarks—thrombocytopenia and hemolytic anemia with schistocytes. Predisposing factors or, rarely, thrombocytopenia or schistocytes are absent, in which case, diagnosis may require a renal biopsy [186, 190, 191]. The hemolytic-uremic syndrome is sometimes mimicked by the HELLP syndrome (hemolysis, elevated liver enzymes, and low platelet count), a variant of preeclampsia. Affected women have microangiopathic hemolytic anemia, elevated liver function tests, a low platelet count, nausea, and upper abdominal pain [192-196]. Complications such as abruptio placenta and cardiac arrest can cause renal failure [192, 193].

    Thrombotic Thrombocytopenic Purpura

    In this rare idiopathic syndrome, platelet aggregation, fibrin formation, and endothelial injury produce arteriolar microthrombi in many organs, but especially in the brain and kidneys [197, 198].

    Clinically, one sees a pentad of thrombocytopenia, microangiopathic hemolytic anemia, neurologic defects, renal abnormalities, and fever. Women 20 to 50 years old are commonly affected, but the condition can strike persons of both sexes and any age group [197, 199, 200]. Thrombotic thrombocytopenic purpura usually occurs without predisposing illness, although a temporal relation to drugs, pregnancy, collagen vascular diseases, and infection, such as with E. coli 0157:H7 [140] or the human immunodeficiency virus [201, 202], has been seen. The thrombocytopenia and anemia are usually severe and symptomatic. The central nervous system manifestations [197, 199, 203-207] are transient and mild initially but may progress to coma and death; they may be focal (such as aphasia and paresthesias) or diffuse (such as headache or seizures). Involvement of different organs results in nausea, vomiting, abdominal pain, pancreatitis, jaundice, vision problems, myalgias, arthralgias, and cardiac dysfunction and conduction defects [6, 7, 197, 204, 208].

    Azotemia occurs in one half of cases but is rarely severe [197, 199, 203, 205-207]. The ratio of blood urea nitrogen to creatinine is frequently high, perhaps because of hypovolemia or protein catabolism [203, 206]. Hypertension is uncommon [203].

    Leukocytosis and microangiopathic hemolytic anemia are usually seen [197, 204]. Sometimes fibrin degradation product levels are increased and fibrinogen concentrations are low, but the results of coagulation tests are usually normal or nearly normal [197]. Most patients have gross or microscopic hematuria and mild to nephrotic proteinuria; some have erythrocyte casts [197, 199, 203, 209].

    Left untreated, thrombotic thrombocytopenic purpura is a fulminant disorder, and most patients die in days to weeks [197]. Alternatively, the onset can be insidious and the course chronic [209].

    The diagnosis is usually made clinically on the basis of thrombocytopenia and anemia with schistocytes on a peripheral smear, and it is buttressed by unexplained neurologic and mild renal abnormalities. In atypical cases, the physician should look for hyaline microthrombi on biopsy of the bone marrow, gingiva, or petechial skin lesions [197, 199, 204, 206, 207]. Renal biopsy specimens show microthrombi but are often contraindicated by thrombocytopenia.

    All of the manifestations of the hemolytic-uremic syndrome may occur in thrombotic thrombocytopenic purpura, and the pentad of thrombotic thrombocytopenic purpura may be seen in the hemolytic-uremic syndrome. This clinical overlap and the similarity of the microthrombi in both illnesses have led several authorities to classify the conditions as variations of thrombotic microangiopathy [198, 209, 210]. Nevertheless, most cases may be classified as one condition or the other. Onset after childbirth, mitomycin C, or diarrhea, especially diarrhea in early childhood, are typical of the hemolytic-uremic syndrome. Moderate to severe azotemia and hypertension and absent or mild neurologic signs also support this diagnosis. On the other hand, the absence of predisposing conditions, absent or mild azotemia and hypertension, and severe central nervous system disturbances characterize thrombotic thrombocytopenic purpura [209].

    Thrombotic thrombocytopenic purpura may be difficult to diagnose early when symptoms are mild and anemia, schistocytes, and severe thrombocytopenia have not yet appeared [197, 198]. At this stage, the disease can mimic an infection with weakness, headache, myalgias, leukocytosis, and fever. Later, neurologic symptoms may be ascribed to uremia or cerebrovascular disease, the renal abnormalities attributed to glomerulonephritis, and the anemia ascribed to bleeding or uremia. Repeating the hemoglobin assessment and platelet count and reexamining the peripheral smear should show the worsening microangiopathic hemolytic anemia and thrombocytopenia.

    Normal fibrinogen concentration and prothrombin time should exclude disseminated intravascular coagulation, if suggested by elevated fibrin degradation products. A negative result on the Coombs test excludes the Evan syndrome—that is, autoantibody-mediated hemolytic anemia and thrombocytopenia.

    Acute (Bilateral or Renal) Cortical Necrosis

    In this rare disease, thrombosis of small arteries, arterioles, and glomerular capillaries produces total or patchy cortical necrosis [211-214]. Hemorrhage, hemolysis, shock, infection, and intravascular coagulation are often present, but the pathogenesis is unknown. Causes include gastroenteritis, sepsis, snake bites, use of nonsteroidal anti-inflammatory drugs, poisons, the hemolytic-uremic syndrome, and pregnancy complicated by induced septic abortion, puerperal sepsis, intrauterine fetal death, preeclampsia, or peripartum hemorrhage [211-218]. Patients may report flank pain and usually have prolonged oligoanuria [219]. Results of urinalysis can be normal [220] but typically reveal microscopic hematuria, granular casts, and up to 4 plus proteinuria [213, 217]. Gross hematuria or erythrocyte casts may be observed [221, 222].

    Acute cortical necrosis should be considered when oligoanuria develops after a complication of pregnancy or after one of the other predisposing factors, particularly if oliguria lasts more than 3 weeks. Renal computed tomography with contrast enhancement shows ischemic cortex as a radiolucent band between the enhanced medulla and subcapsular cortex [221, 223-225]. Although it can help the physician to diagnose acute cortical necrosis with less risk than renal biopsy or arteriography, its sensitivity is not known. If the results of enhanced renal computed tomography are negative, a renal biopsy should be considered. Alternatively, if the renal failure has lasted more than 1 month, unenhanced computed tomography may show scattered single- or double-line cortical calcifications, which confirm the diagnosis [212, 222, 226].

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    Large-Vessel Diseases

    Occlusion of the main renal arteries is a common cause of azotemia in elderly persons. If just one artery is involved, the unaffected contralateral kidney keeps the serum creatinine concentration less than 220 µmol/L [227, 228]. Severe renal failure occurs, however, when the contralateral kidney is damaged or absent [227, 229-231] or when the occlusion is bilateral [227, 228, 232-234].

    Progressive ischemia from renal artery stenosis is a more common form of occlusion than sudden infarction from embolism or thrombosis.

    Renal Artery Stenosis

    Renal failure due to arterial stenosis (ischemic nephropathy) is caused by atherosclerosis of the main renal arteries or by aortic plaques at the ostia; other causes, such as fibromuscular hyperplasia, are rare [230, 235-239].

    Renal artery stenosis can be bilateral but usually begins on one side [236, 240]. As perfusion pressure decreases, the ischemic kidney releases renin, causing hypertension. With further reduction in perfusion, kidney size and glomerular filtration decrease and eventually urine production stops [241-243], although perfusion may suffice to sustain tissue viability [241, 244, 245]. Sometimes this state may be sustained by collaterals, despite total renal artery occlusion [241, 244, 245]. With progressive ischemia, the kidney becomes atrophie with sclerotic glomeruli, focal infarctions [244], and multiple cysts [246]. Atheromatous emboli may aggravate the damage [90].

    Renal artery stenosis is less common in women [227, 228, 247, 248] and in black persons [121, 233, 249-251]. The typical patient is a white man older than 50 years who smokes and has hypertension and coronary, cerebrovascular, or peripheral atherosclerosis [227, 228, 233, 243, 247]. The hypertension is often unusual in its severity, its onset late in life (after 50 years of age), or its escape from good control. In addition, control of hypertension may be difficult or may aggravate azotemia [228, 252]. Recurrent pulmonary edema can also be seen [253, 254].

    Mild proteinuria often occurs, but it is rarely in the nephrotic range [90, 241, 245, 255]. Urine sodium concentration may be low [241]. Peripheral venous renin activity is typically elevated and may lead to hypokalemic metabolic alkalosis [228, 230, 241, 256-259]. Different degrees of stenosis between the two kidneys often produce asymmetrical kidney size [227, 257] or function [233, 241, 260].

    The diagnosis of ischemic nephropathy should be considered whenever an older hypertensive patient has hypertension with unusual features, atherosclerosis, unexplained hypokalemia (or metabolic alkalosis), or asymmetrical kidney size or function [251, 257, 261, 262]. Kidney size is determined by ultrasonography; asymmetrical function is detected using captopril radionuclide scanning.

    Once renal artery stenosis is considered, the physician has three choices: to order arteriography, to do nothing, or to do noninvasive tests. The decision to do arteriography is appropriate if ischemic nephropathy is likely. This decision also assumes that the benefits of improved hypertension and azotemia outweigh the risks of arteriography (bleeding, contrast nephrotoxicity, and atheroemboli), angioplasty (5% to 15% complications, 0% to 6% mortality) [240, 263-266], or surgery (> 10% mortality in some series) [237, 240, 253, 267, 268].

    The decision to do nothing is appropriate if the hazards of arteriography or correction outweigh the benefits. For example, the risk for a poor outcome may be increased by erosive aortic atherosclerosis or serious cardiovascular or other disease; and the potential benefits may be decreased if the hypertension and azotemia are mild or if the chance for success is low, as when both kidneys are small or the serum creatinine concentration is greater than 265 µmol/L [264, 266, 267, 269].

    The decision to do noninvasive tests is appropriate if evidence for ischemic nephropathy is weak, but the benefit-to-risk ratio would be favorable if such evidence was found. The peripheral venous renin level may be measured. A high level makes ischemic nephropathy more likely if diuretics or converting enzyme inhibitors are not stimulating renin production. A radionuclide scan often detects asymmetrical renal function or may do so after a dose of captopril, which impairs glomerular filtration in kidneys with functionally important arterial stenosis. Captopril-induced changes in the radionuclide scan suggest renal artery stenosis; specificity and sensitivity are 70% to 95% in renovascular hypertension [270-274] but are not known for renovascular renal failure. A positive test result suggests reversible ischemic nephropathy, but this is not certain. Doppler sonography of the main arteries may detect increased blood velocity in stenoses. Inadequate visualization is a problem. Specificity and sensitivity range from 70% to 100% for detecting renovascular hypertension [274-276]. Diagnostic accuracy in ischemic nephropathy is unknown, but positive results probably support the diagnosis. Magnetic resonance angiography and spiral computed tomographic angiography were sensitive and specific tests for renal artery stenosis in a few studies [276-279], but further investigations are needed. Thus, in unclear cases, the physician may use peripheral venous renin assessments, captopril scans, or one of three imaging studies to decide whether to do renal arteriography.

    Previous SectionNext Section

    Renal Infarction

    Sudden embolism or thrombosis produces renal infarction and causes azotemia if the infarction is bilateral or in a solitary kidney. Unilateral embolism normally causes little or no azotemia in patients with two kidneys; however, in rare cases, patients show marked but transient renal failure thought to result from contralateral reflex vasospasm or from contrast nephrotoxicity [280]. Renal infarction has many causes (Table 4) but usually involves emboli from hearts with valvular disease or recent myocardial infarction or in atrial fibrillation [280-283]. Polyarteritis nodosa impairs renal function through a secondary glomerulonephritis but only rarely produces azotemia through infarction [289, 290]. Renal vein thrombosis often causes renal failure due to infarction in neonates [173, 304-307]. Venous thrombosis is probably less complete in older children and adults [308-310] and causes kidney failure only rarely and mostly without infarction.

    View this table:
    Table 4. Diseases That Cause Renal Failure through Renal Infarction*

    Renal infarction typically affects older persons with cardiac disease, particularly atrial fibrillation, and is accompanied by chest, flank, back, or abdominal pain, suggesting myocardial infarction, nephrolithiasis, pyelonephritis, or cholecystitis [280, 281, 283]. Patients may have had previous emboli and often report nausea, vomiting, oliguria, or gross hematuria. Fever, recent-onset hypertension, and renal tenderness are common physical findings, and laboratory abnormalities typically include proteinuria (up to 4+), hematuria, pyuria, leukocytosis, azotemia, and a high serum lactic dehydrogenase level. Serum alkaline phosphatase and aspartate and alanine aminotransferase levels may also be elevated. Sonography should be ordered to exclude hydronephrosis, but infarcted kidneys will appear normal. Intravenous pyelograms obtained to rule out ureteral calculi show poor function on one or both sides.

    Once infarction is suspected, the lactic dehydrogenase level should be determined and a radionuclide scan obtained. Focal perfusion defects or unilateral nonfunction suggest infarction. In contrast, bilateral nonfunction can occur with bilateral embolism or parenchymal disease and is nonspecific. Thrombus visualized on an echocardiogram suggests an embolism, but to make a definitive diagnosis, the physician should obtain a renal arteriogram with views of the venous phase if renal vein thrombosis is suspected. Doppler sonography showing no renal arterial flow may confirm the diagnosis, but this has not been studied sufficiently [232, 311]. Renal infarction can be overlooked in persons without cardiac disease, flank pain, or high lactic dehydrogenase levels; urinalysis might suggest glomerulonephritis, but a renal biopsy will lead to the correct diagnosis.

    Previous SectionNext Section

    Conclusions

    Vascular diseases are common causes of renal failure. Usually these conditions are suspected through syndrome recognition and their diagnoses confirmed by one or two additional tests or by a response to treatment (Table 5). In patients without classic features, the condition will initially be difficult to diagnose; such patients generally should have a renal biopsy. The biopsy specimen will show renal infarction or any of the small-vessel diseases. Ischemic nephropathy may show nonspecific changes on biopsy and may offer few clinical clues; arteriography should then be considered.

    View this table:
    Table 5. Diagnosing Vascular Causes of Renal Failure*
    Previous Section
     

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