Renal Artery Stenosis, Thrombosis, and Embolism

Partial or total occlusion of the vasculature of the kidney, which can cause renal insufficiency and hypertension.

Renal artery stenosis is common in the elderly and is usually due to atherosclerosis. Although often totally asymptomatic, renal artery stenosis should be considered in an elderly patient with a sudden onset of hypertension, exacerbation of previous well-controlled hypertension, unexplained hypokalemia (eg, from hyperaldosteronism), or an unexplained increase in blood urea nitrogen or creatinine, especially after treatment with an angiotensin-converting enzyme inhibitor. The captopril renogram is the most sensitive screening procedure, but the test can be difficult to interpret when stenosis is bilateral. Unless medical therapy can achieve normotension with stable renal function, percutaneous transluminal renal angioplasty with stent placement is the procedure of choice, even in a very old person.

Renal artery thrombosis may complicate severe aortic and renal arterial atherosclerosis, especially when renal blood flow is reduced because of heart failure or volume depletion. Symptoms may be absent. If renal function previously was good, the only manifestation of unilateral thrombosis may be a small increase in blood urea nitrogen and creatinine levels and a modest increase in blood pressure. In patients with preexisting renal impairment and azotemia, renal artery occlusion may precipitate heart failure, marked hypertension, and renal failure.

Renal ultrasonography is as informative as intravenous urography and is safer. Differential diagnosis includes a coexisting abdominal aortic aneurysm, which may lead to renal artery occlusion by extension of atheroma or dissection.

Prompt revascularization can lead to a substantial return of renal function, and some patients recover even if surgery is delayed by several months.

Renal arterial embolism can occur in any patient with peripheral embolization (eg, from acute myocardial infarction, chronic atrial fibrillation, subacute bacterial endocarditis, aortic surgery, or aortography). Symptoms and signs may vary from essentially none to a full-blown syndrome of severe flank pain and tenderness, hematuria, hypertension, spiking fevers, markedly reduced renal function, and elevated serum lactic dehydrogenase levels.

Small emboli are difficult to detect, because renal scanning shows focal perfusion defects in many apparently healthy elderly patients. Major emboli may be suggested by differential contrast excretion on urography and confirmed by renal scanning and aortography.

Surgery is generally not indicated, and anticoagulant therapy is unlikely to be beneficial. In many cases, even when renal function is impaired, improvement may occur spontaneously over several days to weeks.

Renal cholesterol embolization, which may occur spontaneously or after aortic surgery or angiography in patients with diffuse atherosclerosis, is specific to the elderly. The clinical course varies, with most patients developing progressive renal failure. However, some patients have only moderate impairment and may eventually regain renal function. Definitive diagnosis may be difficult and requires visualization of cholesterol crystals on renal biopsy; diagnosis is often masked by other possible causes of reduced renal function (eg, hypotension, administration of angiographic contrast material). No specific treatment is available.