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Ischemic injury to the kidney depends on the rate, site, severity, and duration of vascular compromise. Manifestations range from painful infarction to acute kidney injury (AKI), impaired glomerular filtration rate (GFR), hematuria, or tubular dysfunction. Renal ischemia of any etiology may cause renin-mediated hypertension.


Can be due to thrombosis or embolism (from valvular disease, endocarditis, mural thrombi, or atrial arrhythmias) or to intraoperative occlusion, e.g., during endovascular repair of abdominal aortic aneurysms.

Thrombosis of Renal Arteries

Large renal infarcts cause pain, vomiting, nausea, hypertension, fever, proteinuria, hematuria, and elevated lactate dehydrogenase (LDH) and aspartate aminotransferase. In unilateral lesion, renal functional loss depends on contralateral function. IV pyelogram or radionuclide scan shows unilateral hypofunction; ultrasound is typically normal until scarring develops. Renal arteriography establishes diagnosis. With occlusions of large arteries, surgery may be required; anticoagulation should be used for occlusions of small arteries. Pts should be evaluated for a thrombotic diathesis, e.g., antiphospholipid syndrome. Occlusion of one or both of the renal arteries can also rarely occur in pts treated with angiotensin-converting enzyme (ACE) inhibitors, typically in association with significant underlying renal artery stenosis.

Renal Atheroembolism

Usually arises when aortic or coronary angiography or surgery causes cholesterol embolization of small renal vessels in a pt with diffuse atherosclerosis. May also be spontaneous or associated with thrombolysis, or rarely may occur after the initiation of anticoagulation (e.g., with warfarin). Renal insufficiency may develop suddenly, a few days or weeks after a procedure or intervention, or gradually; the pace may alternatively be progressive or "stuttering," with punctuated drops in GFR. Associated findings can include retinal ischemia with cholesterol emboli visible on funduscopic examination, pancreatitis, neurologic deficits (especially confusion), livedo reticularis, peripheral embolic phenomena (e.g., gangrenous toes with palpable pedal pulses), abdominal pain from mesenteric emboli, and hypertension (sometimes malignant). Systemic symptoms may also occur, including fever, myalgias, headache, and weight loss. Peripheral eosinophilia, eosinophiluria, and hypocomplementemia may be observed, mimicking other forms of acute and subacute renal injury. Indeed, atheroembolic renal disease is the "great imitator" of clinical nephrology, presenting in rare instances with malignant hypertension, with nephrotic syndrome, or with what looks like rapidly progressive glomerulonephritis with an "active" urinary sediment; the diagnosis is made by history, clinical findings, and/or the renal biopsy.

Renal biopsy is usually successful in detecting the cholesterol emboli in the renal microvasculature, which are seen as needle-shaped clefts after solvent fixation of the biopsy specimen; these emboli are typically associated with an exuberant intravascular inflammatory response.

There is no specific therapy, and pts have a poor overall prognosis due to the associated burden of atherosclerotic vascular disease. However, there is often a partial improvement in renal function several months after the onset of renal impairment.


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