Section 11 -

Cholesterol Atheroemboli Donna J. Lager, M.D. Matthew Lewin, M.D.

Case 10: Cholesterol Atheroemboli A 66 year old man presented with sudden onset of edema and was found to have renal insufficiency. His serum creatinine was 2.1 mg/dl and urinary protein excretion was 14 grams/24 hours. Atheroembolic disease involving the kidney is a common finding, especially in older patients with severe atherosclerosis. Emboli can cause catastrophic damage to the kidney (such as large or small infarcts) or they may cause reversible renal dysfunction. Predisposing factors for developing atheroemboli include hypertension (61%), coronary artery disease (44%), aortic aneurysm (25%), cerebrovascular disease (21%), congestive heart failure (21%) and diabetes mellitus (11%). Large "shaggy" atheromatous plaques in the aorta predispose patients to multiple emboli. Autopsy studies have shown the most common organ involved by atheroemboli is the kidney in 75% of cases; the next most common was the spleen (52%). Clinical Presentation and Diagnosis Atherosclerotic plaques can ulcerate sporadically or can be damaged from intra-arterial procedures (for example cardiac catheterization). When this happens the organs down stream in the blood flow receive a shower of plaque material including cholesterol and other atheromatous material. When material embolizes within a large artery, it will cause a segmental infarct of the renal tissue. When more numerous, smaller emboli involve the kidney, it causes patchy acute tubular necrosis. The diagnosis rests upon the correlation between the clinical history (often instrumentation or surgery) and renal dysfunction. Biopsy is not commonly utilized to diagnose atheroemboli. Laboratory Findings: The laboratory findings of atheroemboli are similar to those of ATN, including increasing creatinine and BUN. Leukocytosis and an increased sedimentation rate are also often noted. Eosinophilia is present in many cases. As is typical for many causes of renal failure, some degree of proteinuria and hematuria can occur and the urinary sediment is non-specific. Morphologic Findings Atheroemboli are typically seen as cholesterol clefts in arteries, arterioles or glomerular capillary loops, though medium sized arteries are most commonly involved. Regular tissue processing using formaldehyde dissolves the cholesterol, however the cholesterol clefts may be observed on frozen sections and with polarized light. As the emboli age a giant cell reaction and fibrosis develops around the cholesterol clefts. Cholesterol clefts may be difficult to see and must be kept in mind in cases of acute renal failure. Also typically found in association with cholesterol atheroemboli, is patchy acute tubular necrosis with small emboli and zonal infarction with larger ones. The cholesterol clefts can remain for up to nine months in vivo. References: Renal Biopsy Interpretation, Ed. FG Silva, VD D'Agati, T Nadasdy, Churchill Livingstone, 1996 Greenberg A, Cholesterol Atheroembolic Renal Disease in Primer on Kidney Diseases, 3rd Ed., pg 261, 2001. Meyrier A, et al, Atheromatous Renal Disease, Am J Med 85:139, 1988