Tubulointerstitial and Vascular Diseases of the Kidney
Section 11 -
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
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.
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.
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.
- 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