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Diagnosis and Treatment |

Diagnosing Vascular Causes of Renal Failure

Gary J. Abuelo, MD
[+] Article, Author, and Disclosure Information

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.

Copyright ©2004 by the American College of Physicians

Ann Intern Med. 1995;123(8):601-614. doi:10.7326/0003-4819-123-8-199510150-00007
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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.


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Figure 1.
Synergism in the production of renal failure by vasomotor disturbances.

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 2.
Simplified diagram of intrarenal mechanisms for glomerular filtration rate (GFR) maintenance under reduced perfusion pressure, and GFR reduction by drugs.

+ = 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 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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