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(Hypertension. 2005;45:1042.)
© 2005 American Heart Association, Inc.

Brief Reviews

Kidney in Early Atherosclerosis

Alejandro R. Chade; Amir Lerman; Lilach O. Lerman

From the Department of Internal Medicine, Divisions of Nephrology and Hypertension (A.R.C., L.O.L.) and Cardiovascular Diseases (A.L., L.O.L.), Mayo Clinic, Rochester, Minn.

Correspondence to Lilach O. Lerman, MD, PhD, Division of Nephrology and Hypertension, Mayo Clinic College of Medicine, 200 First St SW, Rochester, MN, 55905. E-mail Lerman.Lilach{at}Mayo.Edu

Atherosclerosis represents one of the major causes of premature death in the United States today, and it is frequently associated with, exacerbates, and is aggravated by chronic kidney disease (CKD). Atherosclerosis integrates the response to a number of insults, and consequently, the accelerated atherosclerosis found in CKD patients is associated with activation of a variety of humoral and tissue mechanisms. Hypertension, diabetes, dyslipidemia, obesity, metabolic syndrome, and additional nontraditional risk factors can damage the kidney directly and by promoting intrarenal atherogenesis, even in the absence of obstructive lesions in the renal artery. Evidence indicates that increased oxidative stress and inflammation may mediate a large part of the effects of risk factors on the kidney. In turn, progressive deterioration of renal function in CKD may lead to dyslipidemia or accumulation of uremic toxins, which can induce production of free radicals and activate proinflammatory and fibrogenic factors, leading to vascular endothelial cell dysfunction and injury, and favoring development of atherosclerosis. Therefore, the kidney can be a villain or a victim during atherogenesis. The purpose of this review is to provide new insights into the mechanisms by which atherogenic factors may instigate early renal injury.

Key Words: kidney • atherosclerosis • oxidative stress • fibrosis

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