Kidney in Early Atherosclerosis

• Published in: Hypertension (Dallas, Tex. 1979) Vol. 45; no. 6; pp. 1042 - 1049
• Main Authors: Chade, Alejandro R, Lerman, Amir, Lerman, Lilach O
• Format: Journal Article
• Language: English
• Published: Philadelphia, PA American Heart Association, Inc 01.06.2005; Hagerstown, MD Lippincott
• Subjects: Arterial hypertension. Arterial hypotension; Atherosclerosis (general aspects, experimental research); Atherosclerosis - complications; Atherosclerosis - physiopathology; Biological and medical sciences; Blood and lymphatic vessels; Cardiology. Vascular system; Cardiovascular Diseases - etiology; Chronic Disease; Experimental diseases; Humans; Kidney Diseases - complications; Kidney Diseases - etiology; Medical sciences; Oxidative Stress; Risk Factors; United States; North America; America; Human; Hypertension; Premature; Kidney disease; Obesity; Oxidative stress; Endothelial cell; Urinary system disease; Renal function; Renal artery; Nutrition disorder; Cardiovascular disease; Inflammation; Intrarenal; Free radical; Vascular disease; Toxin; kidney; Atherosclerosis; Risk factor; Fibrosis; Nutritional status
• ISSN: 0194-911X; 1524-4563
• DOI: 10.1161/01.HYP.0000167121.14254.a0

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.