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Current Controversies in Managing End-Stage Renal Disease Patients |
Department of Medicine, Divisions of Cardiology, Nutrition, and Preventive Medicine, William Beaumont Hospital, Royal Oak, Michigan
Address correspondence to: Dr. Peter A. McCullough, Division of Nutrition and Preventive Medicine, William Beaumont Hospital, 4949 Coolidge, Royal Oak, MI 48073. Phone: 248-655-5765; Fax: 248-655-5714; E-mail: pmc975{at}yahoo.com
Coronary artery calcification (CAC) reflects the anatomic presence of coronary atherosclerosis and the relative burden of coronary artery disease (CAD). Higher levels of CAC are seen in the presence of CAD risk factors, older age, and chronic kidney disease. The lipid profile (primarily low HDL cholesterol, elevated triglycerides, elevated LDL cholesterol, and elevated total cholesterol) are important factors in the calcification process. The annual progression of CAC can be reduced from 25 to 30% to 0 to 6% with LDL cholesterol reduction caused by statins and possibly sevelamer. At treated LDL cholesterol levels somewhere below 100 mg/dl, several sources of data suggest the anatomic burden of CAD, including CAC, regresses. Additional supportive studies indicate that carotid intimal medial thickness and the volume of coronary atheroma also can be reduced by LDL cholesterol reduction in concert with elevation of HDL cholesterol. This article reviews the data in support of altering the natural history of CAC with lipid modification.
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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673