Divisions of Cardiology, Nutrition and Preventive Medicine, Department of Medicine, William Beaumont Hospital, Royal Oak, Michigan; and Division of Nephrology and Hypertension, Department of Medicine, Veterans Affairs Medical Center, Fargo, North Dakota

Correspondence: Peter A. McCullough, M.D., M.P.H., Division of Nutrition and Preventive Medicine, William Beaumont Hospital, 4949 Coolidge, Royal Oak, MI 48073. E-mail:pmc975@yahoo.com

Abstract

Cardiovascular calcification in patients with chronic renal failure: Are we on target with this risk factor? End-stage renal disease (ESRD) is comprised of conditions associated with metabolic disorders associated with soft tissue and coronary artery calcification (CAC). The most consistent determinants of CAC in these patients are extent and duration of renal dysfunction and older age. The majority of published studies have not found a causal relationship between measures of calcium-phosphorus balance and CAC. When taken into consideration, the lipid profile [primarily low high-density lipoprotein cholesterol, elevated triglycerides, elevated low-density lipoprotein (LDL-C), and elevated total cholesterol] are important factors in the calcification process. Recent data seems to indicate that CAC is regulated both positively and negatively by a wide variety of mechanisms affecting patients with renal disease. The progression of CAC can be reduced from a 25% to 30% to 0% to 6% annual increase with LDL-C reduction caused by statins or possibly sevelamer. It is currently unclear whether the calcium-phosphorus balance and its related treatments are involved in CAC progression in ESRD patients. Further research into the determinants and potential treatments for CAC in association with ESRD is warranted.