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Contribution of Bone and Mineral Abnormalities to Cardiovascular Disease in Patients with Chronic Kidney Disease

Paolo Raggi^*, and Michael Kleerekoper

^* Department of Medicine and Radiology, Emory University School of Medicine, Atlanta, Georgia; and Department of Endocrinology, Saint Joseph Mercy Hospital, Ann Arbor, and Department of Internal Medicine, Wayne State University, Detroit, Michigan

Correspondence: Dr. Paolo Raggi, Emory University School of Medicine, 1365 Clifton Road NE, AT-504, Atlanta, GA 30322. Phone: 404-778-5414; Fax: 404-778-3540; E-mail: praggi{at}emory.edu

1,25-Dihydroxyvitamin D₃ levels begin to drop early in the course of kidney disease, leading to elevated parathyroid hormone levels and disrupted mineral metabolism. Impaired mineral metabolism seems to be associated not only with bone disease but also with vascular calcification. Animal models have identified molecular mechanisms by which high mineral levels and other uremic substances induce vascular smooth muscle cells to undergo phenotypic changes that initiate the calcification process. Moreover, several epidemiologic and clinical studies showed strong associations between bone loss, arterial calcification, and cardiovascular disease in populations with and without kidney disease. This review discusses evidence that two early complications of chronic kidney disease—vitamin D deficiency and secondary hyperparathyroidism—contribute to bone and cardiovascular disease. New treatment strategies aimed at the prevention of bone loss and parathyroid hyperplasia, such as vitamin D receptor ligand therapy, calcimimetic agents, and noncalcifying phosphate binders, are being investigated for their impact on improving overall outcome in dialysis patients.