Pathogenesis and Management of Vascular Calcification in Patients with End-Stage Renal Disease.

Abstract

Vascular calcification is common in patients with end-stage renal disease (ESRD). In addition to traditional cardiovascular risk factors, ESRD patients also have a number of nontraditional cardiovascular risk factors that may play an important role in the pathogenesis of vascular calcification. The transformation of vascular smooth muscle cells into osteoblast-like cells may be a key element in the pathogenesis of vascular calcification in the presence of calcium and phosphate deposition due to abnormal bone metabolism and impaired renal excretion. Vascular calcification causes increased arterial stiffness, left ventricular hypertrophy, decreased coronary artery perfusion, myocardial ischemia, and increased cardiovascular morbidity and mortality. Although current treatment strategies focus on correcting abnormal calcium, phosphate, parathyroid hormone, or vitamin D levels in ESRD patients, a better understanding of the mechanisms of abnormal tissue calcification may lead to the development of new therapeutic agents that are capable of reducing vascular calcification and improving the cardiovascular outcome of ESRD patients. This review summarizes the pathogenesis and management of vascular calcification in ESRD patients.