Vascular calcification in end-stage renal disease patients

Abstract

Vascular calcification is very common in patients with end-stage renal disease (ESRD) and has been found to be associated with mineral and bone disorders. There are two types of vascular calcification: intimal and medial calcification. The transformation of vascular smooth muscle cells into osteoblast-like cells seems to be a key element in the pathogenesis of medial calcification in the presence of calcium and phosphate deposition. Vascular calcification causes increased arterial stiffness by medial calcification, which leads to left ventricular hypertrophy and decreased coronary artery perfusion and causes myocardial ischemia by intimal calcification. Thus, vascular calcification is thought to be associated with 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 vascular calcification may lead to the development of new therapeutic strategies that are capable of reducing vascular calcification and improving the cardiovascular outcome of ESRD patients. This review summarizes the pathophysiology, diagnostic procedure and therapeutic implication of vascular calcification in ESRD patients.