Abstract
Vitamin D(3) needs to be activated into 1,25-dihydroxyvitamin D(3) in order to bind to vitamin D receptor (VDR) for functional responses. Studies in the past have focussed on the role of VDR in mineral homeostasis, with VDR activators used mainly to treat hyperparathyroidism secondary to chronic kidney disease. Chronic kidney disease patients encounter a higher risk of cardiovascular disease than the general public and experience an extremely high cardiovascular-related mortality rate. Recent clinical observations show that VDR therapy reduces mortality and morbidity in chronic kidney disease. Preclinical studies demonstrate that VDR is likely to be involved in the cardiovascular pathophysiology.