Evaluation of the effect of cholecalciferol on vascular calcification in hemodialysis patients

Abstract

The incidence of cardiovascular disease (CVD) in End stage renal disease (ESRD) patients is about 10 to 20 fold higher than that in the general population, and it accounts for more than 50% of mortality rate. Traditional risk factors just as dyslipidemia, hypertension, diabetes mellitus and others, are involved in the pathogenesis of the vasculopathy among this category of patients.

Recently, cardiovascular calcification; which is a prominent feature in arterial disease in ESRD, has been proposed to contribute to this exceptionally increased risk of CVD. Vascular calcification is considered now as an independent important risk factor for cardiovascular events, as well as all-cause mortality in hemodialysis patients.

Hyperphosphatemia, hypercalcemia and hyperparathyroidism all coexist in ESRD patients, having a crucial role on activation the osteogenesis process in vascular smooth muscle cells, resulting in arteriosclerotic calcification.

On the other hand, vitamin D deficiency is also associated with severe vascular calcification in chronic kidney disease (CKD) patients. In CKD, glomerular filtration rate decline limits the delivery of 25(OH)D to the renal tubules. The decreased renal uptake of 25(OH)D limits the formation of the active form of vitamin D; calcitrol.

Furthermore, CKD also reduce the activity of 1-α-hydroxylase, 25-hydroxylase, and increase the activity of 24-hydroxylase, causing prominent reduction of endogenous 25(OH)D and 1,25(OH)2D product, along with increasing their decay.