The Impact of Vitamin D(3) Supplementation on Mechanisms of Cell Calcium Signaling in Chronic Kidney Disease

Intracellular calcium concentration in peripheral blood mononuclear cells (PBMCs) of patients with chronic kidney disease (CKD) is significantly increased, and the regulatory mechanisms maintaining cellular calcium homeostasis are impaired. The purpose of this study was to examine the effect of vitamin D(3) on predominant regulatory mechanisms of cell calcium homeostasis. The study involved 16 CKD stages 2-3 patients with vitamin D deficiency treated with cholecalciferol 7000–14000 IU/week for 6 months. The regulatory mechanisms of calcium signaling were studied in PBMCs and red blood cells. After vitamin D(3) supplementation, serum concentration of 25(OH)D(3) increased (P < 0.001) and [Ca(2+)](i) decreased (P < 0.001). The differences in [Ca(2+)](i) were inversely related to differences in 25(OH)D(3) concentration (P < 0.01). Vitamin D(3) supplementation decreased the calcium entry through calcium release activated calcium (CRAC) channels and purinergic P2X(7) channels. The function of P2X(7) receptors was changed in comparison with their baseline status, and the expression of these receptors was reduced. There was no effect of vitamin D(3) on P2X(7) pores and activity of plasma membrane Ca(2+)-ATPases. Vitamin D(3) supplementation had a beneficial effect on [Ca(2+)](i) decreasing calcium entry via CRAC and P2X(7) channels and reducing P2X(7) receptors expression.