The effect of vitamin D supplementation on bone metabolic markers in chronic kidney disease

Use of active forms of vitamin D is advocated in CKD patients for treatment of mineral bone disease because of the presumption that native forms of vitamin D would not undergo significant activation to calcitriol, the most active biological form of vitamin D. We present secondary analysis looking at bone turnover in subjects who completed the randomized, double blind, placebo controlled trial investigating the effect of cholecalciferol supplementation on vascular function in non-diabetic CKD stage G3-4 and vitamin D ≤20ng/ml [CTRI/2013/05/003648]. Patients were randomized (1:1) to receive either two directly observed oral doses of 300,000 IU of cholecalciferol or matching placebo at baseline and 8 weeks. Of the 120 subjects enrolled, 58 in the cholecalciferol group and 59 in the placebo group completed the study. At 16 weeks, the serum 25(OH)D and 1,25(OH)2D levels increased in the cholecalciferol group but not in the placebo group [between-group difference in mean change: 23.40 ng/ml; 95% CI: 19.76 to 27.06; p<0.001 and 14.98 pg/ml ,95% CI: 4.48 to 27.18, p=0.007, respectively]. Intact parathormone (iPTH) decreased in the cholecalciferol group [between-group difference in mean change -100.73 pg/ml (95% CI: -150.50 to -50.95, p<0.001). Serum total and bone-specific alkaline phosphatase (SAP, BAP) and serum C-terminal cross-linked collagen type I telopeptides (CTX-1) were significantly reduced in cholecalciferol group (between group difference for change in mean: -20.25 U/L (95% CI: -35.14 to-5.38, p=0.008 for SAP; -12.54, 95%CI: -22.09 to -2.98, p=0.013 for BAP and -0.21, 95%CI: -0.38 to -0.05, p=0.05 for CTX-1 ). Correlation analysis showed significant correlation of Δ 25(OH)D with Δ iPTH (r=-0.409, p