Use of active forms of
vitamin D is advocated in patients with
chronic kidney disease (CKD) 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 nondiabetic CKD stage G3-G4 and
vitamin D ≤20 ng/mL (Clinical Trials Registry of India: 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)2 D 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
parathyroid hormone (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 U/L; p = 0.008 for SAP; -12.54 U/L; 95% CI, -22.09 to -2.98 U/L; p = 0.013 for BAP; and -0.21 ng/mL; 95% CI, -0.38 to -0.05 ng/mL; p = 0.05 for CTX-1). Correlation analysis showed significant correlation of Δ25(
OH)D with ΔiPTH (r = -0.409, p < 0.0001), Δ1,25(
OH)2 D (r = 0.305, p = 0.001), ΔSAP (r = -0.301, p = 0.002), ΔBAP (r = -0.264, p = 0.004), and ΔCTX-1 (r = -0.210, p = 0.0230).
Cholecalciferol supplementation corrects
vitamin D deficiency and is effective in lowering serum intact
parathyroid hormone and bone turnover markers in early stages of CKD. © 2017 American Society for Bone and
Mineral Research.