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The effect of calcium with or without calcitriol supplementation on renal function in patients with hypovitaminosis d and chronic kidney disease.

BACKGROUND: Hypovitaminosis D (serum 25-OHD < 30 ng/mL) is common in patients with chronic kidney disease (CKD). Vitamin D is believed to involve in the regulation of renin-angiotensin system and may be renoprotective.

OBJECTIVES: To compare the effects of calcium with or without calcitriol on renal function in patients with CKD.

PATIENTS AND METHODS: A prospective randomized trial was performed involving patients with stages 2-4 CKD and hypovitaminosis D. Baseline demographics data were taken at baseline. Patients were randomized equally into oral calcitriol plus calcium carbonate (calcitriol group) or calcium carbonate alone (non-calcitriol group). Serum levels of 25-hydroxyvitamin D (25-OHD), 1,25-dihydroxyvitamin D3 (1,25-(OH)2D), creatinine, calcium and urine protein creatinine index (uPCI) were measured at 6 and 12 weeks.

RESULTS: Fifty (21 Female: 29 Male) patients with CKD with a median age of 53 (22-65) years were recruited. Their median MDRD eGFR (modification of diet in renal disease, estimation of glomerular filtration rate) was 36.0 (15-89) mL/min/1.73 m(2) with the CKD stage 2 (n = 8, 16%), stage 3 (n = 29, 58%), and stage 4 (n = 13, 26%) respectively. In both study groups serum 25-OHD levels were increased at 12 weeks (P = 0.001), in contrast to serum 1,25-(OH)2D levels which remained unchanged (P > 0.05), serum creatinine and uPCI were also remained unchanged until the end of study (P > 0.05 each). Patients with diabetes had higher serum creatinine (P = 0.01) and lower serum 1,25-(OH)2D (P = 0.02) at baseline. Regardless of the diabetics status, the serum 25-OHD was increased, and 1,25-(OH)2D remained unchanged at 12 weeks in both study groups. At 12 weeks, serum creatinine was decreased in patients with diabetes in the noncalcitriol group (P = 0.03) compared to stabilization of creatinine in the calcitriol group (P > 0.05). Serum calcium was increased, though it was still within the normal range in the calcitriol group (P < 0.001); whereas, in the noncalcitriol group, there was an initial reduction but increased back to baseline (P = 0.007). Urine PCI remained unchanged in both groups.

CONCLUSIONS: We have demonstrated that calcitriol supplementation did not offer any additional benefit to reduce 25-OHD and 1,25-(OH)2D levels over calcium carbonate alone in patients with CKD in this short term study. Overall renal function remained unchanged. However, we found that calcitriol at 0.5 mg daily plus calcium carbonate 500 mg daily could be reno-protective in diabetic nephropathy regardless of their serum 25-OHD levels.

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