Vitamin D deficiency is common in chronic kidney disease (CKD) and becomes more prevalent as kidney function declines because of reduced sun exposure and nutrition, loss of vitamin D–binding protein, diminished renal mass and tubular function, and impaired conversion of 25-hydroxyvitamin D to active 1,25-dihydroxyvitamin D. KDOQI defines deficiency as 25(OH)D less than 20 ng/mL and insufficiency as 20 to 29 ng/mL. Published estimates suggest 30% to 86% of patients with CKD or end-stage kidney disease may be deficient. Nutritional vitamin D remains an option, with cholecalciferol generally more effective than ergocalciferol for raising 25(OH)D, although effects on parathyroid hormone (PTH) and albuminuria have been inconsistent across trials, particularly in advanced CKD and dialysis populations.
Treatment choice may depend on CKD stage, degree of secondary hyperparathyroidism, and the therapeutic goal. Calcifediol has produced more consistent parathyroid hormone (PTH) reductions in stage 3 to 4 CKD with vitamin D insufficiency and secondary hyperparathyroidism, while active agents such as calcitriol and paricalcitol also lower PTH and have shown reductions in albuminuria or proteinuria in some studies. These potential benefits must be weighed against risks, particularly hypercalcemia and hyperphosphatemia with active vitamin D therapy. Although observational studies have linked vitamin D treatment with better survival and slower CKD progression, randomized and meta-analytic evidence has not consistently demonstrated improvements in cardiovascular or all-cause mortality. The review therefore supports individualized vitamin D management while emphasizing that evidence for hard clinical outcomes remains limited.
Reference: Shringi S, Lu J, Tang J. Management of vitamin D in chronic kidney disease. R I Med J (2013). 2026 Jun 1;109(6):62-68.
Link: http://rimed.org/rimedicaljournal/2026/06/2026-06-62-review-shringi.pdf
