Effect of High-Dose Vitamin D Supplementation on Serum Sclerostin Levels in Chronic Kidney Disease Patients: A Randomized Controlled Trial

Background Vitamin D deficiency and altered bone metabolism are common in patients with chronic kidney disease (CKD). Sclerostin, a key inhibitor of bone formation, has been implicated in CKD–mineral and bone disorder (CKD-MBD), but the impact of high-dose vitamin D supplementation on circulating sclerostin is unclear. This work examined the effect of intramuscular cholecalciferol on serum sclerostin and bone-related markers in CKD patients. Methods This randomized controlled trial involved 128 adult CKD patients (stages 3–5), 18–70 years, both sexes, with vitamin D deficiency. Adults were equally randomized into two groups: the intervention group received intramuscular cholecalciferol (300,000 IU at baseline and week 8), while the control one received no supplementation. Results Vitamin D supplementation significantly increased 25(OH)D and 1,25(OH)2D levels (P < 0.001) and reduced iPTH and serum alkaline phosphatase (SAP) compared with controls. Sclerostin levels remained stable in the intervention group but diminished significantly in controls (P < 0.001). Sclerostin correlated positively with BUN, urea, uric acid, vitamin D metabolites, and iFGF-23, while showing negative correlations with eGFR, iPTH, and SAP. No significant associations were noticed with calcium or phosphorus. Conclusions High-dose vitamin D supplementation in CKD patients corrected vitamin D deficiency and improved secondary hyperparathyroidism without dimnished sclerostin levels. Sclerostin regulation in CKD is multifactorial and not directly suppressed by vitamin D therapy.