Effects of high- vs low-dose native vitamin D on albuminuria and the renin-angiotensin-aldosterone system: a randomized pilot study.

Residual albuminuria is associated with an increased risk of progression to ESKD. We tested whether a supplementation with native vitamin D could reduce albuminuria in stable CKD patients under maximal renin-angiotensin system (RAS) blockade. We conducted a randomized controlled study of high (cholecalciferol 100 000 UI per 10 days over 1 month) vs low-dose (ergocalciferol 400 UI/days over 1 month) supplementation with native vitamin D on urinary albumin/creatinine ratio, blood pressure and the RAS over 1 month in stable CKD patients with albuminuria and maximum tolerated RAS blockade. We included 31 patients, 21 in the high dose group and 10 in the low dose group. In contrast with a low dose, high dose vitamin D normalized plasma 25(OH)D, decreased iPTH but slightly increased plasma phosphate. High dose vitamin D decreased geometric mean UACR from 99.8 mg/mmol (CI 95% 60.4–165.1) to 84.7 mg/mmol (CI 95% 51.7–138.8, p = 0.046). In the low dose group, the change in geometric mean UACR was not significant. Blood pressure, urinary 24 h aldosterone and peaks and AUC of active renin concentrations after acute stimulation by a single dose of 100 mg captopril were unaffected by the supplementation in native vitamin D, irrespective of the dose. Native vitamin D supplementation was well tolerated. We found a small (− 15%) but significant decrease in albuminuria after high dose vitamin D supplementation. We found no effect of vitamin D repletion on blood pressure and the systemic RAS, concordant with recent clinical studies.