Allopurinol has no effect on calcitriol or other CKD-MBD biomarkers: a randomized double-blind study

New evidence has emerged linking uric acid levels to Chronic Kidney Disease and Mineral and Bone Disorder (CKD-MBD). However, interventional studies remain scarce. We evaluated the effect of allopurinol on CKD-MBD biomarkers.

This is a randomized, double-blind clinical trial involving adult patients with stage 3-5 CKD under conservative management. Participants received either allopurinol 300 mg or a placebo for at least 90 days. Clinical data and blood samples were collected at baseline and at the end of the follow-up period to assess changes in calcium, phosphate, 25-hydroxyvitamin-D, parathyroid hormone (PTH), 1,25-hydroxyvitamin D, fibroblast growth factor 23 (FGF23), α Klotho, and bone alkaline phosphatase.

Forty-nine patients completed the study (25 in the allopurinol group and 24 in the placebo group). Most participants were women (53.1%), with a mean age of 71 ± 11 years and an average eGFR of 27.8 ± 11.0 mL/min/1.73 m². Uric acid levels were significantly decreased in the allopurinol group (7.49 mg/dL initial vs 3.96 mg/dL final, 43%, P < .001). FGF23 levels increased over time (P = .037), with no difference between groups. 25-hydroxyvitamin-D levels increased in the allopurinol group and decreased in the placebo group, a result that lost significance after adjusting for cholecalciferol supplementation and race. No other CKD-MBD biomarkers were significantly affected by allopurinol treatment.

Despite its urate-lowering effect, allopurinol did not produce meaningful changes in the major CKD-MBD biomarkers over the study period. Our results strengthen existing recommendations to restrict uric acid-lowering treatment to symptomatic gout, as we did not identify any associated improvements in mineral metabolism.