Effect of Allopurinol on Markers of Mineral and Bone Metabolism
Status:
Recruiting
Trial end date:
2023-04-30
Target enrollment:
Participant gender:
Summary
Hyperuricemia is a common condition in patients with chronic kidney disease (CKD) in the
glomerular filtration rate. Recently, it has been suggested that uric acid is related to a
mineral and bone disease of CKD (CKD-MBD) since the high concentration of uric acid is
associated with the harmful effect of vitamin D. The proof of concept of the association
between acid uric acid and CKD-MBD is based on a prospective study (sample size 6) that
observed, after 1 week of use of allopurinol, an increase in the concentration of 1,25(2D, a
result independent of the concentration of calcium, phosphorus, 25(OH)D and PTH. An
experimental study found that hyperuricemia could modify the expression of the 1α-hydroxylase
enzyme, consequently reducing 1,25(OH). The current study aims to evaluate the action of
allopurinol on CKD-MBD biomarkers (25(OH)-vitamin D, 1,25(OH)2D, FGF-23, PTH, calcium and
phosphorus). We hypothesize that allopurinol can improve serum levels of 1,25(OH) 2D and PTH.
This is a controlled, randomized, double-blind study, defined as a filtration rate <
60ml/1.73 m², according to the CKD-EPI equation. Inclusion criteria: patients with stages
III, IV and V CKD who are not on dialysis with a serum level of 25(OH)-vitamin D >20 ng/ml.
Exclusion criteria: Patients diagnosed with gout, undergoing treatment with allopurinol,
patients already in use and drugs with sensitivity to the drug. Based on a previous study, we
calculated a sample for 2 groups (placebo and drug) with pre and post-measurements (a total
of 4). Considering a standard deviation of 4 and a difference of 7 in the treated group, 3 in
the placebo group, and an alpha error of 5%, we calculated a sample of 25 patients in each
arm.