NEW YORK (Reuters Health)—Allopurinol does not appear to contribute to decline in kidney function and may actually protect renal function in patients with gout, according to a large population-based study.
Gout affects around 4% of Americans and often occurs alongside chronic kidney disease (CKD), Dr. Tuhina Neogi from Boston University School of Medicine and colleagues note in an article online Oct. 8 in JAMA Internal Medicine.1
Despite no firm data suggest allopurinol harms renal function in patients with gout, clinicians are often cautious about using it in patients with gout and CKD, either lowering the dose or stopping it entirely when a patient exhibits kidney function decline, “leading to worse gout outcomes,” they point out.
The researchers used data from a primary care database in the U.K. to explore the risk of CKD in association with allopurinol use in patients with newly diagnosed gout. The created two propensity-matched cohorts of 4,760 patients who initiated allopurinol and 4,760 who did not.
Covariates were well balanced between allopurinol initiators and nonusers, with a mean age of 57, mean BMI of 30, and mean glomerular filtration rate (GFR) of 77 mL/min. Overall, 71% of users and nonusers had CKD stage 2 or estimated GFR 60 mL/min to 89 mL/min; the remaining 29% had CKD stage 1 or eGFR of 90 mL/min or more. As expected, males made up the majority of both cohorts (around 83%).
Compared with patients who were not started on allopurinol, those started on allopurinol (300 mg or more per day) had a 13% lower risk of progressing to stage 3 CKD or higher (main outcome) at a mean follow-up of 5 years.
“In contrast, initiation of allopurinol at a dose of less than 300 mg/d had no association with developing CKD stage 3 or higher, consistent with current thinking that most patients need doses higher than 300 mg/d to achieve clinically meaningful outcomes. Nonetheless, at minimum, allopurinol does not seem to have a detrimental effect on renal function in individuals with gout,” Dr. Neogi and colleagues report.
Based on their results, they say “clinicians should consider other potential contributors when faced with kidney function decline in patients with gout.”
In a linked editorial, Dr. Jonathan Zipursky and Dr. David Jurrlink of Sunnybrook Health Sciences Center in Toronto note that while the study has its share of limitations and caveats, the “important message . . . is that allopurinol is unlikely to contribute to progression of CKD; indeed, it might even be protective, presumably by reducing the risk of urate nephropathy.”
