Do not start urate-lowering medication solely for an elevated test result if you have never had gout

You avoid long-term medication and monitoring costs, as well as an unnecessary exposure to drug risks.

The 2020 American College of Rheumatology guideline defines asymptomatic hyperuricemia as serum urate above 6.8 mg/dL without prior gout flares or subcutaneous tophi. It conditionally recommends against initiating allopurinol, febuxostat, or probenecid, rating the evidence certainty high. A table footnote estimates that 24 patients would need treatment for three years to prevent one incident gout flare. CKD-FIX randomized 363 people with stage 3 or 4 chronic kidney disease, no history of gout, and a risk of progression to allopurinol 100–300 mg daily or placebo for 104 weeks. Annual changes in estimated glomerular filtration rate, or eGFR, were −3.33 mL/min/1.73 m² (95% CI −4.11 to −2.55) and −3.23 (−3.98 to −2.47). The difference was −0.10 (−1.18 to 0.97; P=0.85): kidney function declined at similar rates. Serious adverse events occurred in 46% versus 44%. PERL enrolled 530 people with type 1 diabetes and early-to-moderate diabetic kidney disease. They took allopurinol for three years, followed by a two-month washout. Allopurinol reduced serum urate from 6.1 to 3.9 mg/dL, but post-washout GFR differed by only 0.001 mL/min/1.73 m² (−1.9 to 1.9; P=0.99). Urinary albumin excretion was 40% higher in the allopurinol group (0%–80%). Treating a number feels sensible because “an abnormal result should be pushed back down” is such an easy rule to believe.

This concerns starting lifelong medication before any attack, not ignoring high uric acid. The guideline identifies exceptions when considering treatment after a first flare: stage 3 or worse chronic kidney disease, serum urate above 9 mg/dL (about 535 µmol/L), or a history of urinary stones. Previous attacks, tophi, or erosive damage on imaging require a different assessment; see long-term treatment for diagnosed gout. About 7.4% of Han Chinese people carry HLA-B*5801, compared with 0.7% of White people. Carriers have a greater risk of potentially fatal severe skin reactions to allopurinol; the source reports a threefold higher hypersensitivity-syndrome risk in Asian than White patients. When treatment is indicated, discuss testing before starting; see the same gout-treatment entry. The two kidney trials studied chronic kidney disease and type 1 diabetes. They do not prove that high uric acid can never harm kidneys; they challenge the specific strategy of lowering urate with these medicines to protect kidney function in the studied groups.

FitzGerald JD, Dalbeth N, Mikuls T, et al. (2020). 2020 American College of Rheumatology Guideline for the Management of Gout. Arthritis Care & Research, 72(6), 744–760, Table 1 and footnote. https://doi.org/10.1002/acr.24180; Badve SV, Pascoe EM, Tiku A, et al. (2020). Effects of Allopurinol on the Progression of Chronic Kidney Disease. New England Journal of Medicine, 382(26), 2504–2513. https://doi.org/10.1056/NEJMoa1915833; Doria A, Galecki AT, Spino C, et al. (2020). Serum Urate Lowering with Allopurinol and Kidney Function in Type 1 Diabetes. New England Journal of Medicine, 382(26), 2493–2503. https://doi.org/10.1056/NEJMoa1916624.