Losartan, uric acid, and cardiometabolic disease: beyond blood pressure control

Losartan has a unique uricosuric property among angiotensin II receptor blockers and may therefore be advantageous in patients with hypertension and hyperuricemia or gout. The study by Xu et al. combined a meta-analysis of placebo-controlled randomized trials with a target trial emulation using UK Biobank data and demonstrated that losartan reduced serum uric acid by approximately 0.3 mg/dL. Although this effect is modest and substantially smaller than that of established uric acid-lowering therapies, it may be clinically relevant when selecting antihypertensive treatment for patients with borderline hyperuricemia, gout risk, or diuretic-associated uric acid elevation. Losartan may partially counterbalance the uric acid-raising effect of thiazide diuretics, but it should not replace appropriate treat-to-target therapy in patients with gout or marked hyperuricemia. The study is limited by the small emulated cohort and the possibility of residual confounding and selection bias. Nevertheless, the consistency of the findings across different analytical approaches supports a genuine uric acid-lowering effect. Future studies should determine whether this biochemical effect translates into fewer gout flares, improved attainment of serum uric acid targets, or reduced cardiovascular and cardiometabolic events. Overall, losartan should be regarded as an effective antihypertensive agent with a modest but favorable uric acid profile. Clinical interpretation of losartan's uric acid-lowering effect in hypertension care. ARB, angiotensin II receptor blocker; RCT, randomized controlled trial; URAT1, urate transporter 1.