Key result
Larger uric acid reduction fails to lower cardiorenal events or mortality in asymptomatic hyperuricemia.
Why the study?
Does a large reduction in serum uric acid (≥2.0 mg/dL) following urate-lowering therapy reduce cerebral, cardiovascular, and renal events or mortality in patients with asymptomatic hyperuricemia?
Cohort (n=974)
Does a large reduction in serum uric acid (≥2.0 mg/dL) following urate-lowering therapy reduce cerebral, cardiovascular, and renal events or mortality in patients with asymptomatic hyperuricemia?
Hazard Ratio: 1.274 (95% CI 0.907–1.79)
p-value: p=0.1623
In patients with asymptomatic hyperuricemia, achieving a large reduction in serum uric acid (≥2.0 mg/dL) at 6 months with urate-lowering therapy did not significantly reduce subsequent cerebral, cardiovascular, or renal events.
Background Hyperuricemia is associated with gout and several pathological conditions, including cardiovascular, kidney, and metabolic diseases. However, many individuals with hyperuricemia remain asymptomatic. This study evaluated the impact of serum uric acid (SUA) reduction following urate-lowering therapy on subsequent outcomes in patients with asymptomatic hyperuricemia. Methods This study is a post hoc analysis of Febuxostat for Cerebral and CaRdiovascular Events PrEvEntion StuDy (FREED), a randomized controlled trial. Patients were divided into two groups based on the change in SUA levels between study enrollment and six months. A reduction of 2.0 mg/dL was used as the cut-off point to compare the subsequent outcome events. The primary outcome was a composite of cerebral, cardiovascular, and renal events, as well as all-cause mortality. Results In total, 974 (91.0%) of the 1,070 patients from the original FREED trial were included. At baseline, the mean SUA level was 7.52 ± 1.03 mg/dL, which decreased to 5.67 ± 1.88 mg/dL at six months. Of the patients, 461 (47.3%) achieved SUA reduction ≥2.0 mg/dL (mean 4.35 ± 1.42 mg/dL), while 513 (52.7%) had <2.0 mg/dL reduction (mean 6.87 ± 1.42 mg/dL). No significant reduction in the primary composite outcome was observed with SUA reduction ≥2.0 mg/dL (hazard ratio 1.274; 95% confidence interval 0.907–1.790; P = 0.1623). Conclusion In patients with asymptomatic hyperuricemia, a large reduction in SUA levels at 6 months following urate-lowering therapy did not result in a decrease in subsequent outcome events. Treatment strategies for this population require careful consideration.
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Matsui et al. (2025) conducted a cohort in asymptomatic hyperuricemia (n=974). Serum uric acid reduction ≥2.0 mg/dL vs. Serum uric acid reduction <2.0 mg/dL was evaluated on composite of cerebral, cardiovascular, and renal events, as well as all-cause mortality (HR 1.274, 95% CI 0.907-1.790, p=0.1623). A serum uric acid reduction ≥2.0 mg/dL at 6 months did not significantly reduce cerebral, cardiovascular, renal events, or mortality in asymptomatic hyperuricemia (HR 1.274; 95% CI 0.907-1.790).
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