Gout is a heterogeneous, chronic and metabolic disease characterized by the increase of blood uric acid and the deposition of monosodium urate (MSU) crystals in joints or their surrounding tissues, which can cause gouty arthritis, tophus, kidney calculi's disease and urate nephropathy, and even lead to joint deformity and joint movement disorder in severe cases. There are some patients whose blood uric acid is up to standard in clinic, but gout is still recurring. At present, the blood uric acid standard recommended by various guidelines is not suitable for appeal patients. Our aim is to explore a new target of serum uric acid to guide treatment.

This study collected clinical data from 257 patients diagnosed with gout or hyperuricemia at Peking University International Hospital between October 1, 2016, and December 1, 2022, all of whom had not previously received urate-lowering therapy. All patients underwent a 6‑month follow‑up, during which changes in the fractional excretion of uric acid (FEUA), serum uric acid (UUA), and estimated glomerular filtration rate (eGFR) from baseline to post‑treatment were assessed. The patients were grouped according to the type of urate-lowering medication prescribed. A retrospective analysis was conducted to evaluate the effects of these medications, aiming to explore individualized treatment strategies for achieving serum urate targets in patients with gout or hyperuricemia.Statistical analyses were performed using Prism 9.0 (GraphPad, San Diego, CA, USA).

Using the uric acid excretion fraction with predefined cutoff values (<7% for poor excretion, 7–12% for mixed excretion, and >12% for increased excretion, i.e., overproduction). The FEUA was calculated using the following formula: FEUA = (SCr × UUA) / (SUA × UCr), and the result was expressed as a percentage. The overall distribution of patients, irrespective of renal function, was 89.54%, 9.80%, and 0.66%, respectively. Among patients with normal renal function, defined as eGFR > 60 ml/min/1.73 m², the corresponding proportions were 93.27%, 5.77%, and 0.96%. Patients were further divided into three treatment groups: the benzbromarone group, the febuxostat group, and the allopurinol group. In the 4‑week follow‑up cohort (n = 125), benzbromarone significantly increased FEUA (P = 0.0003), whereas febuxostat significantly decreased it (P = 0.034); allopurinol had no significant effect on FEUA (P = 0.3476). With regard to urinary uric acid (UUA), both febuxostat and allopurinol led to significant reductions (P < 0.0001 and P = 0.0087, respectively), while benzbromarone did not produce a significant change (P = 0.7643). Over an 8‑week follow‑up period (n = 82), only benzbromarone showed an increase in estimated glomerular filtration rate (eGFR) from baseline; however, this change did not reach statistical significance, possibly due to the limited sample size. In contrast, no such increase in eGFR was observed with febuxostat or allopurinol. Moreover, no significant intergroup differences in eGFR were detected at any time point.

This study found that the majority of gout patients were of the type with a decreased uric acid excretion fraction. Benzbromarone was shown to increase the uric acid excretion fraction and improve the estimated eGFR, suggesting that benzbromarone may have a renoprotective effect. Based on these findings, we propose the hypothesis that individualized treatment goals for gout patients should be constructed based on the uric acid excretion fraction.