Abstract: Probiotics have demonstrated significant potential in modulating intestinal microecology to intervene in hyperuricemia (HUA); however, the variability in therapeutic outcomes observed in clinical studies suggests that their urate-lowering efficacy is highly strain-specific rather than a universal trait. This review focuses on the strain selection criteria, the mechanisms of action, and the clinical translation of probiotic interventions for HUA. Grounded in the pivotal role of the gut-kidney axis in maintaining uric acid homeostasis, this article critiques the limitations of existing in vitro screening methods that rely on single degradation metrics. Consequently, it proposes a multidimensional screening strategy that integrates colonization capacity with metabolic profiles. Furthermore, the review elucidates the differential mechanisms by which specific strains inhibit hepatic xanthine oxidase, modulate renal urate transporters, and fortify the intestinal barrier via short-chain fatty acid production. Finally, this article discusses current bottlenecks in clinical translation from three aspects: inter-individual variability in therapeutic response, strain stability, and safety assessment, aiming to provide a theoretical basis for the development of precision interventions based on the functional characteristics of probiotic strains for HUA.

Key words: hyperuricemia; probiotics; strain-specific; uric acid metabolism; gut-kidney axis