The Role of the Intestinal Microbiome in the Pathogenesis and Treatment of Hyperuricemia: A Review

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Abstract
Hyperuricemia (HUA), characterized by elevated blood uric acid (UA) levels, is a major risk factor for gout, UA nephropathy, metabolic syndrome, and other related disorders. Traditional drug therapy for HUA includes medications (e.g., allopurinol and febuxostat) and dietary changes; however, it is limited and may be accompanied by adverse side effects such as allergies, prompting the investigation of alternative therapeutic approaches. Although the newly researched “in‐situ graft polymerization” protein drug modification technology and the emerging gut microbiota transplantation technology have demonstrated innovation in regulating blood UA, they still need to overcome bottlenecks in immunogenicity, individual variability, and formulation technology. Recent research has highlighted the potential of modulating the intestinal microbiome as a promising strategy for managing HUA. Nevertheless, the mechanism by which different intestinal microbiomes affect HUA pathogenesis remains unclear. To bridge this gap, this review firstly outlines the characteristics and prevailing conditions of HUA, followed by the current status of treatment. Besides, this review integrates the findings from clinical trials and animal studies to explore in depth the pathogenic mechanisms of HUA and the potential roles and regulatory pathways of the gut microbiota in mitigating HUA. The gut microbiota act as multi‐functional factors that affect HUA by reducing UA production, enhancing purine metabolism, influencing amino acid transport, and increasing UA excretion. This review addresses critical gaps in the extant literature regarding microbiota‐mediated UA homeostasis and provides new perspectives for the future treatment of HUA.

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