The role of gut microbiota dysbiosis in the pathogenesis of hyperuricemic nephropathy.

Hyperuricemic nephropathy (HN) is a renal complication associated with sustained hyperuricemia and urate-related renal injury. Emerging evidence suggests that gut microbiota dysbiosis may participate in HN pathogenesis by influencing uric acid metabolism, intestinal urate excretion, gut barrier integrity, microbial metabolite production, and gut-kidney immune crosstalk. However, the strength of evidence varies substantially across proposed mechanisms, with many findings derived from animal models, in vitro experiments, CKD studies, or human studies of hyperuricemia and gout rather than HN-specific clinical cohorts. This review summarizes current clinical and experimental evidence linking gut microbiota dysbiosis with HUA, gout, CKD, and HN, critically evaluates proposed mechanistic pathways, and discusses microbiota-targeted interventions including probiotics, prebiotics, dietary strategies, fecal microbiota transplantation, and metabolite-based approaches. Particular emphasis is placed on distinguishing association from causality and identifying translational gaps that should be addressed in future HN-specific studies.