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Approximately 75% of uric acid in humans is excreted renally. Excess uric acid deposits in renal tissues, promoting tubulointerstitial fibrosis and leading to hyperuricemic nephropathy (HN), which is characterized by urate crystal deposition, chronic interstitial nephritis, and renal fibrosis. The pathogenesis and progression of HN involves dysregulated activation of multiple signaling pathways, including MAPK, Nrf2\/HO\u20101\/NQO1, PI3K\/AKT, and ASK1\/JNK\/c\u2010Jun pathways, which facilitate disease progression through the production of pro\u2010inflammatory cytokines and other mediators. Current treatments primarily consist of urate\u2010lowering drugs such as allopurinol, febuxostat, benzbromarone, and probenecid, but their use is constrained by adverse effects including hepatotoxicity, nephrotoxicity, and Stevens\u2010Johnson syndrome. Therefore, targeting inflammatory and fibrotic mechanisms presents a promising therapeutic approach. 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