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Uric acid (UA) is the final product of purine metabolism in the human body. Excessive accumulation of UA leads to hyperuricemia (HUA) and the deposition of UA crystals in tissues, including the joints and kidneys. HUA has been identified as an independent risk factor for kidney disease. Although the association between HUA and kidney damage has been long established, the underlying pathological and physiological molecular mechanisms remain incompletely understood. This article reviews the latest advances in the mechanisms of kidney injury caused by HUA, particularly in the context of inflammation, oxidative stress, endothelial dysfunction, renal fibrosis, and imbalanced composition of the intestinal microbiota. Additionally, we discuss the advances in the treatment of HUA, aiming to provide valuable references for the study of HUA-induced kidney diseases and therapeutic strategies.
Zhang et al. (2025) studied this question.