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As the most prevalent internal modification in eukaryotic messenger RNA, m\u2076A dynamically modulates RNA splicing, stability, translation, and localization through the coordinated actions of writer, eraser, and reader proteins. Recent studies have illuminated the critical role of m\u2076A in kidney disease and renal fibrosis. Dysregulation of m\u2076A machinery has been shown to influence key pathogenic pathways in kidney disease development. Moreover, m\u2076A-modified noncoding RNAs further integrate epitranscriptomic signals into fibrogenic and immune regulatory networks. Therapeutically, targeting m\u2076A pathways offers promising avenues, with small-molecule inhibitors, RNA-based therapeutics, and clustered regularly interspaced short palindromic repeats (CRISPR)-based m\u2076A editing technologies under active investigation. However, challenges remain in achieving tissue-specific modulation and avoiding systemic toxicity. This review synthesizes current knowledge on m\u2076A-mediated regulation in kidney disease, highlighting mechanistic insights, disease-specific alterations, and emerging therapeutic strategies. 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