关键词: 急性肾损伤, 慢性肾脏病, 机制, 炎症反应, 纤维化

Abstract: Acute kidney injury (AKI) is a common kidney disease in clinical practice.Recent studies have shown that AKI is not only a short⁃term condition but can also progress to chronic kidney disease (CKD),becoming an important factor contributing to the continuously increasing prevalence of CKD.A deeper understanding of its molecular mechanisms is crucial for improving patient outcomes and preventing CKD.This article provides a systematic review of the core mechanisms underlying the transition from AKI to CKD,analyzing this continuous pathological process from multiple dimensions:at the cellular level,it explores how cell cycle arrest,senescence,and metabolic reprogramming of renal tubular epithelial cells promote their transformation from repair agents to sources of pro⁃fibrotic signals;at the immune level,it examines how persistent macrophage activation and lymphocyte infiltration maintain chronic inflammation and drive fibrosis;at the molecular level,it explains the roles of epigenetic regulation and metabolic memory in forming renal ‘molecular scars.’ By reviewing existing studies,this article aims to explore the potential mechanisms and intervention strategies for the progression of AKI to CKD,providing new insights into improving patient prognosis.

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