高血糖为糖尿病肾脏疾病(diabetic kidney disease, DKD)的核心始动诱因，可通过糖脂代谢紊乱、肾脏血流动力学异常、氧化应激、慢性低度炎症、补体系统凝集素途径过度激活等多条通路交互调控、级联放大，持续造成足细胞结构与功能损伤，继而诱发肾小球硬化、肾小管间质纤维化，介导DKD的发生及进行性发展。作为补体系统三大激活途径之一，凝集素途径发现时间最晚，相关研究热度逐年上升。该通路可在无抗体参与下活化，是固有免疫防御与炎症反应之间的重要连接介质，在DKD的病理生理过程中发挥核心作用。本文综述了补体系统凝集素途径的核心成分在DKD中的作用机制及研究进展，探讨其作为治疗靶点的可行性，为DKD基础研究与临床防治提供新思路。

Chronic hyperglycemia serves as the core initiating trigger of diabetic kidney disease (DKD). Through the interactive regulation and cascade amplification of multiple pathways including disordered glucose and lipid metabolism, abnormal renal hemodynamics, oxidative stress, chronic low-grade inflammation, and excessive activation of the lectin pathway in the complement system, it continuously damages the structure and function of podocytes, subsequently induces glomerulosclerosis and renal tubulointerstitial fibrosis, and mediates the onset and progressive deterioration of DKD. As one of the three major activation pathways of the complement system, the lectin pathway was discovered most recently, and research interest in it has been rising year by year. Characterized by its ability to initiate activation without antibodies, this pathway acts as a critical mediator linking innate immune defense and inflammatory responses, and plays a central role in the pathophysiological processes of DKD. This paper reviews the mechanisms and research progress of the core components of the lectin pathway of the complement system in DKD, discussing their feasibility as therapeutic targets for providing new insights for basic research, clinical prevention and treatment of DKD.