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.