Mechanisms of diabetic nephropathy include abnormal glucose metabolism, altered renal hemodynamics, oxidative stress, immuno-inflammatory factors, and genetic factors. 1. Abnormalities of glucose metabolism: In diabetic state, the whole body organs show impaired glucose metabolism, among which the glucose metabolism of tissues/organs such as kidneys, nerves, eyes, etc. is obviously enhanced, and at this time, about 50% glucose is metabolized in kidneys, which, on one hand, reduces the risk of ketoacidosis and hyperosmolar coma in the body, and, on the other hand, also aggravates the glycemic load of the kidneys. 2. Renal hemodynamic changes: glomerular hyperperfusion, high transmembrane pressure and hyperfiltration play a key role in the development of diabetic nephropathy. 3. Oxidative stress: In diabetic state, glucose self-oxidation causes mitochondrial overload, leading to excessive production of reactive oxygen species (ROS); on the other hand, the body’s antioxidant capacity decreases, and the amount of intracellular antioxidant reduced coenzyme II is insufficient. 4. Immuno-inflammatory factors: There is a complex network of interactions between the complement system and pattern recognition receptors in natural immunity, which may play an important role in the pathogenesis of diabetic nephropathy. In addition, monocyte-macrophages and mast cells, various transcription factors, chemotactic molecules, adhesion molecules, inflammatory factors, and glycosylated metabolic end products may be involved in the pathogenesis. 5. Genetic factors: It is currently believed that diabetic nephropathy is a polygenic disease, and genetic factors play an important role in determining the susceptibility to diabetic nephropathy. Patients with diabetic nephropathy are advised to seek timely medical treatment.