Diabetic nephropathy is a common and serious chronic complication of diabetes and is one of the leading causes of death and disability in diabetes. The incidence of diabetic nephropathy has been reported abroad to be as high as 45%. In the United States, diabetic nephropathy is the leading cause of end-stage renal failure, accounting for about 38%. So why does diabetes complicate diabetic nephropathy? The exact mechanism is not clear. It is generally believed that on the basis of genetic susceptibility, it is associated with pathophysiological changes caused by risk factors such as hyperglycemia, hypertension, lipid metabolism disorders, smoking, and high protein diet. These pathophysiological changes include increased pathogenic cytokines, increased free radicals, hypercoagulable state, renal hemodynamic disturbances, glomerular hyperperfusion and hyperfiltration, and glomerular and glomerular arteriosclerosis. Increased blood glucose is the most important manifestation of diabetes mellitus, and it is also the main cause of renal lesions. Persistent hyperglycemia can lead to the expansion of extracellular fluid lysate, causing continuous expansion of the renal vascular circulatory bed and the formation of glomerular hyperperfusion and hyperfiltration. Glomerular hyperperfusion, hyperfiltration can damage the glomerular thylakoid membrane, basement membrane and capillary endothelium, etc. Together with the deposition of albumin, fibrin, lipids and mucopolysaccharides on the glomerular capillary basement membrane and the bottom membrane of small renal arteries, it can cause glomerular and glomerular arteriosclerosis, resulting in the destruction of renal units. High blood sugar is like a corrosive agent, if the concentration is too high, it will have a “glycation reaction” with the proteins of blood vessels and organs, causing damage to blood vessels and organs. The higher the blood glucose, the more severe the “glycation reaction” will be. If the blood vessels and cells in the kidney are “glycated”, it will cause abnormal kidney function and various manifestations of diabetic nephropathy. Hypertension can cause renal hemodynamic disorders, promote the expansion of the small glomerular arteries and increase the pressure in the kidney capillaries, thus promoting the development of diabetic nephropathy. Diabetes mellitus and hypertension often coexist, and a vicious circle is formed: on the one hand, the vasculopathy and renal damage caused by diabetes mellitus will further increase blood pressure; on the other hand, the increase in blood pressure will certainly aggravate the vasculopathy and renal damage. Because of this vicious circle, patients with diabetes combined with hypertension are prone to kidney damage. In a study of 110 patients with type 1 diabetes, it was found that nephropathy developed much earlier in those with hypertension than in those without hypertension, and that the height of blood pressure was directly proportional to the degree of proteinuria. In another study, researchers observed 54 patients with type 1 diabetes for 7 to 14 years, and the proportion of those with combined hypertension who developed diabetic nephropathy was 55%, compared to 13% of those with normal blood pressure. It can be seen that hypertension increases the incidence of diabetic nephropathy by 4 times, which fully indicates that hypertension can promote the development of diabetic nephropathy. Dyslipidemia is also common in diabetic patients. It is manifested by an increase in cholesterol, triglycerides and low-density lipoprotein cholesterol (LDL-C), which are damaging to the cardiovascular system, and a decrease in high-density lipoprotein cholesterol (HDL-C), which has a cardiovascular protective effect. In the past, not enough attention has been paid to the relationship between dyslipidemia and kidney disease, but recent studies have found that dyslipidemia can also directly induce diabetic nephropathy, causing progressive decline in kidney function in patients. Disturbances in lipid metabolism are involved in glomerulosclerosis and tubular damage, accelerating the progression of diabetic nephropathy. Application of statins to correct dyslipidemia can inhibit glomerular thylakoid cell proliferation and down-regulate the expression of transforming growth factor, while reducing proteinuria and delaying renal arteriosclerosis, which plays a protective role in diabetic nephropathy. In addition, increased blood viscosity and microcirculatory disorders are also closely related to the occurrence and progression of diabetic nephropathy. Recent studies have shown that increased blood viscosity and microcirculatory disorders are also among the pathological changes caused by diabetes. In diabetic patients, the substances that promote blood clotting are increased, while the function of preventing blood clotting is weakened. This makes the blood prone to clotting and the formation of blood clots. If blood clots appear in the microcirculation of the kidney, the kidney unit will be deprived of blood and oxygen, thus increasing urine protein and decreasing kidney function. In conclusion, the pathogenesis of diabetic nephropathy is very complex and has not been fully elucidated, but it is generally believed to be caused by a combination of genetic and environmental factors. Some studies have shown that the occurrence of diabetic nephropathy has considerable familial aggregation, and the incidence of diabetic nephropathy in siblings of patients with diabetic nephropathy is five times higher than that in siblings without diabetic nephropathy; the results of the DCCT study also showed that although the overall incidence of diabetic nephropathy was related to the level of glycemic control, 26% of diabetic patients had an increased urinary albumin excretion rate ( In contrast, some patients did not develop diabetic nephropathy despite years of poor glycemic control. These phenomena strongly suggest that genetic factors play an important role in the development and progression of diabetic nephropathy. To date, there is no treatment to change the genetic factors, and only comprehensive management of the above risk factors can prevent or delay the development of diabetic nephropathy. Therefore, the causes of diabetic nephropathy are multifaceted. Some patients think that as long as they control their blood sugar, everything will be fine, which is not correct. In fact, if the control of risk factors other than blood glucose is neglected, the incidence of diabetic nephropathy will further increase.