As in non-renal transplant patients, the presence of proteinuria in renal transplant recipients was strongly associated with kidney survival. For each 1 g/d increase in proteinuria, the risk of graft failure and creatinine doubling significantly increased (relative risk 2.24, 95% CI 1.71-2.93; P < 0.0001). 5-year survival of transplanted kidneys was found to be only 69% in patients with proteinuria greater than 0.5 g/d compared with 93% in patients with negative proteinuria in a study of 337 patients. Similarly, the 5-year survival rate of transplanted kidneys was found to be 69.4% in patients with proteinuria greater than 1 g/d compared with 86.5% in proteinuria-negative patients, and the risk of transplant failure increased by 27% for every 1 g increase in 24-h urine protein. In addition, the presence of glomerular disease was also associated with transplant kidney failure (hazard ratio 1.58; 95%, 1.02-2.47). Proteinuria was first proposed as a risk factor associated with transplant kidney survival independently of glomerular disease and glomerular filtration rate. In patients with non-transplanted kidneys, it has been shown that proteinuria can stimulate the release of various cytokines from the renal tubules causing interstitial inflammation and fibrotic lesions. In renal transplant patients, it is unclear whether proteinuria affects transplant survival through this mechanism. Proteinuria has also been associated with survival in renal transplant patients. Microalbuminuria significantly increased the risk of death in renal transplant patients (95% CI, 2.08-11.13, P = 0.0003). Several studies have found a 2-fold increased risk factor for death in patients with positive proteinuria compared to those with negative proteinuria. Proteinuria was associated with patient survival when it was greater than 2 g/d. Studies have found that proteinuria, whether continuous or intermittent, leads to increased mortality in patients. After removing the effects of age, race, glucose, and blood pressure, each 1 g/d increase in proteinuria was associated with a 16% increase in the risk of death (P = 0.0001). Proteinuria increased the risk of death from both cardiovascular factors (relative risk 2.27, P<0.0001) and non-cardiovascular factors (relative risk 1.81, P = 0.025). Foreign studies have noted that proteinuria is not only associated with patient survival but also predicts cardiovascular events, including ischemic heart, brain, and vascular disease. The relative risk of new cardiovascular events increased significantly with increasing amounts of proteinuria. In conclusion, proteinuria is more common in patients after renal transplantation. Proteinuria in the early post-transplant period needs to be identified as originating from autologous or transplanted kidney glomerulopathy. The cause of proteinuria in post-transplant patients is significantly different from that in non-transplant patients as confirmed by renal biopsy pathology, and more than half of the patients have transplant glomerulopathy or acute (slow) rejection as confirmed by renal biopsy. Many recent studies have confirmed that proteinuria after renal transplantation is associated with patient and transplanted kidney survival and an increased risk of cardiovascular events. Treatment with ACEI, ARB, and regimen or restriction of protein intake is effective in reducing proteinuria in patients after renal transplantation.