Objective: To explore the role and mechanism of human renal microvascular endothelial-mesenchymal transition (EndMT) in transplant renal interstitial fibrosis formation. Methods:Based on serum and renal allograft tissue samples from 25 cases of chronic renal allograft dysfunction (CAD) patients and 25 normal renal tissue samples and serum, we observed the changes of renal function and the degree of renal tubular atrophy,renal glomerular collapse and interstitial fibrosis by blood biochemical,periodic acid-schiff staining (PAS) and Mason trichromatic staining assays. Using immunohistochemical and indirect immunofluorescence double staining assays,we also detected the expression and distributions of vascular endothelial cell marker CD34 and myofibroblast marker α-Smooth muscle actin (α-SMA),and transforming growth factor-β1 (TGF-β1) in renal tissue samples of the two groups. Human umbilical vein endothelial cells (HUVECs) set as the object of study and stimulated by TGF-β1 (5 ng/ml) respectively for 0~72 h in vitro. Western blotting was used to observe the expression of CD34 and α-SMA. Results:Compared with the normal group,serum creatinine levels in the CAD group increased significantly. The results of PAS and Masson staining showed that renal tubular atrophy,glomerular collapse and interstitial fibrosis were more apparent in transplanted kidneys of the CAD group. Indirect immunofluorescence staining and immunohistochemical results showed that the positive stains of CD34 reduced,while the positive expression of α-SMA and TGF-β1 increased significantly in the CAD group compared with the normal group. Indirect immunofluorescence double staining showed that the double positive stains of CD34 and α-SMA could be found in the parts of glomerular and interstitial microvascular endothelial cells in the CAD group. The results of Western blotting demonstrated that after treatment with TGF-β1,the expression of CD34 reduced and α-SMA expression increased in an time-dependent mean in HUVECs as compared with the normal group (P < 0.01). Conclusion:Human renal microvascular EndMT may be mediated by TGF-β1 and plays an important role in transplant renal interstitial fibrosis formation.