Abstract: Objective To investigate the expression of KIF3A in mice with unilateral ureteral obstruction (UUO) and TGF-β1- induced NRK-52E cells and the role of KIF3A in renal tubular epithelial cell transdifferentiation. Methods Thirty-six C57BL/6J mice were randomly divided into the sham group (n=18) and UUO group (n=18). Six mice in each group were sacrificed at 7, 14 and 21days after the operation. The degree of renal tubulointerstitial fibrosis of the mice was observed by HE staining, Masson trichrome staining and Sirius red staining. The expression and distribution of KIF3A in the kidney of the mice was detected using RT-PCR, Western blotting and immunohistochemistry. Western blotting was used to detect the expression of KIF3A, E-cadherin and α-SMA proteins in the renal tissue of the mice. The expressions of KIF3A, E-cadherin, α-SMA, Wnt4 and β-catenin proteins in NRK-52E cells with TGF-β1-induced transdifferentiation were detected by Western blotting. Results Compared with the sham-operated mice, the mice with UUO showed worsened renal interstitial fibrosis with the increase of obstruction time, indicating successful modeling. The expressions of KIF3A mRNA and protein increased progressively and reached the peaked level at 21 days after UUO. The expression of α-SMA protein was significantly increased while E-cadherin protein expression was significantly reduced after UUO. The transdifferentiated NRK-52E cells showed significantly increased expressions of KIF3A (P<0.001), Wnt4 (P<0.05) and β-catenin proteins (P<0.0001). Conclusions KIF3A may participate in the development of renal fibrosis through epithelial-mesenchymal transition mediated by wnt/β-catenin signaling pathway.