In this study, we found that: (1) the CCL17 expression level was negatively associated with renal function in CKD patients; (2) CCL17 overexpression induced phenotype changes in HK2 cells by increasing the expression of α-SMA, collagen, and vimentin in vitro; (3) UUO mice exhibited increased renal interstitial fibrosis, tubular dilatation, and the overexpression of CCL17, α-SMA, collagen I and vimentin in a time-dependent manner. The gene discussed is CCL17; the disease is chronic kidney disease.