We have recently found that cadherin-11 (CDH11) is expressed in proximal tubules of human cases and mouse models of chronic kidney disease (CKD) and that targeting CDH11 in three models of kidney injury reduces fibrosis and improves renal function. Hence, CDH11 appears to be a therapeutic target for CKD. We hypothesize that loss of CDH11 prevents apoptosis of proximal tubule epithelial cells and the progression of CKD by preserving proximal tubule health and function, and that this preservation improves mortality in experimental models of CKD. We will test this hypothesis by developing a mouse model of proximal tubule specific deletion of CDH11 (PT-CDH11). Kidneys from mice lacking PT-CDH11 will be examined for fibrosis following unilateral ureter obstruction.