Chronic kidney disease is manifested by progressive proteinuria, tubulointerstitial fibrosis and renal insufficiency, regardless of whether the initial injury occurs in glomeruli or tubulointerstitial compartment of the nephron.While there are extensive studies on the mechanism by which glomemlar injury and proteinuria lead to tubulointerstitial lesions, how tubular damage causes glomerular injury and proteinuria remains poorly understood.We studied this issue by using tubule-specific β-catenin knockout mice (Ksp-β-cat-/-).