The results of this study indicate that the expression of Nephrin, CD2AP,Synaptopodin mRNA and protein decreased, the expression of TRPC6 mRNA and protein is elevated in mice with 30 min ischemia-reperfusion injury, along with the production of proteinuria and renal function decline, suggesting that cytoskeletal disorganization of the podocyte by Nephrin, CD2AP,Synaptopodinand TRPC6 may to some extent drive AKI and the progression of post- AKI chronic renal fibrosis. The gene discussed is SYNPO; the disease is acute kidney injury.