AKT1 and acute kidney injury: Accumulating evidence demonstrates that the important role of nitric oxide/nitrite in LIPC and/or CI-AKI [7, 13, 14], and “reperfusion injury salvage kinase” (RISK) pathway has been found to be an important target of LIPC-induced protection against CM-AKI, in which Phosphatidylinositol3-kinase (PI3K)/Akt signaling pathway is involved in mediating LIPC-induced renoprotection [15, 16].