Zhang et al. (2018) demonstrated that the mitochondrial complex-1 inhibitor, rotenone, slows the progression of AKI to CKD. By the mitochondrial complex-1 inhibitor, the expression of Mn-SOD and ATP synthase subunit β, mitochondrial DNA copy number, were restored, and inflammation and fibrosis were suppressed, in this model. These data suggest that mitochondrial O2•– may play a crucial role in promoting the pathogenesis associated with the transition from AKI to CKD. This evidence concerns the gene SOD2 and chronic kidney disease.