To understand the involvement of uPA/uPAR in the pathogenesis of AKI, we utilized alpha murine urokinase-type plasminogen activator (αMUPA) transgenic mice whose phenotype is similar to that of caloric restricted (CR) animals and who spontaneously consumed 20% less food and lived 20% longer than their wild-type (WT) counterparts. This evidence concerns the gene PLAU and acute kidney injury.