We observed that both kinins receptors antagonism and deletion have been shown to attenuate cisplatin nephrotoxicity [20, 21]; their role was also observed in several other models of kidney disease, such as renal ischemia–reperfusion, which have demonstrated that both B1R antagonism and genetic deletion can mitigate the transition from AKI to CKD by promoting an increase in the M2 macrophage population. This evidence concerns the gene BDKRB1 and chronic kidney disease.