Second, the reported progressively increasing NLR up to 72 h after intervention pointed to the inflammatory origin of CI-AKI and assured the results obtained using AKI animal models that inhibition of NLRP3 inflammasome attenuated renal apoptosis and upregulated HIF1A and BNIP3-mediated mitophagy in CI-AKI [45] and the study which detected renal neutrophil and macrophage chemotaxis, accumulation of the lymphocyte antigen 6 complex with pyroptosis, mitophagy, and apoptosis in renal tissues of CI-AKI animal model [28]. Here, HIF1A is linked to acute kidney injury.