Acute kidney injury(AKI)is a reversible but may be a life-threatening condition,can be caused by a variety of reasons.The immune system plays a key role in the pathology of AKI because its response to the injury includes an inflammatory response that may further damage renal tissue.Inflammatory cell death(PANoptosis)pathway in the process of immune response is activated and leads to the release of pro-inflammatory cytokines and further tissue damage.In this study,mononuclear RNA sequencing data from the NCBI Gene Expression Omnibus(GEO)public database were used to analyze gene expression differences between acute kidney injury(AKI)and normal kidney tissues.The cell clusters of AKI and normal group were annotated to identify and extract the immune cells;hub genes adjusting PANoptosis were screened and verified by RT-qPCR.So as to evaluate the interaction and mechanism of immune cells in proinflammatory responses inducing cell death in AKI.Finally,an interaction network of 12 hub genes was constructed,which provides a solid foundation for further investigation of the detailed mechanisms by which immune cells regulate cell death in AKI and opens insights into potential therapeutic target strategies.The expression levels of five genes(JUN,IL1RAP,PIK3R1,IRAK3,NLRP3)in the AKI group were significantly higher than those in the NC group.In addition,we have identified and defined a novel inflammatory proximal flexotubular cell and suggest future intensive investigation on this cell subtype in AKI,as they may play an important role in the pathological process of AKI and could be a potential target for therapy.As a conclusion,there are 12 hub genes that interact with each other and play a role in the regulation of cell death in AKI immune cells.A novel class of inflammatory proximal convoluted tubule cells are identified and defined,which play an important role in the pathological process of AKI and may be a potential target for therapy.