SAP130 released from iron-dead tubular epithelial cells (TECs) further activates the Mincle/Syk/NF-κB signaling pathway in macrophages, propelling the formation of M1 macrophages, ultimately exacerbating TEC iron death and initiating an inflammatory feedback loop within the microenvironment of sepsis-associated acute kidney injury (SA-AKI). Here, CLEC4E is linked to acute kidney injury.