Dysregulated iron handling-including catalytic iron and ferroptosis, hepcidin-ferroportin signaling, ferritin dynamics, and neutrophil gelatinase-associated lipocalin (NGAL)-mediated siderophore transport-has been implicated in the initiation and propagation of acute kidney injury (AKI) across ischemia-reperfusion, sepsis, and nephrotoxic contexts. Here, LCN2 is linked to acute kidney injury.