Acute kidney injury (AKI) is a prevalent clinical syndrome characterized by a rapid decline in renal function over a short time and accompanied by symptoms of abnormal urine output and azotemia. The pathological mechanisms underlying AKI are highly complex, primarily involving inflammatory responses, oxidative stress, and cell death. In recent years, the global incidence of AKI has risen annually, making it an urgent public health challenge. Emerging research indicates that macrophages play a dual role in the progression and recovery of AKI by dynamically modulating iron metabolism. This review systematically discusses the mechanisms by which dysregulated macrophage iron metabolism influences AKI progression: iron overload exacerbates inflammation by promoting M1 polarization, lipid peroxidation, and ferroptosis, whereas iron restriction may enhance antioxidant capacity via activation of pathways, such as Nrf2, that facilitate M2 polarization and renal tissue repair. Based on