Acute Kidney Injury is a common clinical syndrome characterized by a rapid decline in renal function over a short period, accompanied by abnormal urine output, azotemia, and other symptoms. The pathological mechanisms of AKI are highly complex, primarily involving inflammatory responses, oxidative stress, and cell death processes. In recent years, the incidence of AKI has continued to rise, particularly among critically ill patients, making it an urgent global public health challenge. Emerging studies suggest that macrophages play a dual role in the progression and recovery of AKI through dynamic regulation of iron metabolism. This article systematically elaborates the mechanisms by which imbalanced macrophage iron metabolism impacts AKI: iron overload exacerbates inflammation by inducing M1 polarization, promoting lipid peroxidation and ferroptosis, whereas iron restriction may enhance antioxidant capacity via activation of pathways such as Nrf2, driving M2 polarization to facilitate tissue repair. These findings provide novel insights into the pathogenesis of AKI and establish a theoretical foundation for developing new therapeutic targets and strategies.