Background: After kidney injury, macrophages transition from initial proinflammatory activation to a proreparative phenotype characterized by expression of arginase-1 (), mannose receptor 1 (), and macrophage scavenger receptor 1 (). The mechanism by which these alternatively activated macrophages promote repair is unknown.
Methods: We characterized the macrophage and renal responses after ischemia-reperfusion injury with contralateral nephrectomy in mice and littermate controls and used coculture of macrophages and tubular cells to determine how macrophage-expressed arginase-1 promotes kidney repair.