(A) Macrophage-based cellular therapies or therapeutic interventions can be envisaged that capitalize on the specialized macrophage secretome that determines differential function. Monocytes might be manipulated ex vivo to migrate to a damaged kidney, where they are preferentially M2 polarized, perhaps by inducing receptors to specific chemokines or chemoattractant molecules. Alternatively M2-type macrophages generated ex vivo from peripheral blood monocytes can be administered. Renal dendritic cells and unpolarized macrophages (M0) might also be skewed to an M2 phenotype by therapeutic manipulation of intrarenal molecular signals, such as specific cytokines, chemokines, or ECM proteins, known to direct this process in situ. (B) As more is learned about which soluble secreted macrophage products are associated with renal injury versus repair, single agents or, more likely, a cocktail of biological agents, drugs, and/or small molecules, might be administered to direct tissue recovery. This might include targeting of secondary intracellular signaling cascades that are activated by specific macrophage-derived products.