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Macrophages play an important role in many aspects of tissue injury, inflammation, and repair. Macrophage accumulation is found in most forms of renal disease and depletion studies have shown that they contribute to injury. However, it is also clear that monocytes and macrophages can develop reparative properties that are critical to disease resolution. A number of studies have now shown that macrophages can be transduced or stimulated ex vivo, injected after the initiation of disease, and localize preferentially to the site of renal inflammation. Such macrophage cell therapy can result in reduced inflammation and fibrosis and lead to improved renal function and attenuation of proteinuria. These studies provide a platform for future translational approaches in human renal disease.

Renal inflammation may result from a myriad of insults and often is characterized by the presence of infiltrating inflammatory leukocytes within the glomerulus or tubulointerstitium. Accumulating evidence indicates that infiltrating leukocytes are key players in the induction of renal injury. Although renal inflammation often is followed by the development of fibrosis with loss of renal function, it can resolve. Resolution may be spontaneous as in poststreptococcal glomerulonephritis or after the administration of effective treatment such as immunosuppressive agents. The mechanisms and cells underlying the resolution process and the exact temporal sequence remains uncertain at present but likely involves the removal of injurious leukocytes, the down-regulation of immune responses, and the alteration of the phenotype of infiltrating macrophages from proinflammatory to prorepair. In this review we examine the role of leukocytes in both renal inflammation and repair.