Macrophages and progressive tubulointerstitial disease

In chronic renal disease, tubulointerstitial inflammation and injury is associated with infiltrating macrophages. As a consequence of primary injury, proteinuria, chronic hypoxia, and glomerular-derived cytokines may all differentially modulate the expression of factors that promote macrophage recruitment. In addition to adhesion molecules and chemokines, products of complement system and renin-angotensin system activation may direct this process. Once present at interstitial sites, macrophages interact with resident cells and extracellular matrix to generate a proinflammatory microenvironment that amplifies tissues injury and promotes scarring. There is now increasing evidence for the efficacy of interventions directed against factors that recruit, activate, or are produced by macrophages. A detailed understanding of the biology of this area may lead to the further development of therapies that will improve the outcome of renal disease.