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PREVIEW
Tubulointerstitial fibrosis, characterized by accumulation of extracellular matrix proteins, is a morphologic hallmark of chronic renal disease as well as a component of normal aging in the kidney and of chronic allograft nephropathy. In this article, the author describes patterns that have recently been proposed to explain the pathogenesis of tubulointerstitial injury. In addition, he discusses available and experimental pharmacologic interventions that may ameliorate renal fibrosis.