Abstract
Progressive chronic renal disease is characterized histologically by the accumulation of extracellular matrix proteins within the renal interstitium and progressive tubular atrophy. A number of kidney diseases and their progression to end-stage renal failure are driven by the intercrine, autocrine, paracrine, and endocrine effects of angiotensin II. Growth factors appear to have an important role in the development and progression of diabetic nephropathy. Substantial evidence indicates that induction of transforming growth factor beta (TGF-beta) is mediated by high levels of glucose. TGF-beta is pivotal for the hypertrophy of mesangial and tubular cells. Other factors such as hypertension, protein glycation products, and other mediators may further amplify the synthesis of TGF-beta and/or the expression of its receptors in the diabetic state. Other cytokines, such as tumor necrosis factor alpha also contribute to the progression of chronic renal disease. The overall picture derived from several studies of chronic renal disease suggests that treatment of the progression of the renal fibrosis may require the use of several strategies to prevent the advent of end-stage renal disease.
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