A large variety of chronic renal diseases exhibit an apparently relentless progression to renal failure. In order to develop prophylactic or therapeutic approaches, both cellular and humoral pathogenetic mechanisms have been studied. This special issue attempts to provide an overview of such mechanisms. The question of how glomerular, mesangial, endothelial and/or podocyte injury contributes to renal failure is dealt with, followed by a discussion of the emerging field of how macrophages can be programmed to exhibit different "phenotypic" activities. Two articles address the question of how primary glomerular damage is propagated into renal tubulointerstitium and reviews of the pathogenetic roles of tubular and interstitial cells. Finally, a review is devoted to insights into diabetic nephropathy derived from cell culture and in vivo studies.
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