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Proteinuria and epithelial-to-mesenchymal transition: the role of complement.

The extent of injury to the tubulointerstitial compartment has been recognized for several decades as closely linked to declining renal function in glomerular diseases. In addition to secondary inflammatory injury and ischemia as mechanisms of injury in the tubulointerstitium downstream from diseased glomeruli, proteinuria itself is now recognized as a pathogenic factor and an independent risk factor for the progression of kidney disease.1–3 Reduction of proteinuria is now a major therapeutic goal in reducing risk for renal progression.4 Current strategies to reduce proteinuria are largely focused on treatment of the underlying glomerular disease and by alteration of glomerular hemodynamics and filtration. With improved understanding of basic mechanisms of proteinuria-induced injury, however, more refined and proximate strategies based on molecular pathogenesis of proteinuria-induced tubulointerstitial injury may be possible.

The damaging effects of proteinuria on the renal tubulointerstitial compartment involve a variety of mechanisms.5 These include tubular cell toxicity, when the lysosomal capacity to degrade …