Abstract

Nephron reduction increases the filtration capacity of the remaining nephrons, which is helpful in the short term, but harmful over the long term The increase in glomerular capillary pressure and in hypertrophy of healthy nephrons stimulates the renin-angiotensin system and TGF-beta. Myofibroblastic transdifferentiation follows, with fibrogenesis and glomerulosclerosis. Converting enzyme inhibitors reduce the expression of genes coding for profibrotic molecules. Proteinuria promotes interstitial fibrosis and must be reduced by drugs that block the renin-angiotensin system.

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