[Lowered intrarenal protein degradation--an alternative path to glomerulosclerosis and tubulo-interstitial fibrosis].
Chronic renal failure is the consequence of progressive glomerulosclerosis and tubulo-interstitial fibrosis. The initiating hallmark of nephrosclerosis represents nephronal hypertrophy, due to an accumulation of proteins in the glomeruli and tubulointerstitium. From experimental and clinical investigations the conclusion can be drawn that the disturbed intrarenal protein balance with the consequent nephronal hypertrophy is at least partly the result of reduced protein degradation. Potential factors involved in impaired renal proteinase activities are cytokines like transforming growth factor beta 1 (TGF-beta 1), angiotensin II and advanced glycation endproducts (AGEs).


CONCLUSIONS
Nephrosclerosis as the common histological endpoint of chronic renal insufficiency is the result of an interaction between many pathogenetic factors. Its growing understanding implies the possibility of new therapeutic options to retard the progressive course of chronic renal failure.
Teschner
M
M
Kuratorium für Dialyse und Nierentransplantation e. V., Würzburg.
Heidland
A
A
D000804:Angiotensin II / Q000378:metabolism; D003928:Diabetic Nephropathies / Q000150:complications / Q000378:metabolism*; D017127:Glycation End Products, Advanced / Q000009:adverse effects; D006801:Humans; D007668:Kidney / Q000378:metabolism*; D007676:Kidney Failure, Chronic / Q000209:etiology* / Q000378:metabolism; D007683:Kidney Tubular Necrosis, Acute / Q000150:complications / Q000378:metabolism*; D011506:Proteins / Q000378:metabolism*; D016212:Transforming Growth Factor beta / Q000378:metabolism
D017127:Glycation End Products, Advanced; D011506:Proteins; D016212:Transforming Growth Factor beta; D000804:Angiotensin II