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2015 ; 8
(ä): 29-40
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Inhibition of RAS in diabetic nephropathy
#MMPMID25926752
Yacoub R
; Campbell KN
Int J Nephrol Renovasc Dis
2015[]; 8
(ä): 29-40
PMID25926752
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Diabetic kidney disease (DKD) is a progressive proteinuric renal disorder in
patients with type 1 or type 2 diabetes mellitus. It is a common cause of
end-stage kidney disease worldwide, particularly in developed countries.
Therapeutic targeting of the renin-angiotensin system (RAS) is the most validated
clinical strategy for slowing disease progression. DKD is paradoxically a low
systematic renin state with an increased intrarenal RAS activity implicated in
its pathogenesis. Angiotensin II (AngII), the main peptide of RAS, is not only a
vasoactive peptide but functions as a growth factor, activating interstitial
fibroblasts and mesangial and tubular cells, while promoting the synthesis of
extracellular matrix proteins. AngII also promotes podocyte injury through
increased calcium influx and the generation of reactive oxygen species. Blockade
of the RAS using either angiotensin converting enzyme inhibitors, or angiotensin
receptor blockers can attenuate progressive glomerulosclerosis in animal models,
and slows disease progression in humans with DKD. In this review, we summarize
the role of intrarenal RAS activation in the pathogenesis and progression of DKD
and the rationale for RAS inhibition in this population.
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