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1 Division of Nephrology, Charité, Campus Mitte, Humboldt-University, D-10098 Berlin, Germany; and 2 Department of Cell Biology and Institute of Nephrology, Niigata University Graduate School of Medical and Dental Sciences, Niigata 951-8510, Japan
Moderate alcohol consumption has shown
beneficial effects in experimental and human cardiovascular disease.
With the use of rat models of acute and chronic progressive anti-thy1
glomerulonephritis (GN), we tested the hypothesis that moderate alcohol
intake is protective in renal fibrotic disease. In acute anti-thy1 GN,
untreated nephritic rats showed marked mesangial cell lysis and induced nitric oxide production at day 1 and high proteinuria,
glomerular matrix accumulation, and transforming growth factor
(TGF)-
1, fibronectin, and plasminogen activator
inhibitor (PAI)-1 expression at day 7 after disease
induction, respectively. In animals 15 wk after induction of chronic
progressive anti-thy1 GN, disease was characterized by significantly
reduced renal function, persisting albuminuria as well as increased
glomerular and tubulointerstitial matrix expansion,
TGF-
1, fibronectin, and PAI-1 protein expression. In
both anti-thy1 GN models, an ethanol intake of ~2 ml per day and
animal was achieved, however, disease severity was not significantly altered by moderate alcohol consumption in any of the protocols. In
conclusion, moderate alcohol intake does not influence renal matrix
protein production and accumulation in acute and chronic progressive
anti-thy1 glomerulofibrosis. The study suggests that, in contrast to
cardiovascular disorders, moderate alcohol consumption might not
provide specific protection in renal fibrotic disease.
fibrosis; transforming growth factor-
; inducible nitric oxide
production; beer
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