title: The influence of chronic ethanol administration on adriamycin-induced nephrotic syndrome in rats.
abstract: Alcoholic liver disease may be frequently complicated by mesangial proliferation with the deposition of IgA in glomeruli and glomerulosclerosis, but these glomerular lesions are usually mild and without greater impact on renal function. To evaluate the putative role of ethanol in glomerular pathology we studied the influence of chronic ethanol administration on the development of experimental adriamycin nephropathy in rats. Nephrotic syndrome was induced by a single i.v. dose of adriamycin (5 mg/kg body wt) both in rats given ethanol at a dose of 4 g/day for 3 months and control rats given standard chow. Further controls on both diets without adriamycin administration were also studied. Blood and urine were examined before and 3 and 6 weeks after adriamycin administration. All rats were killed and examined histologically 6 weeks after adriamycin administration. Ethanol fed nephrotic rats were more catabolic than control nephrotic rats (with higher free fatty acids, lower glycaemia, higher urea with similar creatinine) and had lower proteinuria (0.55 +/- 0.34 versus 5.79 +/- 3.15 g of protein/nmol of creatinine, P < 0.05), higher albuminaemia (5.41 +/- 2.62 versus 1.92 +/- 1.94 g/l, P < 0.01), lower plasma cholesterol (6.54 +/- 2.6 versus 10.57 +/- 2.92 mmol/l, P < 0.01) and triglycerides. The development of nephrotic syndrome and renal morphological changes after adriamycin administration in rats seemed to be ameliorated, or at least delayed by chronic ethanol feeding with much milder and focal glomerulosclerosis as compared with more severe and diffuse glomerulosclerosis in control nephrotic animals. The mechanism of this effect of chronic ethanol feeding remains to be elucidated.(ABSTRACT TRUNCATED AT 250 WORDS)
authors.affiliation: First Department of Medicine, School of Medicine I, Charles University, Prague, Czech Republic.
authors.forename: V
authors.initials: V
authors.lastname: Tesar
authors.forename: T
authors.initials: T
authors.lastname: Zima
authors.forename: R
authors.initials: R
authors.lastname: Poledne
authors.forename: A
authors.initials: A
authors.lastname: Stejskalová
authors.forename: S
authors.initials: S
authors.lastname: Stípek
authors.forename: J
authors.initials: J
authors.lastname: Tĕmínová
mesh_terms: D000818:Animals; D001219:Aspartate Aminotransferases / Q000378:metabolism; D002784:Cholesterol / Q000097:blood; D008076:Cholesterol, HDL; D003401:Creatine / Q000097:blood / Q000652:urine; D004305:Dose-Response Relationship, Drug; D004317:Doxorubicin / Q000009:adverse effects* / Q000097:blood / Q000652:urine; D000431:Ethanol / Q000008:administration & dosage* / Q000494:pharmacology*; D005260:Female; D006943:Hyperglycemia; D007668:Kidney / Q000166:cytology / Q000187:drug effects* / Q000503:physiopathology; D007678:Kidney Glomerulus; D009404:Nephrotic Syndrome / Q000139:chemically induced* / Q000503:physiopathology; D051381:Rats; D017208:Rats, Wistar
chemical_list: D008076:Cholesterol, HDL; D000431:Ethanol; D004317:Doxorubicin; D002784:Cholesterol; D001219:Aspartate Aminotransferases; D003401:Creatine