title: Aldosterone blockage in proliferative glomerulonephritis prevents not only fibrosis, but proliferation as well.
abstract: Studies performed recently have determined that aldosterone has not only a major role in electrolyte and water balance and K excretion, but it also modulates myofibroblast growth in the heart and blood vessels and causes fibrosis. This study investigated the effects of aldosterone blockers in rats with anti-thy 1.1 nephritis, both on proliferation and fibrosis, by comparing it to an angiotensin receptor inhibitor valsartan. Rats with anti-thy 1.1 nephritis were randomly allocated to one of the three following groups of treatment: the control group (group 1); those treated with the aldosterone receptor blocker spironolactone (group 2); and those treated with the ATRB valsartan (group 3). On day 7, the parameters of glomerular fibrosis [transforming growth factor beta, TGF staining areas %], proliferation (Ki-67), and renal damage scores were determined. The TGF-beta and Ki-67 levels of control group were significantly more than the other two groups (p<0.01). The TGF staining areas percentages were significantly decreased compared to control group. The artery, glomerular, and renal injury scores evaluated between the groups were found to be significantly decreased compared to control group. In line with previous studies, this study found that in anti-thy 1.1 mesangioproliferative glomerulonephritis, aldosterone blockage affected proliferation and fibrosis.
authors.affiliation: Department of Nephrology, Uludag University Medical School, Bursa, Turkey.
authors.forename: Mustafa
authors.initials: M
authors.lastname: Gullulu
authors.forename: Ibrahim
authors.initials: I
authors.lastname: Akdag
authors.forename: Serdar
authors.initials: S
authors.lastname: Kahvecioglu
authors.forename: Gülaydan
authors.initials: G
authors.lastname: Filiz
authors.forename: Vahide
authors.initials: V
authors.lastname: Savci
mesh_terms: D000450:Aldosterone / Q000378:metabolism*; D047228:Angiotensin II Type 1 Receptor Blockers / Q000494:pharmacology; D000818:Animals; D000959:Antihypertensive Agents / Q000494:pharmacology; D049109:Cell Proliferation / Q000187:drug effects*; D004195:Disease Models, Animal; D004232:Diuretics / Q000494:pharmacology*; D005355:Fibrosis / Q000473:pathology / Q000517:prevention & control*; D015432:Glomerulonephritis, Membranoproliferative / Q000378:metabolism* / Q000473:pathology / Q000503:physiopathology; D019394:Ki-67 Antigen / Q000378:metabolism; D007668:Kidney / Q000187:drug effects / Q000378:metabolism / Q000473:pathology; D000451:Mineralocorticoid Receptor Antagonists / Q000494:pharmacology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013148:Spironolactone / Q000494:pharmacology*; D013777:Tetrazoles / Q000494:pharmacology; D016212:Transforming Growth Factor beta / Q000378:metabolism; D014633:Valine / Q000031:analogs & derivatives / Q000494:pharmacology; D000068756:Valsartan
chemical_list: D047228:Angiotensin II Type 1 Receptor Blockers; D000959:Antihypertensive Agents; D004232:Diuretics; D019394:Ki-67 Antigen; D000451:Mineralocorticoid Receptor Antagonists; D013777:Tetrazoles; D016212:Transforming Growth Factor beta; D013148:Spironolactone; D000450:Aldosterone; D000068756:Valsartan; D014633:Valine