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Nephrol Dial Transplant (2003) 18: 54-61
© 2003 European Renal Association-European Dialysis and Transplant Association

Estradiol is nephroprotective in the rat remnant kidney

Balazs Antus1,, Peter Hamar1, Gabor Kokeny1, Zoltan Szollosi2, Istvan Mucsi1,3, Zoltan Nemes2 and Laszlo Rosivall1

1 Department of Pathophysiology, Semmelweis University, Budapest, Hungary, 2 Department of Pathology, Medical University, Debrecen, Hungary and 3 First Department of Internal Medicine, Semmelweis University, Budapest, Hungary

Background. Female sex hormones may influence the progression of renal diseases. We therefore evaluated the effects of estradiol on the development of glomerulosclerosis in a remnant kidney model.

Methods. Ovariectomized or intact female Wistar rats underwent 5/6 nephrectomy. Ovariectomized animals were treated with vehicle, 17ß-estradiol alone or in combination with progesterone, intact rats received vehicle only. Twenty-four weeks after renal ablation, histological as well as molecular analysis were performed.

Results. Vehicle-treated ovariectomized animals developed severe proteinuria and glomerulosclerosis as compared with vehicle-treated intact rats. In addition, renal mRNA levels of platelet-derived growth factor-A chain (PDGF-A) were increased. Estradiol replacement reduced proteinuria, which was paralleled by a diminished glomerular injury and reduced transforming growth factor-ß1 (TGF-ß1) and PDGF-A mRNA expression. In animals that received combined hormone treatment there were no significant differences in proteinuria, creatinine clearance, renal histopathology and growth factor mRNA levels compared with those measured in vehicle-treated ovariectomized rats. Serum cholesterol and triglyceride levels were comparable between all groups during the whole follow-up period.

Conclusions. The data suggest that estrogens protect against the development of glomerulosclerosis in the rat remnant kidney model.

Keywords: estradiol; glomerulosclerosis; growth factors; interstitial fibrosis; progesterone

Correspondence and offprint requests to: Dr Balazs Antus, Semmelweis University, Department of Pathophysiology, Nagyvarad ter 4, H-1089 Budapest, Hungary. Email: antbal{at}net.sote.hu


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