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  • Title: Cyclosporin A prevents proteinuria in an active model of membranous nephropathy in rats.
    Author: Thaiss F, Schoeppe W, Willaredt-Stoll JG, Batsford S, Mihatsch MJ.
    Journal: Lab Invest; 1989 Dec; 61(6):661-9. PubMed ID: 2689773.
    Abstract:
    The effect of the immunosuppressant Cyclosporin A on an active model of in situ immune complex glomerulonephritis was evaluated. Wistar rats were preimmunized with human IgG and 2 weeks after the last antigen injection, the left kidney was perfused with cationized human IgG in order to induce unilateral in situ immune complex glomerulonephritis. Three groups of rats were treated orally with Cyclosporin A (15 mg/kg body weight/day) beginning 2 days before induction of disease and continuing for 7 or 14 days afterwards, or alternatively treatment was commenced 5 days after induction of disease and continued until day 14. Cyclosporin A significantly reduced proteinuria (40 +/- 7 mg/day) in rats with immune complex glomerulonephritis when compared with untreated nephritic controls (250 +/- 65 mg/day). This effect was observed when rats were pretreated with Cyclosporin A and even when the drug was given in established disease, 5 days after induction. Proteinuria appeared in rats pretreated with Cyclosporin A when drug administration was stopped at day 7. Cyclosporin A did not alter immune complex formation in glomeruli or serum levels of anti-human-IgG antibody, nor did it reduce inulin clearance (CsA: 234 +/- 31 microliters/minute/100 gm body weight; controls: 119 +/- 27 microliters/minute/100 gm body weight). Morphologic studies did not reveal any differences between controls and the immunosuppressed rats. CsA failed to reduce proteinuria in the nonimmune mediated model of aminonucleoside nephrosis. The data demonstrate that Cyclosporin A can prevent the induction and more importantly ameliorate already established proteinuria in an autologous model of in situ immune complex glomerulonephritis. This latter finding is important since, in general, most treatment schedules have little, if any effect on established experimental glomerular disease.
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