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Nephrol Dial Transplant. 1996 Mar;11(3):507-13.

Prevention of cyclosporin nephrotoxicity with a platelet-activating factor (PAF) antagonist.

Author information

1
Department of Nephrology, Hôpital Pitié Salpêtrière, Paris, France.

Abstract

BACKGROUND:

Cyclosporin (CsA) is a potent immunosuppressive drug whose main side-effect is nephrotoxicity. In the kidney, CsA induces vasoconstriction with a decrease in renal blood flow (RBF) and glomerular filtration rate (GFR) and a significant increase in renal vascular resistance (RVR). CsA enhances platelet-activating factor (PAF) synthesis in mesangial cells in vitro. PAF, a secondary mediator of anaphylaxis and inflammation, exhibits vasoactive properties in the kidney similar to those of CsA.

METHODS:

The in situ autoperfused rat kidney model was used to investigate whether PAF plays a role in the haemodynamic injury induced by CsA.

RESULTS:

In this model, CsA (40 mg/kg and 20 mg/kg i.v.) induced a significant decrease in RBF and in GFR and an increase in RVR. BN 52021, a potent and specific PAF antagonist (20 mg/kg i.v. bolus dose) induced a significant increase in GFR (137 +/- 32% of initial value, P < 0.05). BN 52021 (20 and 10 mg/kg) also significantly prevented the decline in RBF and GFR induced by CsA.

CONCLUSIONS:

We have demonstrated that the PAF antagonist BN 52021 can minimize the alteration of renal function induced by CsA.

PMID:
8671822
[Indexed for MEDLINE]

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