Nephrol Dial Transplant Vol. 20 No. 1 © ERA-EDTA 2005; all rights reserved
Editorial Comment
Nephrotoxicity of rapamycin: an emerging problem in clinical medicine
1 Division of Nephrology, Department of Medicine, University Hospital of Zurich, Zurich and 2 Department of Nephrology and Hypertension, Inselspital, University of Berne, Berne, Switzerland
Correspondence and offprint requests to: Professor Felix J. Frey, Department of Nephrology and Hypertension, Inselspital Berne, University of Berne, 3010 Berne, Switzerland Email: felix.frey@insel.ch
Keywords: cyclosporine; everolimus; nephrotoxicity; rapamycin; renal allograft; sirolimus
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Introduction |
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Rapamycin represents substantial progress as a maintenance immunosuppressive agent to prevent rejection episodes and to decrease steroid and calcineurin inhibitor (CNI) exposure [1–3]. This drug is commonly administered in combination with mycophenolate mofetil, an inhibitor of inosine monophosphate dehydrogenase, or with azathioprine, a purine antimetabolite. Furthermore, rapamycin is prescribed as a substitute for or in combination with CNI.
The macrocyclic lactone rapamycin or sirolimus (Rapamune®) and its more polar derivative everolimus (Certican®) exhibit a similar mode of action but a different pharmacokinetic behaviour. Everolimus shows a shorter elimination half-life (
30 vs 60 h) and a higher bioavailability [4,5].
In the absence of concomitant use of CNI, rapamycin was shown repeatedly to spare renal function. To the surprise of the transplant community, evidence for rapamycin-associated nephrotoxicity has been accumulating in the last few years. In line with such observations, Crew et al. [
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Evidence of rapamycin nephrotoxicity in kidney transplantation |
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Nephrotoxicity of rapamycin in glomerulonephritis |
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Mechanisms of rapamycin-associated nephrotoxicity |
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Conclusions |
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