NDT Advance Access originally published online on May 25, 2006
Nephrology Dialysis Transplantation 2006 21(8):2060-2063; doi:10.1093/ndt/gfl219
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© The Author [2006]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org
Editorial Comment
Nephrotoxicity of ciclosporin A: short-term gain, long-term pain?
Centre for Transplant and Renal Research, Millenium Institute, Westmead Hospital, University of Sydney, Australia
Correspondence and offprint requests to: Jeremy R. Chapman, Centre for Transplant and Renal Research, Millenium Institute, University of Sydney, Westmead Hospital, Westmead NSW 2145, Australia. Email: jeremy_chapman@wsahs.nsw.gov.au
Keywords: chronic allograft nephropathy; ciclosporin; nephrotoxicity
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Historical perspective |
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Ciclosporin (CsA) was first dosed in pilot renal transplant recipients at 25 mg/kg/day, based upon large animal experimental data [1], but was rapidly found to be nephrotoxic and the dose reduced to 10 mg/kg/day. Monotherapy at this dose was, however, found to provide inadequate immunosuppression [2] and a starting dose of 17.5 mg/kg/day was thus used in the early phase II/III of clinical studies [3,4]. This early experience changed the clinical practice of transplantation, since acute rejection became a more subtle clinical syndrome and a differential diagnosis of acute nephrotoxicity had to be considered for renal dysfunction. The therapeutic window of CsA, when used alone, proved too narrow and thus, triple therapy, including azathioprine and low-dose prednisolone was born in the late 1980s [5]. The histological picture of acute CsA nephrotoxicity was defined both in transplanted and native kidneys, with
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Acute nephrotoxicity |
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Chronic nephrotoxicity |
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Histological predictors |
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Exacerbating factors |
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Strategies for avoiding chronic nephrotoxicity |
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