Influence of cyclosporin, tacrolimus and rapamycin on renal function and arterial hypertension after renal transplantation
Autor: | Amado Andrés, Jose L. Rodicio, José M. Morales, Manuel Rengel |
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Rok vydání: | 2001 |
Předmět: |
medicine.medical_treatment
Pharmacology Kidney Function Tests Tacrolimus Nephrotoxicity Chronic allograft nephropathy medicine Humans Antihypertensive Agents Sirolimus Transplantation Kidney business.industry Immunosuppression medicine.disease Kidney Transplantation Calcineurin surgical procedures operative medicine.anatomical_structure Nephrology Hypertension Cyclosporine business Immunosuppressive Agents medicine.drug |
Zdroj: | Nephrology Dialysis Transplantation. 16:121-124 |
ISSN: | 1460-2385 0931-0509 |
Popis: | Cyclosporin and tacrolimus have improved survival figures in organ transplantation. However, both drugs are potentially nephrotoxic. The immunosuppressive and nephrotoxic effects of both drugs appear to depend on the inhibition of calcineurin. Cyclosporin and tacrolimus cause acute (functional changes) and chronic nephrotoxicity (structural lesions in the kidney). These last important lesions include arteriolar hyalinosis, stripped interstitial fibrosis and tubular atrophy. It is possible that repeated episodes of renal ischaemia contribute to the development of chronic nephrotoxicity and then chronic allograft nephropathy. Cyclosporin and tacrolimus also induce arterial hypertension. Therefore, the beneficial effects of immunosuppression have been limited due to nephrotoxicity and arterial hypertension. Rapamycin, a novel immunosuppressive agent, that does not inhibit calcineurin, provides immunosuppression without nephrotoxicity. In fact, in the trials performed in Europe, sirolimus-treated immunosuppression patients exhibited a much better renal function than cyclosporin-treated patients. However, sirolimus can potentiate the nephrotoxic effect of cyclosporin. Therefore, when cyclosporin and sirolimus are used in combination, a reduction of the cyclosporin dose is desirable. |
Databáze: | OpenAIRE |
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