title: [Immunossupresive drugs in renal transplantation].
abstract: Modem immunosupressive agents have greatly reduced incidence and severity of acute renal allograft rejection. One-year graft survival rate of 95% can be easily achieved with optimal immunosuppressive regimens. However, long-term kidney transplant survival has improved poorly. At present, chronic allograft nephropathy (CAN) and recipients death (mainly due to circulatory complications, neoplasms and infections) are most common reasons of graft loss in the second and subsequent years after transplantation. Moreover adverse effects of immunosuppressive drugs (nephrotoxicity, arterial hypertension, dyslipidaemia, post-transplant diabetes mellitus) can account for development of CAN. Regimens with combination of at least two drugs are administered to recipients, as it allows for using minimal effective doses and reduces the risk of adverse effects. Narrow therapeutic window of most immunosuppressive agents forces clinicians to adequately monitor serum concentration of the drug or its metabolite. Early postransplant period requires higher doses, which then are reduced. Immunosuppressive regimen is individualized, to minimize the risk of acute rejection, but also to avoid overimmunosuppression and its complications. Presently there are two trends in immunosuppressive schemes: first one to withdraw glycocorticosteroids and the other one to reduce dose or withdraw calcineurin inhibitors, mostly because of their nephrotoxicity.
authors.affiliation: Klinika Medycyny Transplantacyjnej i Nefrologii Instytutu Transplantologii AM w Warszawie.
authors.forename: Teresa
authors.initials: T
authors.lastname: Baczkowska
authors.forename: Magdalena
authors.initials: M
authors.lastname: Durlik
mesh_terms: D000305:Adrenal Cortex Hormones / Q000494:pharmacology / Q000627:therapeutic use; D000074323:Alemtuzumab; D000911:Antibodies, Monoclonal / Q000494:pharmacology / Q000627:therapeutic use; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000912:Antibodies, Neoplasm / Q000494:pharmacology / Q000627:therapeutic use; D001379:Azathioprine / Q000494:pharmacology / Q000627:therapeutic use; D016572:Cyclosporine / Q000494:pharmacology / Q000627:therapeutic use; D004305:Dose-Response Relationship, Drug; D000068876:Fingolimod Hydrochloride; D006084:Graft Rejection / Q000188:drug therapy* / Q000209:etiology / Q000517:prevention & control*; D006801:Humans; D007166:Immunosuppressive Agents / Q000494:pharmacology* / Q000627:therapeutic use*; D016030:Kidney Transplantation / Q000009:adverse effects / Q000276:immunology / Q000379:methods; D009173:Mycophenolic Acid / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D011409:Propylene Glycols / Q000494:pharmacology / Q000627:therapeutic use; D012307:Risk Factors; D000069283:Rituximab; D020123:Sirolimus / Q000494:pharmacology / Q000627:therapeutic use; D013110:Sphingosine / Q000031:analogs & derivatives; D016559:Tacrolimus / Q000494:pharmacology / Q000627:therapeutic use
chemical_list: D000305:Adrenal Cortex Hormones; D000911:Antibodies, Monoclonal; D061067:Antibodies, Monoclonal, Humanized; D058846:Antibodies, Monoclonal, Murine-Derived; D000912:Antibodies, Neoplasm; D007166:Immunosuppressive Agents; D011409:Propylene Glycols; D000074323:Alemtuzumab; D000069283:Rituximab; D016572:Cyclosporine; D000068876:Fingolimod Hydrochloride; D009173:Mycophenolic Acid; D001379:Azathioprine; D013110:Sphingosine; D020123:Sirolimus; D016559:Tacrolimus