PrefaceKidneyAlemtuzumab Induction in Deceased Donor Kidney Transplantation

PurposeAlemtuzumab (Campath-1H), a humanized monoclonal antibody directed against CD52, is a lymphocyte-depleting agent currently being evaluated as an induction agent in solid organ transplantation. This study analyzed the clinical outcomes and effects on peripheral blood lymphocyte subset counts in adult deceased donor renal transplant recipients who received an alemtuzumab-based induction protocol.MethodsEleven kidney alone or simultaneous pancreas-kidney transplant recipients received 20 mg alemtuzumab on postoperative days 0 and 1, followed by calcineurin inhibitor-based maintenance immunosuppression after postoperative day 5. We collected 1-year data including recipient and donor demographic features, renal function and adverse events including endocrine impact, incidence of acute rejection episodes, infections or malignancies as well as hematologic and late immunologic parameters for correlation with patient or graft survival.ResultsMean HLA mismatch was 3.6 and 8/11 deceased donors were of the extended criteria type. Only 2 (18%) recipients displayed delayed graft function with a failure of the serum creatinine to decrease by 25% on the first day; however, their long-term outcomes were similar to other nonaffected patients. Serious adverse events were absent; there was no hyperlipidemia or new-onset diabetes. We failed to observe an acute rejection. The 3 (27%) recipients with infectious complications experienced pericardial tuberculosis, urinary tract infection, or invasive pulmonary aspergillosis. Two (18%) cases of posttransplantation lymphoproliferative disease were diagnosed in this study during the follow-up. Overall patient and graft survival rates were both 91%.ConclusionThis study demonstrated that preconditioning with antibody-depletion using alemtuzumab was efficient with satisfactory patient and graft survivals at 1 year. Alemtuzumab induction was safe even for recipients of extended criteria donor renal transplantation.