No Increased Risk of Posttransplant Lymphoproliferative Disorder Following Alemtuzumab Induction in Kidney Transplant

Abstract

Objectives: Posttransplant lymphoproliferative disorder is a known complication of solid-organ transplant. The use of depleting induction agents has demonstrated varying associations with incidence of posttransplant lymphoproliferative disorder. Alemtuzumab, a depleting induction agent for kidney transplant patients, has shown promising results in reducing the risk of acute rejection and graft loss in the first year. Its unique mechanism of depleting both T-cell and B-cell populations may be beneficial in preventing the occurrence of posttransplant lymphoproliferative disorder. Materials and Methods:We examined the known risk factors for posttransplant lymphoproliferative disorder in the setting of alemtuzumab induction to determine whether incidence increases with this induction agent. We reviewed medical records of all alemtuzumab-induced kidney transplants from March 2006 to November 2015. Results: Of the 675 transplant patients who received alemtuzumab induction, 10 developed posttransplant lymphoproliferative disorder, with a cumulative incidence rate of 1.5%. All diagnosed patients had several known risk factors associated with post transplant lymphoproliferative disorder: 7 with advanced age over 60 years, 5 being cytomegalovirus-negative recipients, and all 10 donor kidneys being male patients and Epstein-Barr virus positive before transplant. Conclusions: The incidence rate seen in our patient population was within the range of the average in the United States but far lower than the incidence rates associated with other induction agents. Alemtuzumab is associated with a lower cumulative incidence rate of posttransplant lymphoproliferative disorder compared with published reports of other induction treatments. Key words: Campath, Kidney transplant outcomes, Transplantation IntroductionPosttransplant lymphoproliferative disorder (PTLD) is a well-documented complication of solid-organ transplant procedures. 1,2 Most occurrences of PTLD originate from uncontrolled Epstein-Barr virus (EBV) activation, which causes an unregulated transformation and proliferation of nodal and extranodal lymphocytes. 2 Within populations of transplant patients, the disorder usually has an incidence rate that ranges between 1% and 2%; however, it can have a higher incidence in pediatric populations. 3 According to the Organ Procurement and Transplantation Network data of 2012, the risk of developing PTLD after kidney transplant had a cumulative risk of 1.3%. 4 Mortality has been shown to be roughly 50%, with some variations associated with time of diagnosis since transplant, multiple-versus single-site cancer location, B-cell-predominant malignancy, and the continued increased risk after the first year of diagnosis. 3,4,5 A number of factors have been associated with the development of PTLD, including transplant from EBV-seropositive donors to EBV-seronegative recipients, coexisting cytomegalovirus (CMV) infection, and the use of certain immunosuppressive agents such as muromonab-CD3 (OKT3) or tacrolimus. 6,7 Depleting i...