PEDIATRICS

G.C. Wu¹, K.V. Lieberman², L.M. Ettinger², J.M. Abrams³, M.E. Shapiro^3
1Surgery - Organ Transplantation, Hackensack University Medical Center, Hackensack/NJ/UNITED STATES OF AMERICA, ²Pediatric Nephrology, Hackensack University Medical Center, Hackensack/NJ/UNITED STATES OF AMERICA, ³Surgery - Organ Transplantation, Hackensack University Medical Center, Hackensack/UNITED STATES OF AMERICA

Body: Background Alemtuzumab is a humanized anti-CD52 panlymphocytic (both T and B cells) monoclonal antibody that is used as an induction agent in approximately 10% of all renal transplant recipients. There are a few studies that have demonstrated its safety and efficacy. However, more reports have shown that alemtuzumab use has resulted in worse death-censored graft survival and an increase in acute rejection rates. A recent study also demonstrated that alemtuzumab augments B-cell activation. In this retrospective chart review, we report our experience with alemtuzumab induction in our pediatric renal transplant recipients.

Methods Between August 1, 2008 and August 31, 2009, 8 pediatric renal transplant patients at our institution received alemtuzumab induction. Seven patients were low-risk recipients and one patient was highly-sensitized, who received Rituximab pre-transplant for desensitization. They all received Tacrolimus, Mycophenolate Mofetil and Prednisone as their immunosuppressive regimen post-transplant. We reviewed their charts for any complications and recorded their absolute lymphocyte counts (ALC) pre-transplant, immediately post-transplant and at 1 month.

Results Out of the 8 patients, 2 low-risk recipients (25%) developed biopsy-proven antibody-mediated rejection (AMR) within 1 month of transplant. One of these two patients had complete graft failure, which required a transplant nephrectomy. The other was successfully treated with IVIG, plasmapheresis and Rituximab. The remaining 6 patients continued to have normal graft function at mid-term follow-up. No patients developed any opportunistic infections or any cellular rejections. All patients had their ALC drop to less than 2% after alemtuzumab was given. No correlation was observed between the level of the ALC and patients who had AMR.

Conclusion Alemtuzumab is supposed to deplete both mature T and B cells. However, in our small single center experience, despite a very low ALC immediate post-transplant, 25% of all alemtuzumab-induced pediatric renal transplant recipients developed AMR. This observation supports the view that alemtuzumab potentially augments B-cell activation and should be used with caution as an induction therapy for the pediatric renal transplant population. In addition, a low ALC may not be an accurate prediction that antibody-mediated rejection cannot occur. More studies need to be done to confirm such observations.

Disclosure: All authors have declared no conflicts of interest.