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Clinical Significance of MHC‐Reactive Alloantibodies that Develop after Kidney or Kidney–pancreas Transplantation
Author(s) -
Pelletier Ronald P.,
Hennessy Patrice K.,
Adams Patrick W.,
VanBuskirk Anne M.,
Ferguson Ronald M.,
Orosz Charles G.
Publication year - 2002
Publication title -
american journal of transplantation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.89
H-Index - 188
eISSN - 1600-6143
pISSN - 1600-6135
DOI - 10.1034/j.1600-6143.2002.020204.x
Subject(s) - medicine , major histocompatibility complex , immunology , kidney transplantation , transplantation , mhc class i , isoantibodies , histocompatibility , pancreas transplantation , kidney , antigen , human leukocyte antigen
The purpose of this study was to determine the relationships between acute rejection, anti‐major histocompatibility complex (MHC) class I and/or class II‐reactive alloantibody production, and chronic rejection of renal allografts following kidney or simultaneous kidney‐pancreas transplantation. Sera from 277 recipients were obtained pretransplant and between 1 month and 9.5 years post‐transplant (mean 2.6 years). The presence of anti‐MHC class I and class II alloantibodies was determined by flow cytometry using beads coated with purified MHC molecules. Eighteen percent of recipients had MHC‐reactive alloantibodies detected only after transplantation by this method. The majority of these patients produced alloantibodies directed at MHC class II only (68%). The incidence of anti‐MHC class II, but not anti‐MHC class I, alloantibodies detected post‐transplant increased as the number of previous acute rejection episodes increased (p = 0.03). Multivariate analysis demonstrated that detection of MHC class II‐reactive, but not MHC class I‐reactive, alloantibodies post‐transplant was a significant risk factor for chronic allograft rejection, independent of acute allograft rejection. We conclude that post‐transplant detectable MHC class II‐reactive alloantibodies and previous acute rejection episodes are independent risk factors for chronic allograft rejection. Implementing new therapeutic strategies to curtail post‐transplant alloantibody production, and avoidance of acute rejection episodes, may improve long‐term graft survival by reducing the incidence of chronic allograft rejection.