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Kidney Week

Abstract: SA-PO471

Anti-HLA Antibody-Mediated Rejection in ABO-Incompatible (ABOI) Living Donor Kidney Transplant (KT) Patients

Session Information

Category: Transplantation

  • 1702 Transplantation: Clinical and Translational


  • Kwon, Hyuk yong, BHS-Hanseo hospital, Busan, Korea (the Republic of)
  • Kong, Jin M., BHS-Hanseo hospital, Busan, Korea (the Republic of)

Antibody-mediated rejection(AMR) in ABOi KT patients can either be due to donor-specific antiHLA antibody(DSA) or anti-blood group antibody(anti-ABO). The relative frequency and possible differential clinical features of these two types of AMR in ABOi KT patients has not been investigated.


Among 91 ABOi KT patients between 2007 and 2016 in our center, 11(12.1%) patients developed clinical acute AMR. Since there is no histologic distinction between DSA- and anti-ABO-induced AMR, we assumed the causative antibody in each case based on anti-ABO level and DSA, measured in serum collected at the time of AMR. DSA was determined by luminex single antigen beads assay.


Of these 11 cases of AMR, 5 were attributable to anti-ABO since anti-ABO titer was 16 or higher and DSA was undetectable at the time of rejection. Three cases were attributable to DSA since DSA was detectable and anti-ABO was low (≤ 8) during rejection. Another 2 cases with low (2) anti-ABO titer and undetectable DSA were assumed to be DSA-induced, since this low level of anti-ABO is unlikely to cause rejection and DSA can be undetectable in DSA-induced AMR by adsorption of Ab on graft, as frequently seen in ABO-compatible patient. One case with anti-ABO 8 and no detectable DSA was regarded as undetermined. The onset of AMR was within 2 weeks in all cases and comparable between two types of AMR. Initial anti-ABO titer was also not statistically different, median(range) 256(64-4096) in ABO-AMR and 64(16-256) in DSA-AMR. All the 5 patients with ABO-AMR had negative PRA before KT, whereas 4 of 5 patients with DSA-AMR had positive PRA before KT, and one DSA-AMR patient had persistent DSA before KT and at the time of AMR. All the AMR were recovered by treatment and no graft was lost to rejection.


We conclude that a significant proportion of AMR in ABOi KT are caused by DSA, and clinical features and possible differential therapeutic approach of these 2 types of AMR needs to be explored by further studies.