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Abstract: TH-PO652

Identification of Complement Regulatory Proteins in ABO-Incompatible and HLA-Incompatible Kidney Transplantation

Session Information

  • Transplantation: Basic
    November 03, 2022 | Location: Exhibit Hall, Orange County Convention Center‚ West Building
    Abstract Time: 10:00 AM - 12:00 PM

Category: Transplantation

  • 2001 Transplantation: Basic

Authors

  • Jintanapramote, Kavita, Chulalongkorn University Faculty of Medicine, Bangkok, Thailand
  • Bhunyakarnjanarat, Thansita, Chulalongkorn University Department of Microbiology, Bangkok, Bangkok, Thailand
  • Phannajit, Jeerath, Chulalongkorn University Faculty of Medicine, Bangkok, Thailand
  • Surintrspanont, Jerasit, Chulalongkorn University, Bangkok, Bangkok, Thailand
  • Leelahavanichkul, Asada, Chulalongkorn University Faculty of Medicine, Bangkok, Thailand
  • Avihingsanon, Yingyos, Chulalongkorn University Faculty of Medicine, Bangkok, Thailand
  • Eiam-Ong, Somchai, Chulalongkorn University Faculty of Medicine, Bangkok, Thailand
  • Townamchai, Natavudh, Chulalongkorn University Faculty of Medicine, Bangkok, Thailand
Background

ABO incompatible kidney transplantation (ABOi KT) provides better allograft outcomes compared to HLA incompatible KT (HLAi KT), especially a lower incidence of antibody-mediated rejection (ABMR). The findings in ABMR generally consist of the presence of serum anti-donor antibody, C4d staining, and inflammation in the allograft. Despite the positivity of C4d, there is no evidence of inflammation found in ABOi KT, indicating that there must be some mechanisms preventing the allograft from complement mediated injury. We hypothesize that the complement regulatory proteins may play roles in this process.

Methods

This observational, retrospective study was conducted at King Chulalongkorn Memorial Hospital. All living donor KT patients were divided into 4 groups according to pre-transplant antibody: 1) ABOi, 2) HLAi, 3) combined ABOi and HLAi, which considered as high-immunologic risk groups and 4) compatible KT, which served as the control group. The expression of complement regulatory proteins including CD59, CD55, CD46, and CD35 was measured from allograft tissue within 1 year after KT using RNA isolation and quantitative reverse transcription-PCR (qRT-PCR).

Results

There were 87 patients enrolled of which 12 were ABOi KT, 22 were HLAi KT, 6 were combined ABOi and HLAi KT and 47 were compatible KT group. There was no differences in CD59, CD55, CD46, and CD35 expression between all groups. However, CD46 expression was significantly higher in ABOi KT patients with C4d positive (accommodation) who have a high ABO titer (≥ 1:32) compared to a low ABO titer (<1:32) (p = 0.006). In addition, CD 59 was upregulated in high-immunologic risk patients compared with the control group (p = 0.018).

Conclusion

This study found no evidence of increased CD59, CD55, CD46, or CD35 expression in ABOi KT compared with other types of transplantation. However, CD46 expression increased in association with the ABO titer. All types of incompatible KT revealed higher CD59 expression, which may play roles protection of the allograft against preformed antibodies.

Funding

  • Private Foundation Support