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Kidney

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Room: E-Poster Hall

P-11.03 Anti-abo antibody- versus anti-hla antibody-induced antibody mediated rejection in abo-incompatible kidney transplant patients: Relative incidence and phenotype difference

Sung-Hyun Son, Korea

director
Division of Nephrology
BHS-Han Seo Hospital

Abstract

Anti-abo antibody- versus anti-hla antibody-induced antibody mediated rejection in abo-incompatible kidney transplant patients: Relative incidence and phenotype difference

Sung-Hyun Son1, Hyukyong Kwon1, Kitae Kim1, Joon Heun Jeong2, Eun Joo Hwang4, Chul Soo Yoon3, Sun Kim5, Jin Min Kong1.

1Nephrology, BHS-Hanseo Hospital, BUSAN, Korea; 2Transplant Surgery, BHS-Hanseo Hospital, BUSAN, Korea; 3Urology, BHS-Hanseo Hospital, BUSAN, Korea; 4Clinical laboratory, BHS-Hanseo Hospital, BUSAN, Korea; 5Transplant Coordinator, BHS-Hanseo Hospital, BUSAN, Korea

Antibody-mediated rejection(AMR) in ABO incompatible(ABOi) kidney transplant(KT) patients can either be due to donor-specific anti-HLA antibody(DSA) or anti-blood group antibody. The relative frequency and possible phenotype difference of these two types of AMR in ABOi KT patients have not been reported.
Among 111 ABOi KT patients between 2007 and 2019 in our center, 15(13.5%) patients developed acute AMR diagnosed by indication biopsy. 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.
Of these 15 cases of AMR, 5 were attributable to anti-ABO since anti-ABO titer was higher (≥16) and DSA was undetectable at the time of rejection. Four cases were attributable to DSA since DSA was detectable and anti-ABO was lower during rejection. Another 3 cases with lower 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 patients Two cases both with higher anti-ABO titer and detectable DSA were 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 is caused by DSA, and clinical features and possible differential therapeutic approaches of these 2 types of AMR need to be explored by further studies.

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