Evaluation Of Complement-related Factors In Tma Post-kidney Transplantation: A Retrospective Multicenter Study
1Center for Kidney Disease and Transplantaion, Akita University Hospital, Akita, Japan, 2Department of Urology, Niigata University, Niigata, Japan, 3Kidney Transplant Surgery, Sapporo City General Hospital, Sapporo, Japan, 4Department of Urology, Osaka General Medical Center, Osaka, Japan, 5Department of Urology, The University of Tokyo, Tokyo, Japan, 6Department of Nephrolog, Shinsyu University Hospital, Shinsyu, Japan, 7Department of Urology, Tokyo Women’s Medical University, Tokyo, Japan, 8Department of Transplant Surgery, Nagoya Daini Red Cross Hospital, Nagoya, Japan, 9The Japanese Association for Complement Research, Osaka, Japan
Meeting: 2019 American Transplant Congress
Abstract number: D104
Keywords: Gene polymorphism, Hyperacute rejection, Renal thrombosis
Session Information
Session Name: Poster Session D: Kidney Acute Antibody Mediated Rejection
Session Type: Poster Session
Date: Tuesday, June 4, 2019
Session Time: 6:00pm-7:00pm
Presentation Time: 6:00pm-7:00pm
Location: Hall C & D
*Purpose: Post-kidney transplant thrombotic microangiopathy (KT-TMA) is a poor prognostic complication that causes a high rate of graft loss. In this study, we investigated KT-TMA-associated complement factors and blood markers.
*Methods: Kidney transplant patients who had developed KT-TMA since 2010 were enrolled. Their blood samples were subjected to targeting genome sequencing of 136 complement-related genes by NGS and quantitative analysis of blood complement factors (sC5b-9, Ba, CFH, CFH-IgG, CFH, C5a, C3, C4, and CH50), and the patients’ clinical data were collected.
*Results: Eight KT-TMA patients from 5 hospitals were enrolled. The time after KT-TMA until blood sampling was a median of 24 months [range: <1 to 40 months]. Soring by donor, there was one deceased donor and 7 living donors, and all living kidney transplantations were ABO-incomparible. Further, six of seven patients did not undergo plasma exchange and/or double filtration plasmapheresis as a desensitizatation therapy. In the blood complement assay, plasma Ba, a factor B degradation product, in 7 KT-TMA patients was higher than the normal limits [median: 1,079 ng/mL(range: 730 to 6,768) v.s. normal range: 276 to 685]. Especially, levels in the two patients with graft loss was markedly high. In NGS analysis, we detected a new candidate mutation in CHFR1 of atypical HUS-responsible genes, but no common mutation, as well as other candidate gene mutations in 136 complement-related genes.
*Conclusions: Ba produced in an alternative pathway was a candidate KT-TMA blood maker. Further evaluation of candidate mutations is required to identity genes responsible for KT-TMA.
To cite this abstract in AMA style:
Fujiyama N, Tasaki M, Harada H, Tsutahara K, Matsumoto A, Hara Y, Okumi M, Saito K, Watarai Y, Inoue N, Wakamiya N, Satoh S. Evaluation Of Complement-related Factors In Tma Post-kidney Transplantation: A Retrospective Multicenter Study [abstract]. Am J Transplant. 2019; 19 (suppl 3). https://atcmeetingabstracts.com/abstract/evaluation-of-complement-related-factors-in-tma-post-kidney-transplantation-a-retrospective-multicenter-study/. Accessed May 3, 2025.« Back to 2019 American Transplant Congress