ABO-incompatible (ABO-I) living donor liver transplantation (LDLT) can be performed successfully. However, anti-ABO isoagglutinin rebound may cause antibody-mediated rejection (AMR) and graft loss. The risk threshold of isoagglutinin rebound is still not defined. 76 ABO-I LDLT recipients were divided into group A ( = 56) with low isoagglutinin titers (<1:256), and group B ( = 20) with high isoagglutinin titers (≥1:256), at initial assessment for liver transplantation. The last 12 patients in group B received a modified desensitization regimen by adding bortezomib to deplete plasma cells. Six (10.7%) patients in group A and 10 (50.0%) patients in group B had postoperative isoagglutinin rebound ( < 0.001). Three patients (5.54%) in group A and two patients (10%) in group B developed clinical AMR ( = 0.602). The cutoff value of postoperative isoagglutinin rebound to cause clinical AMR was ≥1:1024. Among the 12 patients in group B with bortezomib administration, isoagglutinin rebounded up to 1:128 only, and no clinical AMR occurred. In conclusion, the patients with high isoagglutinin titers had a higher rate of postoperative isoagglutinin rebound. Isoagglutinin rebound ≥1:1024 is risky for developing clinical AMR. Adding bortezomib into the desensitization regimen may mitigate isoagglutinin rebound, and avoid clinical AMR.
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http://dx.doi.org/10.3390/jpm11121300 | DOI Listing |
Cureus
June 2024
Nephrology, Sir Ganga Ram Hospital, New Delhi, IND.
Kidney transplantation is the preferred treatment for end-stage renal disease (ESRD); however, ABO incompatibility (ABOi) poses challenges due to increased graft rejection risk. Desensitization strategies, including immunoadsorption (IA), aim to overcome ABOi barriers. The objective of this case report was to present the initial findings and patient outcomes of ABOi kidney transplantation (KT) using two different brands of IA columns (Glycosorb ABO and SECORIM-ABO) in reducing isoagglutinin titers to the desired target level.
View Article and Find Full Text PDFAsian J Transfus Sci
May 2022
Institute of Liver Disease and Transplantation, Chennai, Tamil Nadu, India.
We report the clinical outcome of an emergency ABO incompatible-liver transplantation (LT) for an 8-year-old child with Wilson's disease-induced acute liver failure. The pretransplant anti-A antibody titer was 1:64, and hence he underwent three cycles of conventional plasma exchange as pretransplant liver supportive treatment for deranged coagulopathy and liver function followed by one cycle of immunoadsorption (IA) prior to LT. The posttransplant immunosuppression consisted of rituximab, tacrolimus, mycophenolate mofetil, and corticosteroid.
View Article and Find Full Text PDFJ Pers Med
December 2021
Division of Liver and Transplantation Surgery, Department of General Surgery, Chang-Gung Memorial Hospital, Linkou 33357, Taiwan.
ABO-incompatible (ABO-I) living donor liver transplantation (LDLT) can be performed successfully. However, anti-ABO isoagglutinin rebound may cause antibody-mediated rejection (AMR) and graft loss. The risk threshold of isoagglutinin rebound is still not defined.
View Article and Find Full Text PDFJ Clin Apher
February 2021
Service de Néphrologie, Hémodialyse, Aphérèses et Transplantation Rénale, CHU Grenoble-Alpes, Grenoble, France.
Introduction: ABO-incompatible (ABOi) kidney transplantation, a well-established procedure, has good long-term results provided pretransplant desensitization that includes immunosuppression and apheresis.
Objective: To compare, within the first pretransplant apheresis session given to 29 ABOi kidney-transplant candidates, the effect on isoagglutinin titers (both IgG and IgM isotypes) of three modalities: centrifugation therapeutic plasmapheresis (cTP; n = 10), filtration TP (fTP; n = 9), and double-filtration plasmapheresis (DFPP; n = 10).
Results: The three groups were comparable according to baseline demographics.
Antiviral Res
September 2019
Department of Chemistry, University of British Columbia, 2036 Main Mall, Vancouver, British Columbia, V6T 1Z1, Canada. Electronic address:
An influenza A(H1N1)pdm09 and an influenza B virus were passaged in 3-fluoro(eq)-4-guanidino difluoro sialic acid (3Feq4Gu DFSA), an inhibitor of the influenza neuraminidase (NA) to determine whether resistant variants could be selected. 3Feq4Gu DFSA is a mechanism-based inhibitor, forming a covalent link to Y406 in the NA active site. Given its similarity to the natural substrate, sialic acid, we predicted resistant variants would be difficult to select.
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