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Late antibody-mediated rejection after ABO-incompatible kidney transplantation during Gram-negative sepsis

Annelies de Weerd1*, Alieke Vonk2, Hans van der Hoek3, Marian van Groningen4, Willem Weimar1, Michiel Betjes1 and Madelon van Agteren1

Author Affiliations

1 Erasmus Medical Center Rotterdam, Department of Nephrology, Room D-411, P.O. Box 2040, 3000 CA Rotterdam, The Netherlands

2 Erasmus Medical Center Rotterdam, Department of Microbiology and Infectious diseases, Rotterdam, The Netherlands

3 Erasmus Medical Center Rotterdam, Department of Hematology, Rotterdam, The Netherlands

4 Erasmus Medical Center Rotterdam, Department of Pathology, Rotterdam, The Netherlands

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BMC Nephrology 2014, 15:31  doi:10.1186/1471-2369-15-31

Published: 12 February 2014



The major challenge in ABO-incompatible transplantation is to minimize antibody-mediated rejection. Effective reduction of the anti-ABO blood group antibodies at the time of transplantation has made ABO-incompatible kidney transplantation a growing practice in our hospital and in centers worldwide. ABO antibodies result from contact with A- and B-like antigens in the intestines via nutrients and bacteria. We demonstrate a patient with fulminant antibody-mediated rejection late after ABO-incompatible kidney transplantation, whose anti-A antibody titers rose dramatically following Serratia marcescens sepsis.

Case presentation

A 58-year-old woman underwent an ABO-incompatible kidney transplantation for end-stage renal disease secondary to autosomal dominant polycystic kidney disease. It concerned a blood group A1 to O donation. Pre-desensitization titers were 64 for anti-blood group A IgM and 32 for anti-blood group A IgG titers. Desensitization treatment consisted of rituximab, tacrolimus, mycophenolate mofetil, corticosteroids, immunoadsorption and intravenous immunoglobulines. She was readmitted to our hospital 11 weeks after transplantation for S. marcescens urosepsis. Her anti-A IgM titer rose to >5000 and she developed a fulminant antibody-mediated rejection.

We hypothesized that the (overwhelming) presence in the blood of S. marcescens stimulated anti-A antibody formation, as S. marcescens might share epitopes with blood group A antigen. Unfortunately we could not demonstrate interaction between blood group A and S. marcescens in incubation experiments.


Two features of this post-transplant course are remarkably different from other reports of acute rejection in ABO-incompatible kidney transplantation: first, the late occurrence 12 weeks after kidney transplantation and second, the very high anti-A IgM titers (>5000), suggesting recent boosting of anti-A antibody formation by S. marcescens.

ABO-incompatible kidney transplantation; Serratia marcescens; Antibody-mediated rejection; Bacteremia-induced anti-ABO antibodies