Passenger Lymphocyte Syndrome: Use of Archived Donor Organ Biopsy Obtained at the Time of Transplantation for Diagnosis


To the Editor:

A recent report by Nadarajah et al. [1] highlighted the rare, but important complication of transplantation known as passenger lymphocyte syndrome (PLS). PLS that occurs with transplantation of mismatched ABO or RhD organs or marrow can be straightforward because the ABO and RhD type of both the donor and recipient is always known. Diagnosis of PLS that occurs when donor lymphocytes and plasma cells react with other recipient red blood cell (RBC) antigens, such as antigens of the Kidd, Duffy, RhCE, or Kell blood groups, is not always straightforward since the extended RBC phenotype is not always known.

We recently encountered a pediatric liver-transplant recipient who developed an immune-mediated hemolysis and thrombocytopenia, with the pathologic RBC antibody having apparent specificity for the Kpb antigen found on the Kell blood group protein. That is, the RBC antibody reacted with all reagent RBCs except those without the Kpb antigen. RBC genotyping of the patient showed she should have the Kpb antigen on her own RBCs, which implies that the pathologic antibody was either an autoantibody or an alloantibody produced from donor plasma cells.

In order to sort out the origin of the anti-Kpb antibody, the wedge biopsy of the donor liver that was obtained during the backroom preparation of the organ was acquired. A 10-µm unstained section of the formalin-fixed, paraffin-embedded tissue was cut, and the genomic DNA was isolated using the QIAamp DNA FFPE Tissue Kit as per the manufacturer's instructions (Qiagen, Valencia, CA). Polymerase chain reactions (PCRs) were performed to amplify the portion of exon 8 that contains the locus for the KEL4 allele using the following primers: Forward-5′-GACCCAAGCAAGGTGC-3′ and Reverse-5′-TGACCATCTGGAAGAGCTTGC-3′. The resulting DNA was sequenced using the same forward and reverse primers used in the PCR reaction.

Sequencing of the PCR product showed that the donor liver tissue had the wild type sequence 5′-CGG-3′ at codon 281, which corresponds to the KEL4 (Kpb) phenotype. This suggested that the RBC antibody was likely an autoantibody with apparent specificity for the Kpb antigen rather than a Kpb-specific graft-versus-host antibody that was being produced by plasma cells derived from the donor liver.

The patient was treated by discontinuing tacrolimus and starting cyclosporine, along with IVIG. The patient's hemolysis subsided, and the pathologic antibody was not detectable 23 days after first being discovered. In addition, the patient's hemoglobin responded well to Kpb-negative blood transfusions.

In summary, we report a pediatric solid organ transplant recipient who developed a warm autoantibody with apparent Kpb-specificity that responded well to treatment. Molecular genotyping performed on the donor liver tissue was utilized to rule out PLS. This case demonstrates that donor-derived organ transplant biopsies that are often routinely collected as part of the transplantation process may be a useful repository of genetic information needed to care for transplant recipients.

  • S. A. Koepsell* and J. D. Landmark

  • Department of Pathology and Microbiology, University of Nebraska Medical Center, Omaha, NE

  • * Corresponding author: Scott A. Koepsell,


The authors of this manuscript have no conflicts of interest to disclose.