(P-TS-96) Severe Post-Transplant Hemolysis. Is It Time To Be Proactive?

A 54-year-old O Rh(D)-positive patient with liver cirrhosis successfully underwent a deceased donor liver transplant from an O Rh(D)-negative donor and received standard post-transplant immunosup- pression and infection prophylaxis. Perioperatively, the patient developed anemia and was transfused with nine O Rh(D)-positive red blood cells (RBC) units; in addition, high bilirubin was present and was attributed to the liverpathology. On POD 25, the patient was readmitted for a hemoglobin level of 5.9 g/dL, with no clinical findings of overt bleeding or retroperitoneal hematoma. The rou- tine antibody screen was positive and subsequent antibody identification panels identified an anti-D antibody.The case was referred to the Transfusion Medicine team.


Study

Design/Methods:

Following the identification of the anti-D antibody, the patient’s chart, including medication and transfusion history, were reviewed. The direct anti-human globulin (DAT) was performed via sero- logical methods and testing for the RHD genotype was sent out to a reference laboratory.Donor history was further investigated.


Results/Findings:

The patient received a total of 12 O Rh(D)-positive and 7 O Rh(D)-negative RBC transfusions before and after the patient’s anti-D detection. NoIVIG or preparations possibly containing anti-D antibody were administered. The direct anti-human globulin was positive with IgG and complement fraction, with the RBC eluate demonstrating the anti-D antibody. Laboratory markers of hemolysis are illustrated in Table 1. The patient’s probable RHD genotype was found to be hemizygous or homozygous RHD*01, with no variant markers detected. Further investigation on the liver donor history revealed that the donor had an anti-D antibody.


Conclusions:

This is a case of an O Rh(D)-positive liver transplant recipient who developed subacute hemolysis following a liver transplant from an O Rh(D)-negative donor who had a history of anti-D antibody. Passive antibody transfer was ruled out and the patient’s genotype confirmed that he did not have variant markers. Therefore, it was concluded that the patient’s anemia was caused by passenger lymphocyte syndrome (PLS) due to anti-D. PLS due to minor ABO/Rh incompatibility is recognized as a cause for post-transplant anemia and PLS due to prior donor sensitization hasbeen reported to lead to more severe hemolysis. However, pre-transplant evaluation does not routinely include investigation beyond blood type and antibody screen. Due to the higher risk of post- transplant hemolysis, proactive identification of patients who receive organs from donors with a history of antibodies against major RBC antigens may allow increased immunosuppression and early transfusion of antigen-negative RBCs.