Passenger Lymphocyte Syndrome in a Kidney Transplant Recipient

Introduction: Passenger Lymphocyte Syndrome (PLS) is an immune mediated disorder that is well described after an ABO mismatch solid organ transplant but is exceedingly rare in kidney transplantation. A high index of clinical suspicion is required for prompt identification, diagnosis, and management of this condition. Case Description: A 77-year-old man with CKD stage IV, blood type AB negative underwent a pre-emptive deceased donor kidney transplant with instant graft function. The donor blood group was A1. He then presented 2 weeks later with fever, cough and lethargy. His respiratory panel was positive for Influenza A and blood cultures were positive for Candida glabrata. He was also noticed to have a dramatic drop in hemoglobin from 12.6 g/dL to 6.8 g/dL over 4 days. Hemolysis was suspected as his total bilirubin increased to 4.6 mg/dL (conjugated bilirubin: 0.5 mg/dL). LDH was 494 U/L and haptoglobin was <8 mg/dL. Direct antiglobulin test was performed which was +1 positive for C3 but negative for IgG. No schistocytes were seen on a peripheral blood smear, and further evaluation showed the presence of anti-B antibodies that were thought to be produced by the donor graft lymphocytes. Diagnosis of PLS was made. Thereafter, the patient received A negative blood to prevent worsening hemolytic anemia and required only 2 red blood cell transfusions with improvement in hemolysis markers. Discussion: PLS is a rare cause of hemolytic anemia in kidney transplant recipients where donor B lymphocytes produce antibodies towards host erythrocytes. It typically occurs within 1-3 weeks after transplantation and is often self-limiting process, as donor B lymphocytes usually disappear, as shown in our case. Rarely, PLS can lead to more severe complications such as disseminated intravascular coagulation and allograft thrombosis. Some proposed therapies to help with severe cases are Rituximab, plasmapheresis, or IVIG which help with the neutralization and/or removal of effector antibodies.Figure 1. Pathophysiology of PLS