*Purpose: PLS can occur soon after solid organ transplantation when donor-derived antibodies against recipient red cell antigens are produced and lead to hemolysis. The anemia generally is self-limiting and resolves when donor-derived B cells fail to self-renew. In some severe cases, however, treatment with plasmapheresis and rituximab is indicated. We report a rare case of severe, immune-mediated hemolysis in an O+ patient who received a kidney from an O- donor.

*Methods: Our patient is a Caucasian male with ESRD secondary to diabetes who received a deceased donor kidney transplantation from a female donor who died from anaphylaxis after a bee sting. He was induced with thymoglobulin, methylprednisolone, and MMF. Estimated blood loss during surgery was 1000cc. His post-transplant course was complicated by delayed graft function, hyperkalemia, and oliguria for which he received dialysis on POD#0. His Hgb dropped to 7.9 mg/dL post-procedure from from 12.7 g/dL, so he received one unit of O+ RBCs with dialysis. The patient was typed pre-transplant as O+ with a negative red cell antibody (Ab) screen. On POD#3, his Hgb dropped to 7.2 g/dL and he received an additional unit of O+ RBCs to keep his Hgb >8. A guaiac-positive stool result led to EGD on POD#5 that showed erosive gastropathy. His PPI dose was increased accordingly. His Hgb peaked on POD#18 at 10.5 g/dL and then started to decline fairly rapidly. On POD#26 it had fallen to 7.6 g/dL and his workup was consistent with hemolysis (elevated LDH, low haptoglobin…etc). Stool was guaiac-negative at this point. Red cell Ab testing was positive for anti-D. He required multiple O- RBCs transfusions over several days. He failed a trial of IVIG and remained transfusion-dependent until POD#39, when he was started on rituximab.

*Results: The deceased donor sample was verified as O-, and anti-D in the donor serum was identified. We therefore attributed the recipient’s delayed presentation of anti-D to production by kidney donor-derived (passenger) B-cells and/or plasma cells. In situations like this, transfusion with donor Rh type-specific RBCs generally restores the patient’s Hgb until the hemolysis resolves. Our patient received rituximab to reduce transfusion dependence. Follow up labs approximately 1 month after completing rituximab showed no evidence of active hemolysis. The patient is now 1 year post transplant and his Hgb is stable (at > 14 g/dL).

*Conclusions: PLS should be suspected in cases of hemolytic anemia following ABO-mismatched solid organ transplant. In our case, we hypothesize that donor-derived B cells were triggered to produce anti-D against both the recipient’s and the transfused O+ RBCs resulting in hemolysis. The patient was successfully treated via the transfusion of donor Rh type-specific RBCs and the administration of rituximab.

« Back to 2020 American Transplant Congress