A 55-year-old female patient underwent deceased-donor kidney transplantation on 11/01/2024, with a cold ischemia time of 12 hours. Thirty days after transplantation, she developed cytomegalovirus viremia, requiring preemptive treatment with ganciclovir followed by valganciclovir for 28 days. At 60 days, she progressed with pancytopenia, splenomegaly, need for red blood cell transfusions and use of filgrastim during hospitalizations in January and February 2025. Initial immunosuppression consisted of tacrolimus, prednisone and mycophenolate, the latter being replaced by sirolimus due to persistent CMV replication. Due to persistent pancytopenia, a bone marrow workup was performed, immunosuppression was changed to cyclosporine, and prophylactic sulfamethoxazole/trimethoprim was discontinued due to the risk of myelotoxicity. Bone marrow aspirate showed dysplasia in all three hematopoietic lineages, and bone marrow biopsy revealed giant erythroblasts with intranuclear inclusions, suggestive of viral infection, without fibrosis. Serologies for HIV, hepatitis and HTLV were negative, and CMV PCR was undetectable. Parvovirus B19 serology showed reactive IgM. After confirmation of viral infection, cyclosporine was reduced to the minimum dose, sirolimus was discontinued, and intravenous immunoglobulin was requested to treat transient aplastic crisis. The patient evolved with good hematologic response and clinical resolution after 60 days, without the need for immunoglobulin. The reduced ability to mount an effective immune response in immunosuppressed patients favors the development of chronic or reactivated parvovirus B19 infection, leading to hypoplasia or aplasia of erythroid precursors and severe, acute or chronic, potentially fatal anemia. Studies describe chronic infection and prolonged anemia in solid organ transplant recipients. In such cases, B19-associated refractory anemia may relapse in approximately 17–18% of cases. By exclusively suppressing erythropoiesis, the infection causes marked reticulocytopenia; in addition, giant pronormoblasts with eosinophilic intranuclear inclusions and vacuolated cytoplasm with marginated chromatin are typically seen in bone marrow. B19 can trigger a transient aplastic crisis (TAC), which is generally self-limited, as erythropoiesis returns to normal usually 7–14 days after the decline of viremia and resolution of infection.
Castro et al. (Sun,) studied this question.