Navigating Therapeutic Challenges: Parvovirus-Induced Pure Red Cell Aplasia in a Kidney Transplant (KT) Recipient Who Declines Blood Transfusions

Introduction: Parvovirus B19 causes anemia by destroying erythroid progenitor cells. In immunocompromised patients, particularly KT recipients, persistent infection can lead to pure red cell aplasia (PRCA). Management is challenging in Jehovah’s Witnesses (JWs), who refuse allogenic blood products. Case Description: A 54-year-old JW female who received a living donor KT (2011) with current CKD IV from chronic antibody-mediated rejection, presented with symptomatic anemia. She refused blood transfusions. On admission, her hemoglobin (Hg) 5.1 g/dL, platelets 264 k/μL and creatinine 3.1 mg/dL (baseline 2.4). Severe anemia-induced hypoxemia was believed to cause the acute kidney injury. There was no evidence of gastrointestinal bleeding, iron deficiency (ferritin was elevated and iron saturation was normal), or hemolysis. Reticulocyte (R) production index was 0.3, consistent with bone marrow suppression. CMV and HHV6 were negative; EBV was detected at low levels. Parvovirus B19 infection was confirmed by qualitative PCR leading to a diagnosis of viral-induced PRCA. Mycophenolate Mofetil (MMF) was stopped, and the due dose of Belatacept was held. She received IVIG 2 g/kg in 2 doses, IV Iron Dextran 1,000 mg, and Epoetin Alfa 40,000 units daily for 2 days, then 10,000 units daily. Her Hb dropped to 4.7 g/dL by hospital day 3 but rose to 6.7 g/dL by day 12. Absolute R count increased from 0 to 600,000/μL. By discharge, Belatacept 5 mg/kg was resumed while MMF was kept on hold. Discussion: This case illustrates the complexity of managing severe anemia in a JW KT recipient with parvovirus-induced PRCA. Parvovirus B19 anemia occurs in up to 9% of KTs in the U.S., though PRCA remains rare. Despite a nadir Hb was 4.7 g/dL, and though she was symptomatic, she had no signs of critical anemia such as myocardial ischemia, hypotension, or shock. Aggressive anemia management must be promptly initiated with high dose erythropoietin stimulating factors, iron and vitamin B12/folate repletion. Compassionate use of hemoglobin-based oxygen carriers should be considered in cases of critical anemia (Hb<4 g/dL). In the absence of antivirals, reducing immunosuppression and providing passive immunity with IVIG can help as seen in this case by a dramatic increase in the R count.

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Publication Details

Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025b1s7ngbh
Primary Topic
Parvovirus B19 Infection Studies
Type
article
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article

Navigating Therapeutic Challenges: Parvovirus-Induced Pure Red Cell Aplasia in a Kidney Transplant (KT) Recipient Who Declines Blood Transfusions

Journal of the American Society of Nephrology
Parvovirus B19 Infection Studies
article

Navigating Therapeutic Challenges: Parvovirus-Induced Pure Red Cell Aplasia in a Kidney Transplant (KT) Recipient Who Declines Blood Transfusions

article en

Abstract

Introduction: Parvovirus B19 causes anemia by destroying erythroid progenitor cells. In immunocompromised patients, particularly KT recipients, persistent infection can lead to pure red cell aplasia (PRCA). Management is challenging in Jehovah’s Witnesses (JWs), who refuse allogenic blood products. Case Description: A 54-year-old JW female who received a living donor KT (2011) with current CKD IV from chronic antibody-mediated rejection, presented with symptomatic anemia. She refused blood transfusions. On admission, her hemoglobin (Hg) 5.1 g/dL, platelets 264 k/μL and creatinine 3.1 mg/dL (baseline 2.4). Severe anemia-induced hypoxemia was believed to cause the acute kidney injury. There was no evidence of gastrointestinal bleeding, iron deficiency (ferritin was elevated and iron saturation was normal), or hemolysis. Reticulocyte (R) production index was 0.3, consistent with bone marrow suppression. CMV and HHV6 were negative; EBV was detected at low levels. Parvovirus B19 infection was confirmed by qualitative PCR leading to a diagnosis of viral-induced PRCA. Mycophenolate Mofetil (MMF) was stopped, and the due dose of Belatacept was held. She received IVIG 2 g/kg in 2 doses, IV Iron Dextran 1,000 mg, and Epoetin Alfa 40,000 units daily for 2 days, then 10,000 units daily. Her Hb dropped to 4.7 g/dL by hospital day 3 but rose to 6.7 g/dL by day 12. Absolute R count increased from 0 to 600,000/μL. By discharge, Belatacept 5 mg/kg was resumed while MMF was kept on hold. Discussion: This case illustrates the complexity of managing severe anemia in a JW KT recipient with parvovirus-induced PRCA. Parvovirus B19 anemia occurs in up to 9% of KTs in the U.S., though PRCA remains rare. Despite a nadir Hb was 4.7 g/dL, and though she was symptomatic, she had no signs of critical anemia such as myocardial ischemia, hypotension, or shock. Aggressive anemia management must be promptly initiated with high dose erythropoietin stimulating factors, iron and vitamin B12/folate repletion. Compassionate use of hemoglobin-based oxygen carriers should be considered in cases of critical anemia (Hb<4 g/dL). In the absence of antivirals, reducing immunosuppression and providing passive immunity with IVIG can help as seen in this case by a dramatic increase in the R count.

Journal of the American Society of NephrologyVol. 36(10S)
University of Virginia (US)
Good health and well-being, Gender equality
Openalex Percentile: Top 36%
Parvovirus B19 Infection Studies
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