Diagnosis And Treatment Of Parvovirus B19-induced Pure Red Cell Aplasia After Renal Transplantation: A Case Report And Review Of Literature

Objective: Chronic aplasia is common in clinic after renal transplantation, maybe 39% of the recipients. Parvovirus B19-induced hematological toxicity, which has been reported in solid organ transplant recipients, may result in anemia episodes especially pure red cell aplasia, reported mainly in kidney transplant recipients. We aim to analyze the causes of pure red cell aplasia after renal transplantation and summarize the experience of diagnosis, treatment and prevention of parvovirus B19 infection causing pure red cell aplasia after transplantation.Methods: We describe the case of a renal transplant recipient with pure red cell aplasia due to parvovirus B19 infection that appeared during immunosuppressive therapy and discuss causes, diagnosis, treatment and prevention of the disease by reviewing relevant literature.Results: A 37-year-old male with mesangial proliferative glomerulonephritis received a renal allograft for end-stage renal disease. Immunosuppression in the first 29 days after the renal transplant was with cyclosporine, mycophenolate, and prednisolone, and thereafter it was changed to tacrolimus, mycophenolate, and prednisolone. After transplantation, this patient suffered from progressive anemia. Fifty-three days later, the hemoglobin had dropped to 47 g/L. Blood transfusions, colony stimulating factor, folate, iron, and erythropoietin supplements failed to raise the hemoglobin levels. And bone marrow biopsy showed selectively inhibited erythropoiesis. The anemia was unresponsive to replacement of tacrolimus by cyclosporine A and discontinuing mycophenolate. Detection of parvovirus B19-DNA with real time polymerase chain reaction revealed a severe parvovirus B19 infection(5.0×10~9 genome copies /ml). A course of intravenous immunoglobulin(20g/d for 5 days) was performed. Ten days after the administration, hemoglobin levels were stably elevated to 76g/L and parvovirus B19-DNA was 4.9 ×10~6 genome copies per milliliter. Ten days later, a remarkable decline of hemoglobin levels(61g/L) and a large amount of parvovirus B19-DNA in blood emerged again(4.8×10~9 genome copies /ml). Another course of intravenous immunoglobulin(25g/d for 5 days) was performed. After the third course of intravenous immunoglobulin(25g/d for 10 days) his hemoglobin level rose to 112 g/L but parvovirus B19-DNA was still detectable in blood with low level (3.8×10~5 genome copies /ml). Three months later, his hemoglobin level was normal. The parvovirus B19-DNA was negative 6 months after the treatment. Conclusions: Parvovirus B19 infection is the most common cause of virus-induced pure red cell aplasia after kidney transplantation. Diagnosis is based on bone marrow examination and detection of parvovirus B19 DNA by polymerase chain reaction in serum and/or bone marrow. Intravenous immunoglobulin is an effective and safe treatment but the disease easily recurs. There is no proven specific strategy available to prevent parvovirus B19 infection after kidney transplantation. We recommend further research on exploring most effective modality of therapy without recurrence and preventative strategies.