To the Editor,

Parvovirus B19 infection has an incidence of 2% after solid organ transplants. Parvovirus B19 is an erythrovirus belonging to the Parvoviridae family, which usually replicates in human erythrocyte precursor cells. Clinical symptoms include fever, joint pains, and a rash in 25%, 7%, and 6% of cases, respectively. Anaemia is the most common expression of the virus (99%). Diagnosis of the infection by serology (IgM and IgG) is not reliable due to the delayed and inadequate antibody-mediated immune response in immunocompromised patients. Using polymerase chain reaction (PCR) improved the detection of parvovirus B19 infection, and the precision rate for positive PCR in immunocompromised hosts is higher when associated with red cell aplasia. If serology and PCR tests are negative, a bone marrow study with in situ hybridization and immunohistochemical techniques may also clarify the diagnosis. At present, no treatment with anti-viral drugs has been described. However, high doses of immunoglobins (IVIg therapy) were shown to have a beneficial effect on the infection in patients receiving kidney transplants. The optimal dose and duration of treatment have not been established as some patients require additional courses of drugs. Furthermore, reducing immunosuppression is a priority.

We present the case of a 36-year-old male diagnosed with chronic kidney failure of unknown aetiology. He was admitted for haemodialysis in 2008 and then in January 2010 he received a kidney transplant from a 9-year-old cadaveric donor with a history of cranio-encephalic trauma (CET). He was given thymoglobulin induction therapy, corticosteroids and mycophenolate sodium. Tacrolimus, deltisone and mycophenolate sodium were given as maintenance treatment. He received ganciclovir prophylaxis for cytomegalovirus (CMV), and trimethoprim-sulfamethoxazole (TMP-SMX) for PCP. The patient had urinary fistula on the third day after the transplantation, which was corrected with surgery. Two weeks later, he suffered diarrhoea associated with mycophenolate sodium, and severe normocytic anaemia (Hct 19%), normochromic anaemia with reticulocytopenia, without changes in the series of white blood cells, and negative Coombs’ test on platelets. He needed multiple transfusions due to symptomatic anaemia. In February 2010, he had a fever syndrome and a urinary infection due to Acinetobacter sp., and was given treatment with amikacin. The patient continued with anaemia with the same characteristics described above, associated with joint and muscle pain. A ferrokinetic study was requested, showing normal parameters. The maximum dose of erythropoietin was increased with no response. A study of blood in stools and  serial parasitological examinations of faecal samples were negative. We performed an upper and lower endoscopy with no signs of haemorrhages; a video capsule endoscopy: s/p, blood smear analysis with PAMO: erythroid hypoplasia, with normal white blood cell and platelet counts. Parvovirus B19 IgG and IgM antibodies tests were positive, and PCR test for parvovirus B19 was positive. Treatment with IVIg at 400 mg/kg/day (30 g/day) was prescribed for 5 days. Mycophenolate sodium treatment was stopped. Kidney function remained stable (average creatinine 1.4 mg/dl); Hct levels increased 10 (35%) and 14 (38%) days after treatment, as did the number of reticulocytes. The follow-up parvovirus PCR (8 weeks after treatment) was negative. Immunosuppression treatment with tacrolimus and deltisone was continued. DNA PCR testing will continue on a regular basis.