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Thrombotic Microangiopathy Associated with Parvovirus B 19 Infection after Renal Transplantation

LUISA MURER^*, GRAZIELLA ZACCHELLO^*, DANIELA BIANCHI, ROBERTO DALL'AMICO^*, GIOVANNI MONTINI^*, BARBARA ANDREETTA^*, MARINO PERINI, ELISABETTA CURRÒ DOSSI^*, GIANFRANCO ZANON^* and FRANCO ZACCHELLO^*

^* Department of Pediatrics, University of Padova, Italy.
Research and Development Department, DiaTech Srl, Jesi (An)-, Italy.

Correspondence to Dr. Luisa Murer, Department of Pediatrics, Via Giustiniani 3 35128 Padova, Italy. Phone: +39 49 8213505; Fax: +39 49 8213509; E-mail: luisam{at}child.pedi.unipd.it

Abstract. Human parvovirus B19 is considered an etiologic agent of aplastic anemia in immunosuppressed patients. Microscopic vasculitis, with or without renal involvement, has recently been attributed to this viral infection in immunocompetent patients. This study describes four cases of thrombotic renal graft microangiopathy presumably secondary to B19 infection. Twelve to 50 days after transplantation, four patients presented a renal graft dysfunction with creatinine rising to 360 to 1088 µmol/L and requiring hemodialysis in three cases. Renal involvement appeared after a systemic illness characterized by fever, fatigue and arthralgia, aplastic anemia (hemoglobin ranged from 5.3 to 7.8 g/dl), and thrombocytopenia. A thrombotic microangiopathy was observed in the renal biopsies, and the parvovirus B19 genome was isolated by PCR from the specimens. All four patients also became IgM-positive for parvovirus. Three of the four renal biopsies taken at the time of transplantation (T0) from the same patients were found positive for the B19 genome. Graft function recovered, with resolution of the aplastic anemia, within 22 to 110 d. Twenty biopsies performed as routine controls or for suspected acute rejection and nine T0 biopsies of patients with no signs of B19 infection were used. The B19 genome was found in two of 20 posttransplant biopsies and in one of nine T0 biopsies. The temporal association between aplastic anemia and the onset of thrombotic graft microangiopathy, isolation of the viral genome in renal specimens, seroconversion, and endothelial tropism of the virus suggests that B19 could be the etiologic agent of thrombotic microangiopathy in these cases. The development of the disease after infection could depend on other detrimental cofactors, which make the patient more susceptible to microthrombi formation in the renal microvasculature. The renal graft could represent the route of B19 transmission.

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Copyright © 2008 by the American Society of Nephrology. Online ISSN: 1533-3450 Print ISSN: 1046-6673