Thrombotic microangiopathy associated with parvovirus B19 infection after renal transplantation

Citation
L. Murer et al., Thrombotic microangiopathy associated with parvovirus B19 infection after renal transplantation, J AM S NEPH, 11(6), 2000, pp. 1132-1137
Citations number
34
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Urology & Nephrology","da verificare
Journal title
JOURNAL OF THE AMERICAN SOCIETY OF NEPHROLOGY
ISSN journal
1046-6673 → ACNP
Volume
11
Issue
6
Year of publication
2000
Pages
1132 - 1137
Database
ISI
SICI code
1046-6673(200006)11:6<1132:TMAWPB>2.0.ZU;2-R
Abstract
Human parvovirus B19 is considered an etiologic agent of aplastic anemia in immunosuppressed patients. Microscopic vasculitis, with or without renal i nvolvement, has recently been attributed to this viral infection in immunoc ompetent patients. This study describes four cases of thrombotic renal graf t microangiopathy presumably secondary to B19 infection. Twelve to 50 days after transplantation, four patients presented a renal graft dysfunction wi th creatinine rising to 360 to 1088 mu mol/L and requiring hemodialysis in three cases. Renal involvement appeared after a systemic illness characteri zed by fever, fatigue and arthralgia, aplastic anemia (hemoglobin ranged fr om 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 transplan tation (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 a cute rejection and nine T0 biopsies of patients with no signs of B19 infect ion were used. The B19 genome was found in two of 20 posttransplant biopsie s 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 o f the virus suggests that B19 could be the etiologic agent of thrombotic mi croangiopathy in these cases. The development of the disease after infectio n could depend on other detrimental cofactors, which make the patient more susceptible to microthrombi formation in the renal microvasculature. The re nal graft could represent the route of B19 transmission.