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J Am Soc Nephrol 10:1080-1089, 1999
© 1999 American Society of Nephrology


REGULAR ARTICLES

Polyomavirus Infection of Renal Allograft Recipients

From LatentInfection to Manifest Disease

VOLKER NICKELEIT*, HANS H. HIRSCH{dagger}, ISABELLE F. BINET{ddagger}, FRED GUDAT*, OLIVER PRINCE*, PETER DALQUEN*, GILBERT THIEL{ddagger} and MICHAEL J. MIHATSCH*

* Institute for Pathology, University of Basel, Switzerland.
{dagger} Institute for Medical Microbiology, University of Basel, Switzerland.
{ddagger} Division of Nephrology, Kantonsspital, University of Basel, Switzerland.

Correspondence to Dr. Michael J. Mihatsch, Institute of Pathology, University of Basel, Schoenbeinstrasse 40, CH-4003, Basel, Switzerland. Phone: 41 61 265 2872; Fax: 41 61 2653194; E-mail: mjmihatsch{at}uhbs.ch

Abstract. Polyomavirus (PV) exceptionally causes a morphologically manifest renal allograft infection. Five such cases were encountered in this study, and were followed between 40 and 330 d during persistent PV renal allograft infection. Transplant (Tx) control groups without PV graft infection were analyzed for comparison. Tissue and urine samples were evaluated by light microscopy, immunohistochemistry, electron microscopy, and PCR. The initial diagnosis of PV infection with the BK strain was made in biopsies 9 ± 2 mo (mean ± SD) post-Tx after prior rejection episodes and rescue therapy with tacrolimus. All subsequent biopsies showed persistent PV infection. Intranuclear viral inclusion bodies in epithelial cells along the entire nephron and the transitional cell layer were histologic hallmarks of infection. Affected tubular cells were enlarged and often necrotic. In two patients, small glomerular crescents were found. In 54% of biopsies, infection was associated with pronounced inflammation, which had features of cellular rejection. All patients were excreting PV-infected cells in the urine. PV infection was associated with 40% graft loss (2 of 5) and a serum creatinine of 484 ± 326 µmol/L (mean ± SD; 11 mo post-Tx). Tx control groups showed PV-infected cells in the urine in 5%. Control subjects had fewer rejection episodes (P < 0.05) and stable graft function (P = 0.01). It is concluded that a manifest renal allograft infection with PV (BK strain) can persist in heavily immunosuppressed patients with recurrent rejection episodes. PV mainly affects tubular cells and causes necrosis, a major reason for functional deterioration. A biopsy is required for diagnosis. Urine cytology can serve as an adjunct diagnostic tool.




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