Polyomavirus nephropathy after renal transplantation: A single centre experience
- Author(s)
- HYUN CHUL KIM; EUN AH HWANG; SEUNG YEUP HAN; SUNG BAE PARK; KWAN KYU PARK
- Keimyung Author(s)
- Kim, Hyun Chul; Hwang, Eun Ah; Han, Seung Yeup; Park, Sung Bae; Park, Kwan Kyu
- Department
- Dept. of Internal Medicine (내과학)
Dept. of Pathology (병리학)
Kidney Institute (신장연구소)
- Journal Title
- Nephrology
- Issued Date
- 2005
- Volume
- 10
- Issue
- 2
- Keyword
- graft failure; polyomavirus nephropathy (BK virus nephropathy); renal
transplantation
- Abstract
- Background: Polyomavirus associated nephropathy (PVN) in renal transplant recipients has been
observed with increasing frequency recently and has emerged as a cause of allograft failure linked to
highly potent new immunosuppressive regimens containing tacrolimus or mycophenolate mofetil
(MMF).
Methods: Polyomavirus associated nephropathy was identified in nine out of 182 patients who
received renal transplantation between October 1998 and July 2003. PVN was confirmed by allograft
biopsy. The clinical records of these nine patients were reviewed, as were all of the allograft biopsies.
Electron microscopy was performed in all nine cases. After the diagnosis of PVN, maintenance immu-
nosuppression was reduced. The clinical course and outcome of the PVN patients were reviewed in
relation to manipulation of immunosuppressive agents.
Results: There were nine cases of PVN in renal transplant recipients and the incidence of PVN was
4.9%. All patients with PVN were under triple immunosuppression comprising tacrolimus and MMF.
The mean time to a diagnosis of PVN was 7.8 months after transplantation. Three of the nine patients
received antirejection therapy prior to PVN. Seven out of nine PVN patients presenting acute allograft
dysfunction were initially treated with high-dose intravenous steroid pulse or OKT3 before reduction
of the immunosuppression. After reduction of the immunosuppression, seven patients stabilized their
renal function. Two (22%) lost their grafts due to persistent PVN and chronic rejection. Two (22%)
patients later developed acute rejection after reduction of the immunosuppression.
Conclusion: PVN can cause allograft dysfunction and graft loss. Renal allograft recipients who are
at risk of PVN should be routinely screened with urine cytology and quantitative measurements of viral
load in the blood, particularly patients who had graft dysfunction. Early diagnosis and judicious alter-
ation of immunosuppressive agents might permit a superior prognosis and reduce the graft loss from
PVN in renal transplant recipients.
KEY WORDS: graft failure, polyomavirus nephropathy (BK virus nephropathy), renal
transplantation.
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