Literature DB >> 12138148

Clinical course of polyoma virus nephropathy in 67 renal transplant patients.

Emilio Ramos1, Cinthia B Drachenberg, John C Papadimitriou, Omar Hamze, Jeffrey C Fink, David K Klassen, Rene C Drachenberg, Anne Wiland, Ravinder Wali, Charles B Cangro, Eugene Schweitzer, Stephen T Bartlett, Matthew R Weir.   

Abstract

Polyoma virus (PV) can cause interstitial nephritis and lead to graft failure in renal transplant recipients. The clinical course of patients with polyoma virus nephritis (PVN) is not well understood, partially due to its relatively low incidence. This study is a retrospective analysis of our experience over 4 yr. The specific purpose is to outline the clinical course and outcome of patients with PVN and to study the relationship between immunosuppression and the disease process. Between June 1997 and March 2001, 67 patients with graft dysfunction were found to have biopsy-proven PVN. The diagnosis was made at a mean of 12.8 +/- 9.9 mo posttransplantation. The majority of patients were men (79%) with a mean age of 54 +/- 14 yr (range, 28 to 75). All patients received immunosuppression with a calcineurin inhibitor (tacrolimus in 89% of patients). All patients except two received mycophenolate mofetil and prednisone. After the diagnosis of PVN, maintenance immunosuppression was reduced in 52 patients and remained unchanged in 15 patients. After reduction of immunosuppression, eight patients (15.3%) developed acute rejection and six (11.5%) became negative for PV in biopsy and urine. After a mean observation period of 12.6 mo (mean of 26 mo posttransplantation), 16.4% of patients had lost their grafts (8 of 52 in the reduction group and 3 of 15 in the no change group). In comparison to a case-matched polyoma virus-negative control group, the PVN patients were older (P =.0004) and there was a predominance of men (P = 0.02). Kaplan-Meier analysis demonstrated that patients with PVN had reduced graft survival compared with negative controls (P =.0004). It is concluded that PVN is a serious hazard for renal transplant recipients and contributes directly to graft loss. Antiviral drugs are needed, as the reduction of immunosuppression alone may not significantly improve graft function in patients with already established PVN. Although multiple factors probably play a role in the development of PVN, judicious use of immunosuppressive agents is indicated to minimize the occurrence of this infection.

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Year:  2002        PMID: 12138148     DOI: 10.1097/01.asn.0000023435.07320.81

Source DB:  PubMed          Journal:  J Am Soc Nephrol        ISSN: 1046-6673            Impact factor:   10.121


  77 in total

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3.  [Polyomavirus associated nephropathy. A new opportunistic complication after kidney transplantation].

Authors:  H H Hirsch
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4.  Impact of genomic sequence variability on quantitative PCR assays for diagnosis of polyomavirus BK infection.

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Authors:  Bradley H Collins; Carlos E Marroquin; Janet E Tuttle-Newhall; Paul C Kuo; Glenn M Preminger; David W Butterly
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Review 6.  Canadian Society of Transplantation: consensus guidelines on eligibility for kidney transplantation.

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7.  Urine cytology screening for polyoma virus infection following renal transplantation: the Oxford experience.

Authors:  Thomas P Thamboo; Katie J M Jeffery; Peter J Friend; Gareth D H Turner; Ian S D Roberts
Journal:  J Clin Pathol       Date:  2006-12-08       Impact factor: 3.411

8.  Antirejection treatment in kidney transplant patients with BK viruria.

Authors:  Liise K Kayler; Ibrahim Batal; Ravi Mohanka; Claire Morgan; Amit Basu; Ron Shapiro; Parmjeet S Randhawa
Journal:  Transplantation       Date:  2008-09-27       Impact factor: 4.939

Review 9.  The role of polyomaviruses in human disease.

Authors:  Mengxi Jiang; Johanna R Abend; Silas F Johnson; Michael J Imperiale
Journal:  Virology       Date:  2008-11-07       Impact factor: 3.616

10.  HLA-A01-, -A03-, and -A024-binding nanomeric epitopes in polyomavirus BK large T antigen.

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Journal:  Hum Immunol       Date:  2009-05-14       Impact factor: 2.850

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