Detection of Polyomavirus BK Reactivation After Renal Transplantation Using an Intensive Decoy Cell Surveillance Program Is Cost-Effective

Detection of Polyomavirus BK Reactivation After Renal Transplantation Using an Intensive Decoy Cell Surveillance Program Is Cost-Effective: Background. Reactivation of polyomavirus BK (BKV) after renal transplantation can lead to allograft dysfunction or loss with early detection improving outcomes. Current guidelines recommend quantitative polymerase chain reaction for surveillance; however, urinary decoy cell detection is a potentially cost-effective alternative. We present the outcomes from an early intensive BKV surveillance program using decoy cell detection for initial screening starting 2 weeks after transplantation.
Methods. Records for all recipients of kidney (n=211) or simultaneous kidney and pancreas (n=102) transplants performed over 2 years in a single center were reviewed. Follow-up was for a minimum of 1 year. Urine cytology screening was performed fortnightly from 0 to 3 months after transplantation, monthly from 3 to 6 months then every 2 months from 6 to 12 months.

Results of Repeat Renal Transplantation After Graft Loss From BK Virus Nephropathy

Results of Repeat Renal Transplantation After Graft Loss From BK Virus Nephropathy: Background. BK virus nephropathy (BKVN) is an important cause of renal graft loss in recent years. The aims of this study are to (1) describe the management of patients undergoing retransplantation after allograft loss in the setting of BKVN and (2) to identify risk factors for BK virus replication in the retransplant.

Mammalian target of rapamycin signal inhibitors could play a role in the treatment of BK polyomavirus nephritis in renal allograft recipients

Mammalian target of rapamycin signal inhibitors could play a role in the treatment of BK polyomavirus nephritis in renal allograft recipients: "

A.I. Sánchez Fructuoso, N. Calvo, I. Perez-Flores, R. Valero, B. Rodríguez-Sánchez, D. García de Viedma, P. Muñoz, A. Barrientos. Mammalian target of rapamycin signal inhibitors could play a role in the treatment of BK polyomavirus nephritis in renal allograft recipients. Transpl Infect Dis 2011. All rights reserved

Abstract: BK virus (BKV) nephropathy is a common viral infection in renal transplant patients, with a prevalence of 1–9% at approximately 12 months after surgery. While it is widely agreed that reduction of immunosuppression should be the first intervention after diagnosis of BKV infection, there is no consensus on whether calcineurin inhibitors or antiproliferative drugs should be reduced first. Furthermore, target levels of immunosuppressive drugs are poorly defined, as are criteria for replacing one immunosuppressive agent with another.

Prospective monitoring of BK virus reactivation in renal transplant recipients in North India

Prospective monitoring of BK virus reactivation in renal transplant recipients in North India: "

R. Thakur, S. Arora, R. Nada, M. Minz, K. Joshi. Prospective monitoring of BK virus reactivation in renal transplant recipients in North India. Transpl Infect Dis 2011. : xx: 000–000. All rights reserved

Abstract: Background. BK nephropathy (BKN) is an important complication of renal transplantation with a reported incidence between 1% and 10% in different parts of the world. Early diagnosis is important to plan early therapeutic strategies. The epidemiology and evolution of BKN is relatively unknown in India and hence, the present study has been designed to prospectively monitor the activation of BK virus (BKV) in renal transplant recipients in India.

Patients and methods. In this study, 32 renal allograft recipients were prospectively monitored with protocol biopsies of allografts, BKV DNA load in plasma, and viral particles in urine by electron microscopy (EM) on day 1, and at 1, 3, and 6 months. Additionally, the baseline BKV DNA load in plasma was quantitated in 21 corresponding donors.

Results. On follow-up in 32 recipients, 9.7%, 23.8%, 19.2%, and 13.3% of patients showed viral profiles by EM at day 1, 1 month, 3 months, and 6 months, respectively. BKV DNA positivity in plasma was 25.8%, 42.9%, 15.4%, and 20% at day 1, 1 month, 3 months, and 6 months, respectively, with mean BKV copy number/mL plasma of 1796, 1029, 2611, and 3318, respectively. A total of 15.7% (17/108) urine samples of 32 renal recipients were positive by urine EM. Out of 100 protocol biopsies, none developed histologically demonstrable cytopathic effects of BKN, although 8% biopsies were SV-40 large T antigen (SV-40 T Ag) positive. By quantitative real-time polymerase chain reaction assay, 27/108 (25%) of recipients' plasma samples were positive for BKV. Peak viremia and viruria occurred at 1–3 months post transplantation. The baseline viremia in donors was predictive of viremia positivity in the post-transplantation period at 1 month. Twenty-four episodes of graft dysfunction were attributed mainly to rejection.

Conclusion. The study shows a total of 15.7% and 25% urine and plasma samples were positive for BKV at any time during a 6-month follow-up. The highest incidence of BK viruria and viremia occurred at 1 month. In protocol biopsies, focal positivity of SV-40 T Ag was seen in 8% biopsies.

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