Donor and Recipient BKV-Specific IgG Antibody and Posttransplantation BKV Infection

Sood, Puneet; Senanayake, Shamila; Sujeet, Kumar; Medipalli, Radhika; Van-Why, Scott K.; Cronin, David; Johnson, Christopher P.; Hariharan, Sundaram

doi:10.1097/tp.0b013e318282ba83

Cited by 47 publications

(52 citation statements)

References 21 publications

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“…showed that the cumulative proportion of subjects BKV viremia free in the first year posttransplant was significantly decreased if the pre-implantation graft biopsy, preservation and washing solutions contained BKV DNA (12). High BKV-specific antibody titers in donors (possibly representing recent BKV exposure / higher graft load) and detection of BKV infection within 5 days of transplantation are risk factors for BKV nephropathy in kidney recipients (13). Therefore, the association of donor BKV replication and posttransplant recipient BKV viremia is likely due to tropism of BKV for the kidney and the high BKV antibody prevalence in healthy adult (14, 15) kidney donors.…”

Section: Discussionmentioning

confidence: 99%

The Impact of Donor Viral Replication at Transplant on Recipient Infections Posttransplant

et al. 2015

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Background Organ donors are often implicated as the source of posttransplant recipient infection. We prospectively studied kidney and liver donor-recipient pairs to determine if donor viral replication of cytomegalovirus (CMV), Epstein-Barr virus (EBV), and BK polyomavirus (BKV) at transplant was a risk factor for posttransplant recipient infection and disease. Methods Donors and recipients were studied for antibodies against CMV and EBV and for quantitative viral replication of CMV, EBV and BKV in oral washes, urine, and whole blood pretransplant. Recipient testing continued every 3 months posttransplant. Demographic and clinical data on infections and graft and subject outcomes were obtained. Results The 98 donor-recipient pairs included 15 liver and 83 kidney transplants (18 of whom were children). No donor had detectable CMV replication; therefore its impact on recipient CMV replication could not be analyzed. Donor EBV replication occurred in 22%, mostly in the oral wash and had no impact on posttransplant recipient EBV replication (p 0.9) or EBV viremia (p 0.6) in kidney or liver recipients. Donor BKV replication occurred in 17%, mostly in the urine and although not associated with posttransplant recipient urinary BKV replication in recipients, it was associated with BKV viremia (p 0.02), and a significantly shorter time to BKV viremia (p 0.01) in kidney recipients. Conclusion Donor replication of CMV or EBV did not impact posttransplant recipient viral replication in kidney/liver transplants. Donor urinary BKV replication is associated with recipient BKV viremia in kidney transplants.

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Section: Discussionmentioning

confidence: 99%

The Impact of Donor Viral Replication at Transplant on Recipient Infections Posttransplant

et al. 2015

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“…Additionally, in this study no predictive value of BKPyV serology of the recipient’s pre-transplant was found. Yet others have shown that high BKPyV-IgG titers in the donor and low BKPyV-IgG titers in the recipient, have a negative effect on the BKPyV infection post transplantation [29–31]. …”

Section: Discussionmentioning

confidence: 99%

A delicate balance between rejection and BK polyomavirus associated nephropathy; A retrospective cohort study in renal transplant recipients

et al. 2017

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BackgroundThe immunosuppressive agents mycophenolate acid (MPA) and tacrolimus (Tac) are associated with a higher incidence of BK polyomavirus nephropathy (BKPyVAN).In this observational retrospective cohort study, the frequency of BK polyomavirus (BKPyV) complications over a 24-month period was studied.Methods358 renal transplant recipients (RTR) treated with MPA, with either cyclosporine A (CsA) (CsAM group) or Tac (TacM group) and mostly prednisolone, were included.ResultsIncidence of BKPyV-viremia was not significantly different between the CsAM (n = 42/191) (22.0%) and the TacM (n = 36/167) (21.6%) group. Biopsy proven BKPyVAN occurred more often in the TacM group (6.6%) versus the CsAM group (2.1%) (p = 0.03). Longitudinal data analysis showed a significant earlier decline of viral load in plasma in the CsAM group compared to the TacM group (p = 0.005).The incidence of biopsy proven acute rejection (BPAR) was significantly higher in the CsAM (19.9%) compared to the TacM (10.8%) (p = 0.02) group. Graft loss, estimated glomerular filtration rate and mortality rate did not differ in both treatment groups.ConclusionIn conclusion, this study shows that immunosuppressive treatment with Tac and MPA compared to CsA and MPA is associated with a lower incidence of BPAR, but at the cost of an increased risk of developing BKPyVAN in the first two years post-transplant.

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“…However, another group found a higher risk for BK viremia in seronegative recipients who received a kidney from a seropositive donor. 94 These discrepancies may be accounted by variability in the assays used to detect BK-specific antibodies and quantitative differences in anti-BK antibody titers. It was previously shown that viremic patients had a lower antibody level pretransplant than those who never developed BK viremia.…”

Section: Qualitative and Quantitative Serostatusmentioning

confidence: 99%

BK Polyomavirus and the Transplanted Kidney

et al. 2016

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BK polyomavirus is ubiquitous, with a seropositivity rate of over 75% in the adult population. Primary infection is thought to occur in the respiratory tract, but asymptomatic BK virus latency is established in the urothelium. In immunocompromised host, the virus can reactivate but rarely compromises kidney function except in renal grafts, where it causes a tubulointerstitial inflammatory response similar to acute rejection. Restoring host immunity against the virus is the cornerstone of treatment. This review covers the virus-intrinsic features, the posttransplant microenvironment as well as the host immune factors that underlie the pathophysiology of polyomavirus-associated nephropathy. Current and promising therapeutic approaches to treat or prevent this complication are discussed in relation to the complex immunopathology of this condition.

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Donor and Recipient BKV-Specific IgG Antibody and Posttransplantation BKV Infection

Abstract: BKV serostatus can be used to risk stratify patients for posttransplantation infection.

Cited by 47 publications

References 21 publications

The Impact of Donor Viral Replication at Transplant on Recipient Infections Posttransplant

The Impact of Donor Viral Replication at Transplant on Recipient Infections Posttransplant

A delicate balance between rejection and BK polyomavirus associated nephropathy; A retrospective cohort study in renal transplant recipients

BK Polyomavirus and the Transplanted Kidney

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