BK Virus-Associated Nephropathy in Renal Allograft Recipients: Rescue Therapy by Sirolimus-Based Immunosuppression

Wali, Ravinder K.; Drachenberg, Cinthia; Hirsch, Hans H.; Papadimitriou, John C.; Nahar, Anita; Mohanlal, Viresh; Brisco, Meredith A.; Bartlett, Stephen T.; Weir, Matthew R.; Ramos, Emilio

doi:10.1097/01.tp.0000142127.84497.50

Cited by 70 publications

(45 citation statements)

References 23 publications

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“…Although IVIG may contain high levels of anti-BKV antibodies (29), our analysis of recipients receiving IVIG following diagnosis of PVAN also does not indicate a robust effect on functional stability or on viral elimination from the graft. Whether conversion from calcineurin inhibitor to mTOR inhibitorbased immunosuppression has specific functional benefit in PVAN (40) has not been tested here but may merit consideration for cases with progressive decline in GFR.…”

Section: Discussionmentioning

confidence: 99%

Kidney Transplant Function and Histological Clearance of Virus Following Diagnosis of Polyomavirus-Associated Nephropathy (PVAN)

Wadei

Rule

Lewin³

et al. 2006

American Journal of Transplantation

137

136

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Section: Discussionmentioning

confidence: 99%

Kidney Transplant Function and Histological Clearance of Virus Following Diagnosis of Polyomavirus-Associated Nephropathy (PVAN)

Wadei

Rule

Lewin³

et al. 2006

American Journal of Transplantation

137

136

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“…Different centers have reported different approaches, and there have been variable results with both immunoreduction and class switching. 2,20 Our quantification of BK viremia in renal transplant patients with stable graft function may therefore provide useful baseline data, with which comparative clinical trials can use to delineate whether decrement or class switching of immunosuppression is superior.…”

Section: Discussionmentioning

confidence: 99%

Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

Chan¹,

Leung²,

Wong³

et al. 2012

Renal Failure

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Introduction: Polyoma BK virus (BKV) has recently been identified to cause renal allograft dysfunction, which manifests as polyomavirus-associated nephropathy (PVAN). However, the presence and level of BKV DNA in renal allograft patients with good and stable renal function have remained undetermined. Methods: In this prospective study, serum samples were collected from a total of 45 renal allograft recipients with serum creatinine <155 μmol/L. In 17 patients, whose duration of transplantation was under 2 years, samples were collected at 3-4-month intervals for up to 2 years after transplantation. BK viral load was quantified using quantitative polymerase chain reaction (Q-PCR). Results: The BK viral load in asymptomatic renal allograft recipients was independent of the duration of transplantation and did not correlate with allograft function. The mean (AE SD) level of viremia was 552.80 AE 1931.00 genome copies/mL, with 92.9% of patients having low levels of viremia corresponding to <1 Â 10 3 copies/mL. In contrast, patients with proven PVAN had levels in the range of 10 6 copies/mL. Conclusions: The prevailing BK viral load in asymptomatic renal allograft patients is quantifiably low. Our findings may guide optimal immunosuppressive modulation in PVAN cases, where judicious manipulation of immunosuppression is required without inciting allograft rejection.

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“…Because histologic clearance of the virus (79) and disappearance of decoy cells (87) precede clearance from the blood, monitoring should be performed with quantitative assays, preferably BKV PCR, until the viral level is undetectable or at least falls below the threshold value that is associated with BKV nephropathy. On the basis of kinetic models (123) and prospective monitoring (57,79,87,123), viremia clears in 7 to 20 wk, but the initial decrease may be delayed by 4 to 10 wk after immunosuppression reduction. If viremia persists, then further reduction of current maintenance therapy, conversion to sirolimus, or addition of leflunomide can be considered.…”

Section: Postinfection Monitoringmentioning

confidence: 99%

BK Virus Nephropathy and Kidney Transplantation

Bohl

Brennan

2007

Clinical Journal of the American Society of Nephrology

220

175

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Nephropathy from BK virus (BKV) infection is an evolving challenge in kidney transplant recipients. It is the consequence of modern potent immunosuppression aimed at reducing acute rejection and improving allograft survival. Untreated BKV infections lead to kidney allograft dysfunction or loss. Decreased immunosuppression is the principle treatment but predisposes to acute and chronic rejection. Screening protocols for early detection and prevention of symptomatic BKV nephropathy have improved outcomes. Although no approved antiviral drug is available, leflunomide, cidofovir, quinolones, and intravenous Ig have been used. Retransplantation after BKV nephropathy has been successful.Clin J Am Soc Nephrol 2: S36 -S46, 2007. doi: 10.2215/CJN.00920207 P olyomavirus infection in kidney transplant recipients is of increasing interest and research. Although the two human polyomaviruses, BK virus (BKV) and JC virus (JCV), were reported in 1971 (1,2), their influence and importance were limited. The emergence of polyomavirus nephropathy has coincided with the use of new potent immunosuppressive medications (3,4). It is usually associated with BKV, affects up to 8% of recipients, and frequently results in allograft loss or permanent dysfunction (5). It presents as an asymptomatic gradual rise in creatinine with a tubulointerstitial nephritis that mimics rejection, producing a treatment dilemma. The decrease in immunosuppression that is needed to treat infection is opposite to the increases that are needed to treat rejection.Two studies in kidney transplant recipients who were treated with prednisone and azathioprine in the early 1980s have provided the foundation for much of our current understanding of polyomaviruses in transplant recipients. Hogan et al. (6) and Gardner et al. (7) found that the pretransplantation seroprevalence was 80 to 88% for BKV and 54 to 55% for JCV. The posttransplantation rates of polyomavirus infection were 18 to 44% for BKV and 30 to 35% for JCV. Most polyomavirus infections were asymptomatic and occurred within the first 3 mo after transplantation. BKV infection was associated with a rising creatinine. More than 20 yr ago, Gardner et al. (7) warned, "The detection of polyomavirus infection is important as increased immunosuppression needs to be avoided to prevent possible complications."

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BK Virus-Associated Nephropathy in Renal Allograft Recipients: Rescue Therapy by Sirolimus-Based Immunosuppression

Abstract: Further studies are needed, but at present these preliminary results offer a new direction for therapeutic intervention in recipients of renal allografts with BKN.

Cited by 70 publications

References 23 publications

Kidney Transplant Function and Histological Clearance of Virus Following Diagnosis of Polyomavirus-Associated Nephropathy (PVAN)

Kidney Transplant Function and Histological Clearance of Virus Following Diagnosis of Polyomavirus-Associated Nephropathy (PVAN)

Quantification of BK Viral Load in Asymptomatic Renal Allograft Recipients

BK Virus Nephropathy and Kidney Transplantation

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