Polyomavirus BK Nephropathy: The Effect of an Early Diagnosis on Renal Function or Graft Loss

Burgos, D.; López, Verónica; Cabello, Mercedes; Sola, E.; Gutiérrez, Cristina; García, Iván García; Siles, J.A.; Flórez, Pablo; Molina, M. González

doi:10.1016/j.transproceed.2006.08.027

Cited by 16 publications

(14 citation statements)

References 11 publications

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Section: Immunosuppressive Reductionmentioning

confidence: 88%

“…However, results evidenced a scarce, if any, significant effect in clearing viruria or viremia [75][76][77][78] . Other studies reported clearance of viremia in 50% to 100% of the cases [75,[79][80][81][82] . The effect of cidofovir on renal function was variable, with some studies evidencing stabilization of creatinine [79][80][81] and others Table 4 Recommended treatment of polyomavirus-associated nephropathy by reduction or switching of immunosuppression [49] …”

Section: Immunosuppressive Reductionmentioning

confidence: 88%

“…Tacrolimus → Cyclosporine A (trough levels 100-150 ng/mL) Tacrolimus (trough levels < 6 ng/mL) Mycophenolate mofetil → Azathioprine (dose ≤ 100 mg/d) Cyclosporine A (trough levels 100-150 ng/mL) Tacrolimus → sirolimus (trough levels < 6 ng/mL) Mycophenolate mofetil dose ≤ 1 g/d Mycophenolate mofetil → sirolimus (trough levels < 6 ng/mL) Cyclosporine A (trough levels 100-150 ng/mL) Mycophenolate mofetil → leflunomide showed no effect on renal function [75,77] . The pronounced nephrotoxicity limits the use of cidofovir particularly in renal transplantation and an adequate hydratation is required.…”

Section: Switching Decreasingmentioning

confidence: 99%

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Polyomavirus-associated nephropathy

Costa¹

2012

WJT

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Polyomaviruses BK and JC are ubiquitous viruses with high seroprevalence rates in general population. Following primary infection, polyomaviruses BK and JC persist latently in different sites, particularly in the reno-urinary tract. Reactivation from latency may occur in normal subjects with asymptomatic viruria, while it can be associated to nephropathy (PVAN) in kidney transplantat recipients. PVAN may occur in 1%-10% of renal transplant patients with loss of the transplanted organ in 30% up to 80% of the cases. Etiology of PVAN is mainly attributable to BK virus, although approximately 5% of the cases may be due to JC. Pathogenesis of PVAN is still unknown, although viral replication and the lack of immune control play a major role. Immunosuppression represents the condicio sine qua non for the development of PVAN and the modulation of anti-rejection treatment represents the first line of intervention, given the lack of specific antiviral agents. At moment, an appropriate immunemodulation can only be accomplished by early identification of viral reactivacation by evaluation of polyomavirus load on serum and/or urine specimens, particularly in the first year post-trasplantation. Viro-immunological monitoring of specific cellular immune response could be useful to identify patients unable to recover cellular immunity posttransplantation, that are at higher risk of viral reactivation with development of PVAN. Herein, the main features of polyomaviruses BK and JC, biological properties, clinical characteristics, etiopathogenesis, monitoring and diagnosing of PVAN will be described and discussed, with an extended citation of related relevant literature data.

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Section: Immunosuppressive Reductionmentioning

confidence: 88%

Section: Immunosuppressive Reductionmentioning

confidence: 88%

Section: Switching Decreasingmentioning

confidence: 99%

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Polyomavirus-associated nephropathy

Costa¹

2012

WJT

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“…More than half of biopsies may show tubulitis (5,43,47,80), and reduction in immunosuppression can precipitate rejection in 10 to 30% of recipients (51, 53,57,86,108,124). The infiltrating mononuclear cells may represent a BKV-specific and/or allospecific response, and treatment is debatable (133,134).…”

Section: Bkv Nephropathy and Acute Rejectionmentioning

confidence: 99%

BK Virus Nephropathy and Kidney Transplantation

Bohl

Brennan

2007

Clinical Journal of the American Society of Nephrology

222

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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“…Therefore, effective screening in renal transplant recipients could reduce allograft losses. 7 It has been shown that viremia precedes PVAN by a median of 12 weeks 8 and that levels of viremia correlate with emergence of BKV associated disease. 9 These data suggest that BKV blood viral load measurement could be used as a screening tool for PVAN.…”

Section: Introductionmentioning

confidence: 99%