Quantitative viral load monitoring and cidofovir therapy for the management of BK virus-associated nephropathy in children and adults1

Vats, Abhay; Shapiro, Ron; Randhawa, Parmjeet; Scantlebury, Velma P.; Tüzüner, Acar; Saxena, Malika; Moritz, Michael L.; Beattie, Tom F.; Gonwa, Thomas A.; Green, Michael D.; Ellis, Demetrius

doi:10.1097/00007890-200301150-00020

Cited by 236 publications

(203 citation statements)

References 23 publications

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“…There is no uniform agreement in the approach toward the diagnosis and management of BKVN (13)(14)(15). Diagnostic tests such as urinary decoy cells and BK Viremia have low positive predictive values.…”

Section: Discussionmentioning

confidence: 99%

BK Virus‐Specific Antibodies and BKV DNA in Renal Transplant Recipients with BKV Nephritis

Hariharan

Cohen

Vasudev

et al. 2005

American Journal of Transplantation

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We evaluated twenty renal transplant subjects at various stages of BKV nephritis (BKVN) for BKV-specific IgG and IgM antibodies using ELISA technique and BKV-DNA using PCR. They were divided as early onset (n = 7), stabilizing (n = 3), resolved (n = 8) and late onset (n = 2) BKVN. BKV-specific antibodies and BKV-DNA were simultaneously determined. The mean BKV-specific IgG level in early onset and stabilizing BKVN were 64 and 39 EIA units, and were significantly lower than 138 EIA units seen in resolved BKVN, P = 0.007, P = 0.008. The mean BKV-specific IgM levels in stabilizing BKVN was higher than resolved BKVN (130 vs 51 EIA units), P = 0.006. Mean plasma BKV loads for each group were 955 925, 5642 and 42 copies/mL of plasma, respectively. Prospective study in six BKVN cases revealed mean IgG, IgM levels and BKV-DNA at the time of diagnosis of BKVN as 39, 110 EIA units and 586 758 copies/mL of plasma, respectively. After a mean period of 5.2 months, IgG level increased to 120 EIA units (p = 0.0058) and had no detectable viral copies in circulation.Recovery from BKVN and elimination of BKV is associated with the development of BKV-specific IgG antibodies and this provides insight into the role of humoral immunity to BKV in the pathogenesis of BKVN.

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Section: Discussionmentioning

confidence: 99%

BK Virus‐Specific Antibodies and BKV DNA in Renal Transplant Recipients with BKV Nephritis

Hariharan

Cohen

Vasudev

et al. 2005

American Journal of Transplantation

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“…Low-dose cidofovir has been used to treat BK nephropathy (143)(144)(145)(146). Renal toxicity may result, especially with calcineurin inhibitors, although it is unclear how much BK infection also contributes to the renal dysfunction.…”

Section: Bk Polyomavirusmentioning

confidence: 99%

Viral Infection in the Renal Transplant Recipient

Kotton

Fishman²

2005

Journal of the American Society of Nephrology

197

181

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Viruses are among the most common causes of opportunistic infection after transplantation and the most important. The risk for viral infection is a function of the specific virus encountered, the intensity of immune suppression used to prevent graft rejection, and other host factors governing susceptibility. Viral infection, both symptomatic and asymptomatic, causes the "direct effects" of invasive disease and "indirect effects," including immune suppression predisposing to other opportunistic infections and oncogenesis. Rapid and sensitive microbiologic assays for many of the common viruses after transplantation have replaced, for the most part, serologic testing and in vitro cultures for the diagnosis of infection. Furthermore, quantitative molecular tests allow the individualization of antiviral therapies for prevention and treatment of infection. This advance is most prominent in the management of cytomegalovirus, Epstein-Barr, hepatitis B, and hepatitis C viruses. Diagnostic advances have not been accompanied by the development of specific and nontoxic anti-viral agents or effective antiviral vaccines. Vaccines, where available, should be given to patients as early as possible and well in advance of transplantation to optimize the immune response. Studies of viral latency, reactivation, and the cellular effects of viral infection will provide clues for future strategies in prevention and treatment of viral infections.

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“…10,11 Viruria was observed in 17.6% of graft recipients in our study with low positive predictive value Acute cellular rejection Grade 1A with chronic allograft nephropathy (1) Acute rejection (4) Borderline rejection (2) Isometric vacuolisation (2) Within normal histological limits (9) 3 Graft dysfunction with viruria + viraemia 3 Acute rejection grade IIA (1) without immunohistochemical evidence of BKVAN Acute rejection grade IB (1) Acute rejection grade IB with interstitial nephritis (1) 4 Graft dysfunction with viruria + viraemia with 5 Detailed histopathological features as per Table 1 immunohistochemical evidence of BKVAN BKVAN: BK polyoma viral nephropathy. for the diagnosis of BKVAN.…”

Section: Viruria Viraemia and Bk Viral Infectionmentioning

confidence: 99%

BK polyoma viral infection in renal allograft recipients

Badwal

Chopra

Varma³

et al. 2011

Medical Journal Armed Forces India

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Quantitative viral load monitoring and cidofovir therapy for the management of BK virus-associated nephropathy in children and adults1

Abstract: Quantitative PCR for BKV is a sensitive and reliable method for following the course of the infection in renal transplant patients. In addition, cidofovir therapy may be useful in the treatment of some of these patients, and its role needs to be investigated further.

Cited by 236 publications

References 23 publications

BK Virus‐Specific Antibodies and BKV DNA in Renal Transplant Recipients with BKV Nephritis

BK Virus‐Specific Antibodies and BKV DNA in Renal Transplant Recipients with BKV Nephritis

Viral Infection in the Renal Transplant Recipient

BK polyoma viral infection in renal allograft recipients

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