Polyomavirus Nephropathy in Pediatric Kidney Transplant Recipients

Smith, Jodi M.; McDonald, Ruth A.; Finn, Laura S.; Healey, Patrick J.; Davis, Connie L.; Limaye, Ajit P.

doi:10.1111/j.1600-6143.2004.00629.x

Cited by 142 publications

(150 citation statements)

References 29 publications

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“…Recipient serostatus did not show a statistically significant difference in viremia, however. In contrast, Smith et al (27) found recipient seronegativity to be a significant risk for development of BKVN (P ϭ 0.01) in a pediatric population. Donor serostatus was not analyzed because of paucity of data from all donors.…”

Section: Pathogenesis Of Bkv Infectionmentioning

confidence: 89%

BK Virus Nephritis after Renal Transplantation

Dall

Hariharan²

2008

Clinical Journal of the American Society of Nephrology

124

108

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BK virus nephritis is an increasing problem and is posing a threat to improving renal transplant graft survival. The pathogenesis of this condition remains to be investigated. Higher prevalence of BK virus infection in recent years has been correlated with declining acute rejection rates and the use of potent immunosuppressive agents. Patients with this infection usually have asymptomatic viremia and/or nephritis with or without worsening of renal function. The diagnosis of this disease is based on detecting the virus or its effects in urine, blood, and renal tissue. In the past, approximately 30 to 60% of patients with BK virus nephritis developed graft failure. In recent years, the combination of early detection, prompt diagnosis, and therapies including preventive measures have resulted in better outcomes.Clin J Am Soc Nephrol 3: S68 -S75, 2008. doi: 10.2215/CJN.02770707 T he term "BK" originated from a patient's initials, in whom it was first detected in 1971 (1). The next observed case was published by investigators from the University of Pittsburgh in 1995 (2). Since then, there have been numerous reports on BK virus (BKV) infection and BKV nephritis (BKVN) in renal transplant recipients (3-8). The factors that lead to its higher incidence in recent years and its pathogenesis remain poorly understood. Increased awareness, the ability of clinicians to recognize this infection, and the availability of better diagnostic tools may be contributing to higher prevalence of this disease in recent years (9). The use of potent immunosuppressive combination therapy with mycophenolate mofetil (MMF) and tacrolimus has been thought to play a role in the occurrence of this infection (10 -12); however, this infection is also seen with cyclosporine and sirolimus therapy (13). Prevalence of BK viremia within 1 yr after transplantation is approximately 20% (6,14) and is higher than the prevalence of acute rejection of 13% reported for the year 2003 (15). This review discusses the pathogenesis, clinical features, therapy, and the short-and long-term renal graft survival with reference to BKV infection. Pathogenesis of BKV InfectionPotential factors that contribute to the pathogenesis of BKVN may be a combination of (1) ineffective immune surveillance by the host T lymphocytes, (2) the absence of previous humoral immunity to BKV, (3) molecular sequence variability of the virus, and (4) alloimmune activation. These details have been reviewed elsewhere (9) and are also discussed next.Cellular immunity in the development and clearance of BKV infection has remained an important area of research in the past several years. Comoli et al. (16) showed a reduction in BKVspecific IFN-␥-secreting lymphocytes in patients with BKVN compared with healthy control subjects. The authors noted an increase in patient IFN-␥-secreting lymphocyte levels with reduction in immunosuppressive therapy similar to that of their healthy counterparts (16). Prosser et al. (17) used an IFN-␥ enzyme-linked immunosorbent spot (ELISPOT) assay to measure cellula...

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Section: Pathogenesis Of Bkv Infectionmentioning

confidence: 89%

BK Virus Nephritis after Renal Transplantation

Dall

Hariharan²

2008

Clinical Journal of the American Society of Nephrology

124

108

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“…The importance of cellular immunity has been studied in healthy subjects (19) and recently in renal transplant subjects with BKVN (20). Recently investigators have explored the role of pre-transplant humoral antibody status in donor recipient pairs in children (21). However, they studied few cases with hemagglutination tests for detecting antibody as their methodology over ELISA technique and their study did not evaluate the concomitant utility of BKV-specific antibody with BKV DNA in subjects with BKVN.…”

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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“…Donor seropositivity has been implicated in development of BK viruria, viremia or BKVN in pediatric and adult transplant recipients (6)(7)(8)(9). The mode of viral transmission in the general population is incompletely understood, but multiple routes of infection are likely involved (1).…”

Section: Mode Of Transmissionmentioning

confidence: 99%

BK Virus Infection in Transplant Recipients: An Overview and Update

Randhawa

Brennan

2006

American Journal of Transplantation

189

152

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BK virus infection after kidney transplantation has been a subject of great interest in the past decade. This article traces the discovery of BK virus and the subsequent development of our knowledge about this emerging pathogen. The pathobiology of the virus is summarized with particular reference to epidemiology, interactions with host cell receptors, cell entry, cytoplasmic trafficking and targeting of the viral genome to the nucleus. This is followed by a discussion of clinical features, laboratory monitoring and therapeutic strategies. Finally, we present potential cellular mechanisms that explain the basis of virus-mediated damage to the human kidney.

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Polyomavirus Nephropathy in Pediatric Kidney Transplant Recipients

Cited by 142 publications

References 29 publications

BK Virus Nephritis after Renal Transplantation

BK Virus Nephritis after Renal Transplantation

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

BK Virus Infection in Transplant Recipients: An Overview and Update

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