Renal Failure Five Years After Lung Transplantation Due to Polyomavirus BK‐Associated Nephropathy

Egli, Adrian; Helmersen, Douglas; Taub, Ken; Hirsch, Hans H.; Johnson, Alice

doi:10.1111/j.1600-6143.2010.03265.x

Cited by 41 publications

(33 citation statements)

References 39 publications

(18 reference statements)

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“…Clinical impact is relevant, as loss of the renal graft ranges from 30% up to > 80% of cases [12][13][14] ; in transplant centres where screening for polyomavirus replication in the urine and plasma is performed, the rate of graft loss is lower [15] . Several studies evidenced that BK viremia is only rarely observed in non-kidney solid organ transplant recipients and biopsy-confirmed cases of nephropathy have been described in few case reports [16][17][18][19][20][21][22] , despite the similar or even higher level of immunosuppression, thus supporting the role of organ determinants in the pathogenesis of PVAN.…”

Section: Human Polyomaviruses and Nephropahtymentioning

confidence: 99%

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: Human Polyomaviruses and Nephropahtymentioning

confidence: 99%

Polyomavirus-associated nephropathy

Costa¹

2012

WJT

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“…For example, in lung-transplant recipients, it is reported that 9% will have ESRF and 53% double their serum creatinine by 5 years posttransplant (130,184). Although this is most commonly an effect of calcineurin antagonist, other transplant-specific factor such as infection with polyomavirus BK may be important (73).…”

Section: Other Factorsmentioning

confidence: 98%

Exercise Limitation Following Transplantation

Williams

McKenna

2012

Comprehensive Physiology

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Organ transplantation is one of the medical miracles or the 20th century. It has the capacity to substantially improve exercise performance and quality of life in patients who are severely limited with chronic organ failure. We focus on the most commonly performed solid‐organ transplants and describe peak exercise performance following recovery from transplantation. Across all of the common transplants, evaluated significant reduction in o 2 peak is seen (typically renal and liver 65%‐80% with heart and/or lung 50%‐60% of predicted). Those with the lowest o 2 peak pretransplant have the lowest o 2 peak posttransplant. Overall very few patients have a o 2 peak in the normal range. Investigation of the cause of the reduction of o 2 peak has identified many factors pre‐ and posttransplant that may contribute. These include organ‐specific factors in the otherwise well‐functioning allograft (e.g., chronotropic incompetence in heart transplantation) as well as allograft dysfunction itself (e.g., chronic lung allograft dysfunction). However, looking across all transplants, a pattern emerges. A low muscle mass with qualitative change in large exercising skeletal muscle groups is seen pretransplant. Many factor posttransplant aggravate these changes or prevent them recovering, especially calcineurin antagonist drugs which are key immunosuppressing agents. This results in the reduction of o 2 peak despite restoration of near normal function of the initially failing organ system. As such organ transplantation has provided an experiment of nature that has focused our attention on an important confounder of chronic organ failure‐skeletal muscle dysfunction. © 2012 American Physiological Society. Compr Physiol 2:1937‐1979, 2012.

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“…The impact of BKV on kidney function and long-term outcomes in nonrenal SOT recipients is not well established (113,114). Although case reports of potential BKV-associated nephropathy in native kidneys, mainly of heart and lung transplant recipients, have been published (115)(116)(117), the majority of studies prospectively assessing the role of BKV in nonrenal SOT recipients have found low rates of BKV viremia and no association between BK viruria and renal dysfunction (113,114,(118)(119)(120)(121).…”

Section: Type Of Organ Transplantmentioning

confidence: 99%

The Impact of Infection on Chronic Allograft Dysfunction and Allograft Survival After Solid Organ Transplantation

Martín-Gandul

Mueller

Pascual

et al. 2015

American Journal of Transplantation

131

103

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Infectious diseases after solid organ transplantation (SOT) are a significant cause of morbidity and reduced allograft and patient survival; however, the influence of infection on the development of chronic allograft dysfunction has not been completely delineated. Some viral infections appear to affect allograft function by both inducing direct tissue damage and immunologically related injury, including acute rejection. In particular, this has been observed for cytomegalovirus (CMV) infection in all SOT recipients and for BK virus infection in kidney transplant recipients, for community-acquired respiratory viruses in lung transplant recipients, and for hepatitis C virus in liver transplant recipients. The impact of bacterial and fungal infections is less clear, but bacterial urinary tract infections and respiratory tract colonization by Pseudomonas aeruginosa and Aspergillus spp appear to be correlated with higher rates of chronic allograft dysfunction in kidney and lung transplant recipients, respectively. Evidence supports the beneficial effects of the use of antiviral prophylaxis for CMV in improving allograft function and survival in SOT recipients. Nevertheless, there is still a need for prospective interventional trials assessing the potential effects of preventive and therapeutic strategies against bacterial and fungal infection for reducing or delaying the development of chronic allograft dysfunction.

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Renal Failure Five Years After Lung Transplantation Due to Polyomavirus BK‐Associated Nephropathy

Cited by 41 publications

References 39 publications

Polyomavirus-associated nephropathy

Polyomavirus-associated nephropathy

Exercise Limitation Following Transplantation

The Impact of Infection on Chronic Allograft Dysfunction and Allograft Survival After Solid Organ Transplantation

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