Prospective study of the human polyomaviruses BK and JC and cytomegalovirus in renal transplant recipients.

Gardner, S. D.; Mackenzie, E. F. D.; Smith, Corey; Porter, Allison

doi:10.1136/jcp.37.5.578

Cited by 239 publications

(147 citation statements)

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“…At the site of entry, which is normally the respiratory tract, these viruses replicate and traffic to the tissues of the kidneys (Heritage et al 1981, McCance 1983) and the central nervous system, where they sustain a long-term infection (Elsner & Dörries 1992, Quinlivan et al 1992. A recurrence of the infection may be induced by significant immunosuppression, as in the case of kidney (Hogan et al 1980, Kahan et al 1980, Gardner et al 1984) and bone marrow transplants (O'Reilly et al 1981, Arthur et al 1988) and other factors such as immunodeficiency diseases, diabetes, other chronic diseases, immunosuppressive chemotherapy, pregnancy ) and old age (Tajima et al 1990). …”

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confidence: 99%

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JC polyomavirus infection in candidates for kidney transplantation living in the Brazilian Amazon Region

Melo¹,

Bezerra

Ishak

et al. 2013

Mem. Inst. Oswaldo Cruz

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confidence: 99%

“…In these patients, the virus can cause haemorrhagic cystitis, nephritis, urethral stenosis and a loss of function of the transplanted kidney (Coleman et al 1978, Gardner et al 1984, Chan et al 1994, Weiskittel 2002.…”

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confidence: 99%

JC polyomavirus infection in candidates for kidney transplantation living in the Brazilian Amazon Region

Melo¹,

Bezerra

Ishak

et al. 2013

Mem. Inst. Oswaldo Cruz

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“…The association between renal transplantation and shedding of polyomavirus in the urine was established firmly by subsequent studies (10,(12)(13)(14). The reported incidence of viruria in patients who received azathioprine and prednisone ranged from 14 to 68%, depending on the method used to demonstrate the infection (10,(12)(13)(14)(15)(16).…”

Section: Bk Virus and Renal Transplantation: Historical Perspectivementioning

confidence: 99%

Histologic versus Molecular Diagnosis of BK Polyomavirus–Associated Nephropathy

Drachenberg

Papadimitriou²,

Ramos³

2006

Clinical Journal of the American Society of Nephrology

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Although discovered in 1970 the BK virus infections had no significant clinical impact until the emergence of BK virusassociated allograft nephropathy (BKPVAN). Escalating clinical challenges required better diagnostic tools and delineation of uniform criteria for diagnosis. In recent years, the widespread use of real-time PCR for measuring viral loads has confirmed that BK viruria and viremia are consistently identified before the development of overt nephritis. The identification of this viruria-viremia-nephritis sequence has provided tools for screening renal transplant patients and the possibility of earlier intervention with improved outcomes. Analysis of current clinical trends indicates that despite the fact that a positive renal biopsy is the "gold standard" for the diagnosis of BKPVAN, clinical interventions often are based on the surrogate markers of the disease rather than on tissue diagnosis. This is conceptually supported by the fact that early BKPVAN is focal and liable to tissue sampling errors. Strong arguments remain, however, in favor of retaining the requirement for tissue evaluation in patients who are suspected of having BKPVAN. BKPVAN selectively affects the graft and is likely to occur in a background of immune and/or nonimmune renal injury. A renal biopsy is necessary to exclude other pathologic processes (e.g., acute rejection) that could coexist with BKPVAN or be the main cause of allograft dysfunction. Evaluation of a renal biopsy for the purpose of staging is important for prognosis and is also of paramount importance for the rational assessment of therapeutic success.

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“…It was first isolated in 1970 from a kidney transplant recipient with a ureteric stricture [1]. Studies show that up to 90% of the general adult human populations become exposed to BK virus at some point, usually early in life [1][2][3]. While this is usually inconsequential in the immunocompetent patient, BK replication in immunocompromised patients can result in graft dysfunction and loss.…”

Section: Introductionmentioning

confidence: 99%

“…However specific pathological hallmarks ascribed to tissue invasive disease not only improved the detection and description of BK nephropathy, but led to alteration in post-transplant immunotherapy to minimize the damage [4]. Today, BK virus nephropathy is an important and emerging cause of renal transplant dysfunction and loss [2,3,5].…”

Section: Introductionmentioning

confidence: 99%

Long-Term Results of a Screening and Immunosuppression Protocol for Polyoma BK Viremia after Renal Transplantation

Schuster¹,

Eldor²,

Leutters³

et al. 2017

Glob Surg

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There is currently no treatment consensus with regards to BK Nephropathy (BKN). Thus, balancing minimization of immunosuppression with the attendant risk of acute rejection remains paramount for long-term allograft survival.Between Jan. 1, 2006 and Dec. 31, 2012, 371 adult renal transplants were performed at our center. Immunosuppression consisted of Thymoglobulin induction followed by maintenance therapy with Tacrolimus, Mycophenolate Mofetil (MMF) and either Sirolimus (88%) or prednisone (12%). Serum PCR screening for BK virus was obtained monthly. BK viremia was detected in 66 (18%) recipients (Group A) while the remaining 305 recipients were never detected to have viremia (Group B). Minimizing immunosuppression for Group A recipients occurred in a stepwise fashion and consisted of an immediate 50% reduction in MMF dosing following by complete discontinuation if viremia did not clear within 3 months. No MMF dosing adjustments were made in Group B patients. All recipients were followed longterm for patient survival and graft function and survival.Group A patient survival at 1, 3, and 5 years was 100%, 98.5%, and 97% compared to 99.3%, 98.4%, and 95.4% in Group B. Graft survival at the same time intervals in Group A was 100%, 98.5%, and 93.9% versus 99%, 97.7%, and 92.5% in Group B recipients. Mean serum creatinine, mg/dl, levels at 1, 3, and 5 years in Group A were 1.6, 1.7 and 1.6 compared to 1.5, 1.5, and 1.6 in Group B. Subsequent to MMF dose reduction/elimination, only on Group A patient progressed to BKN (1.5%) and only 2 patients suffered from an episode of acute rejection (3%).This pre-emptive reduction in immunotherapy at the detection of BK viremia was associated with a low rate of progression to BKN and the development of acute rejection. In addition to comparable long-term function.

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Prospective study of the human polyomaviruses BK and JC and cytomegalovirus in renal transplant recipients.

Cited by 239 publications

References 10 publications

JC polyomavirus infection in candidates for kidney transplantation living in the Brazilian Amazon Region

JC polyomavirus infection in candidates for kidney transplantation living in the Brazilian Amazon Region

Histologic versus Molecular Diagnosis of BK Polyomavirus–Associated Nephropathy

Long-Term Results of a Screening and Immunosuppression Protocol for Polyoma BK Viremia after Renal Transplantation

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