Evaluating the impact of pre‐transplant desensitization utilizing a plasmapheresis and low‐dose intravenous immunoglobulin protocol on <scp>BK</scp> viremia in renal transplant recipients

Gabardi, Steven; Townsend, Keri; Martin, Spencer T.; Chandraker, Anil

doi:10.1111/tid.12087

Cited by 15 publications

(16 citation statements)

References 25 publications

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“…(ii) treatment protocols; (iii) treatment endpoints; (iv) antibody evaluation; (v) crossmatch procedures; (vi) assessment of graft function; (vii) donor type (living or deceased); (viii) DSA strength pretreatment and at transplant; (ix) length of follow-up; and (x) additional risk factors such as repeated mismatches. Tables 1 and 2 give AMR rates and graft survival data, respectively, for selected studies representing variations of the high dose IVIG and PP/low dose IVIG protocols (35,39,40,65,71,75,(81)(82)(83)(84)(85)(86). Because of the variability noted above, these data cannot be taken as a meaningful comparison of the different protocols but, rather, show that despite the increased risk of AMR, good graft and patient survival can be achieved.…”

Section: Desensitization For Hla Antibodymentioning

confidence: 99%

Desensitization for solid organ and hematopoietic stem cell transplantation

Zachary

Leffell

2014

Immunological Reviews

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Desensitization protocols are being used worldwide to enable kidney transplantation across immunologic barriers, i.e. antibody to donor HLA or ABO antigens, which were once thought to be absolute contraindications to transplantation. Desensitization protocols are also being applied to permit transplantation of HLA mismatched hematopoietic stem cells to patients with antibody to donor HLA, to enhance the opportunity for transplantation of non-renal organs, and to treat antibody-mediated rejection. Although desensitization for organ transplantation carries an increased risk of antibody-mediated rejection, ultimately these transplants extend and enhance the quality of life for solid organ recipients, and desensitization that permits transplantation of hematopoietic stem cells is life saving for patients with limited donor options. Complex patient factors and variability in treatment protocols have made it difficult to identify, precisely, the mechanisms underlying the downregulation of donor-specific antibodies. The mechanisms underlying desensitization may differ among the various protocols in use, although there are likely to be some common features. However, it is likely that desensitization achieves a sort of immune detente by first reducing the immunologic barrier and then by creating an environment in which an autoregulatory process restricts the immune response to the allograft.

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Section: Desensitization For Hla Antibodymentioning

confidence: 99%

Desensitization for solid organ and hematopoietic stem cell transplantation

Zachary

Leffell

2014

Immunological Reviews

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“…5,12 Recently pretransplant desensitization with PEx/IVIg has shown to increase the risk for BKV viremia and nephropathy. 13 Recipient risk factors including older age, male sex and donor related risk factors including female sex, active BKV and cytomegalovirus infection and deceased donor transplant are also thought to influence BKV infection. 5,12 In our study all recipients were on tacrolimus-mycophenolate based immunosuppression, a large proportion were elderly males who had received deceased donor transplants, and had additional immunosuppression either in the form of Previous studies have reported that most (95%) BKVN occurs in the first 2 years after transplantation.…”

Section: Discussionmentioning

confidence: 99%

BK Virus Associated Nephropathy, a Cause of Early Renal Allograft Dysfunction: A Single Centre Study

Shrestha¹,

Kerr

Kanellis

et al. 2017

Kathmandu Univ. Med. J.

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Background BK virus associated nephropathy (BKVN) is an important cause of early graft dysfunction in renal transplant recipients. The present study was carried out to determine the burden of BKVN in a single renal transplant centre in Australia.Method A retrospective analysis of de novo renal transplant recipients from 2010 to 2013 was performed to identify biopsy proven BKVN. Estimated glomerular filtration rate (eGFR) was compared at baseline, at BKVN diagnosis and 3 and 12 months post-diagnosis.Result Of the 317 de novo renal transplants recipients in the study period, 20 (6.3%) developed BKVN. The mean age was 54.8 ± 13.1 years and 13 (65%) were male. The mean time from transplant to BKVN was 8.7 ± 6.7 months with 17 (85%) diagnosed within 12 months. Four recipients each were diagnosed BKVN on 3 and 12 month surveillance biopsy. Six (30%) had normal eGFR at diagnosis. Mean eGFR at diagnosis was 38.8 ± 19.2 ml/min/1.73 m2, which was significantly lower (p < 0.01) than that at baseline (50.3 ± 16.4 ml/min/1.73 m2). eGFR improved numerically at 3 and 12 months post-diagnosis, however the difference was not significant. One patient had graft failure, 19 months after diagnosis.Conclusion BKVN generally occurs in first post-transplant year and is an important cause of early graft dysfunction. Surveillance biopsy helps in detecting subclinical BKVN.

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“…13 Biopsy proven "definite" PVN has an incidence of 5-6%, with a higher incidence in ABO-incompatible donors and following desensitization in highly sensitized recipients. [14][15][16] The Banff Working Group on Polyomavirus Nephropathy recently published a morphologic classification of definite PVN into three groups, Class I, II, and III, based on polyomavirus load and Banff ci score (interstitial fibrosis) for ease of diagnostic communication and comparative data analysis. 17 However, this was a retrospective observational analysis which has not been validated in a mixed population.…”

Section: Prevalencementioning

confidence: 99%

“…6,14,41,42 Recipient factors include old age, male sex, desensitization, and prior kidney transplant with PVN. 16,43…”

Section: Management Strategies Risk Factorsmentioning

confidence: 99%

<p>BK Virus Nephropathy: Prevalence, Impact and Management Strategies</p>

Sharma¹,

Zachariah²

2020

IJNRD

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BK virus reactivation as a result of therapeutic immunosuppression following renal transplant can result in BK polyomavirus nephropathy and renal allograft loss. This is a complex and challenging clinical problem with a range of management options and practices reported in literature. The current standard for early diagnosis and treatment is surveillance by measuring viral DNA in blood using qPCR. Immunosuppression reduction is the cornerstone of effective management but is associated with a risk of acute rejection following treatment.

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Evaluating the impact of pre‐transplant desensitization utilizing a plasmapheresis and low‐dose intravenous immunoglobulin protocol on BK viremia in renal transplant recipients

Abstract: This analysis reveals that pre-transplant desensitization significantly increases the risk for BKV viremia and nephropathy.

Cited by 15 publications

References 25 publications

Desensitization for solid organ and hematopoietic stem cell transplantation

Desensitization for solid organ and hematopoietic stem cell transplantation

BK Virus Associated Nephropathy, a Cause of Early Renal Allograft Dysfunction: A Single Centre Study

<p>BK Virus Nephropathy: Prevalence, Impact and Management Strategies</p>

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