Humoral Rejection of Organ Allografts

Moll, Solange; Pascual, Manuel

doi:10.1111/j.1600-6143.2005.01086.x

Cited by 101 publications

(51 citation statements)

References 59 publications

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“…The development of de novo antibodies may increase the risk for acute and chronic rejection and decrease allograft survival (1)(2)(3)(4). Because of insufficient routine posttransplantation monitoring of de novo antibody production, the exact incidence of humoral alloimmune responses after kidney transplantation is still uncertain.…”

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confidence: 99%

Sensitization after Kidney Transplantation

Akalin¹,

Pascual²

2006

Clinical Journal of the American Society of Nephrology

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Kidney transplant recipients may develop de novo anti-HLA and non-HLA antibodies after transplantation. Although these antibodies may be donor-specific or non-donor-specific, their presence may increase the risk for acute and chronic rejection, thereby decreasing allograft survival. The introduction of more sensitive and specific methods to detect anti-HLA antibodies, such as Flow Specific Beads and FlowPRA, both before and after transplantation, will help to define immunologically high-risk kidney transplant recipients. Thus, posttransplantation monitoring of anti-HLA antibody production will allow the identification of kidney transplant recipients who might be at increased risk for late allograft failure. Moreover, knowledge of alloantibody status after transplantation may help to guide the appropriate use of immunomodulatory agents to downregulate anti-HLA antibody production.

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Sensitization after Kidney Transplantation

Akalin¹,

Pascual²

2006

Clinical Journal of the American Society of Nephrology

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“…31 Deposition of C4d, a complement split product, on the capillary endothelium has been suggested as a surrogate marker for AMR in heart, kidney, liver, and pancreas transplants. [32][33][34][35][36][37][38][39][40][41][42] The role of C4d deposition in the diagnosis of AMR in lung allografts, however, is still unclear. Moreover, reproducibility of C4d deposition in allograft lung transbronchial biopsies is problematic, even among pathologists who routinely evaluate C4d in lung allograft biopsies.…”

Section: Diagnosis Of Antibody-mediated Rejection Inmentioning

confidence: 99%

Diagnosis of Acute Cellular Rejection and Antibody-Mediated Rejection on Lung Transplant Biopsies: A Perspective From Members of the Pulmonary Pathology Society

Roden¹,

Aisner²,

Allen³

et al. 2016

Archives of Pathology &Amp; Laboratory Medicine

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Context.— The diagnosis and grading of acute cellular and antibody-mediated rejection (AMR) in lung allograft biopsies is important because rejection can lead to acute graft dysfunction and/or failure and may contribute to chronic graft failure. While acute cellular rejection is well defined histologically, no reproducible specific features of AMR are currently identified. Therefore, a combination of clinical features, serology, histopathology, and immunologic findings is suggested for the diagnosis of AMR. Objective.— To describe the perspective of members of the Pulmonary Pathology Society (PPS) on the workup of lung allograft transbronchial biopsy and the diagnosis of acute cellular rejection and AMR in lung transplant. Data Sources.— Reports by the International Society for Heart and Lung Transplantation (ISHLT), experience of members of PPS who routinely review lung allograft biopsies, and search of literature database (PubMed). Conclusions.— Acute cellular rejection should be assessed and graded according to the 2007 working formulation of the ISHLT. As currently no specific features are known for AMR in lung allografts, the triple test (clinical allograft dysfunction, donor-specific antibodies, pathologic findings) should be used for its diagnosis. C4d staining might be performed when morphologic, clinical, and/or serologic features suggestive of AMR are identified.

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“…Approximately 30% of patients active in the United Network for Organ Sharing waiting list are sensitized. [1][2][3] Pretransplant sensitization is indeed a major risk factor for acute antibody-mediated rejection (ABMR) after transplant, with an increased risk of allograft loss. [1][2][3][4] Despite its recognition for .20 years as a defined clinicopathologic entity, [4][5][6][7] treatment strategies for acute biopsyproven ABMR are still not standardized.…”

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“…[1][2][3] Pretransplant sensitization is indeed a major risk factor for acute antibody-mediated rejection (ABMR) after transplant, with an increased risk of allograft loss. [1][2][3][4] Despite its recognition for .20 years as a defined clinicopathologic entity, [4][5][6][7] treatment strategies for acute biopsyproven ABMR are still not standardized. In general, therapeutic strategies have been based on the removal of antidonor alloantibodies (eg, by series of plasmapheresis or immunoadsorption sessions), associated with attempts to suppress antidonor humoral responses (eg, by using intravenous immunoglobulin [IVIg] or the anti-CD20 monoclonal antibody rituximab).…”

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confidence: 99%

“…Activation of the complement cascade in acute ABMR rejection has been identified as a major pathophysiological mechanism leading to allograft damage and dysfunction. 1,2,[8][9][10] As a consequence, it has been proposed that specific inhibition of the recipient's complement system of limited duration may be useful to prevent acute ABMR. 1 Dr Chehade collected and analyzed the data and wrote the manuscript; Dr Rotman was the pathologist who reviewed the biopsy and critically reviewed the manuscript; Dr Matter performed the transplant, participated in collecting the data, and critically reviewed the manuscript; Prof Girardin participated in patient management and data collection and critically reviewed the manuscript; Dr Aubert participated in performing the Luminex and serologic assays and critically reviewed the manuscript; Prof Pascual collected and analyzed the data, wrote the manuscript, and critically reviewed the manuscript; and all authors approved the final manuscript as submitted.…”

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Eculizumab to Treat Antibody-Mediated Rejection in a 7-Year-Old Kidney Transplant Recipient

et al. 2015

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We report on successful early eculizumab administration to treat acute antibody-mediated rejection (ABMR) in a highly sensitized kidney transplant recipient. The recipient is a 7-year-old boy who received, 6 months after a desensitization protocol with monthly intravenous immunoglobulin infusion, a second kidney transplant in the presence of low donor-specific antibodies (DSAs). Both pretransplant lymphocytotoxic and flow cytometric crossmatch were negative. Allograft function recovered promptly, with excellent initial function. On postoperative day (POD) 4, the child developed significant proteinuria with an acute rise in serum creatinine. Allograft biopsy showed severe acute ABMR. Intravenous eculizumab (600 mg), preceded by a single session of plasmapheresis, was administered on POD 5 and 12 along with a 4-day thymoglobulin course. After the first dose of eculizumab, a strikingly rapid normalization of allograft function with a decrease in proteinuria occurred. However, because circulating DSA levels remained elevated, the child received 3 doses of intravenous immunoglobulin (POD 15,16,and 17), with a significant subsequent decrease in DSA levels. At 9 months after transplant, the child continues to maintain excellent allograft function with undetectable circulating DSA levels. This unique case highlights the potential efficacy of using early eculizumab to rapidly reverse severe ABMR in pediatric transplantation, and therefore it suggests a novel therapeutic approach to treat acute ABMR.

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Humoral Rejection of Organ Allografts

Cited by 101 publications

References 59 publications

Sensitization after Kidney Transplantation

Sensitization after Kidney Transplantation

Diagnosis of Acute Cellular Rejection and Antibody-Mediated Rejection on Lung Transplant Biopsies: A Perspective From Members of the Pulmonary Pathology Society

Eculizumab to Treat Antibody-Mediated Rejection in a 7-Year-Old Kidney Transplant Recipient

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