Clinical relevance of complement-fixing antibodies in cardiac transplantation

Rose, Marlene L.; Smith, John D.

doi:10.1016/j.humimm.2009.04.016

Cited by 54 publications

(52 citation statements)

References 44 publications

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“…50 Many solid-phase assays were unable to distinguish between activating-and nonactivating-complement antibodies. Although the frequency of nonactivating-complement antibodies in patients awaiting a second renal transplant has been shown to be approximately 40%, there are no convincing data to show the clinical significance or otherwise of nonactivating-complement HLA antibodies.…”

Section: Introductionmentioning

confidence: 99%

Current Concepts in Histocompatibility During Heart Transplant

Picascia

Grimaldi²,

Zullo³

et al. 2012

Exp Clin Transplant

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Sensitized candidates for heart transplant usually end up on a long waiting list and have an increased risk of rejection, graft loss, and incidence of cardiac allograft vasculopathy. An increasing number of studies have demonstrated the negative effect of preformed and posttransplant antibodies on graft survival. Thus, in sensitized patients, the combination of new, appropriate, desensitization protocols, and monitoring of posttransplant development of donor-specific antibodies may improve short-term and long-term outcomes. Introduction of more-sensitive and more-specific techniques for antibody detection provides a valid tool for assessing the degree of pretransplant HLA histocompatibility, and, therefore, predicting the results of crossmatch in sensitized patients, which are difficult to transplant. Currently, there are no accurate and standard methods to determine the functional characteristics of antibodies detected by solid-phase assay and, therefore, to predict their clinical relevance. Therefore, the future of heart transplantation requires a better understanding of tissue typing techniques and the effect of anti-HLA antibodies on clinical outcome to prevent discrimination against sensitized patients at the time of organ allocation.

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Section: Introductionmentioning

confidence: 99%

Current Concepts in Histocompatibility During Heart Transplant

Picascia

Grimaldi²,

Zullo³

et al. 2012

Exp Clin Transplant

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“…Autoimmunity confers risk to the development of AMR and CAV. Antibodies against non-HLA antigens have gained attention in the pathogenesis of AMR and CAV [75][76][77]. Antibodies against cardiac self-antigens such as cardiac myosin and vimentin (cytoskeleton protein) are found to be associated with development of AMR and CAV and are considered to be independent risk factor for CAV [66][67][68].…”

Section: Immunologic Factorsmentioning

confidence: 99%

“…Development of donor specific HLA antibodies has been associated with chronic rejection. Both acute cellular rejection (ACR) and AMR have been inferred in the pathogenesis of allograft vasculopathy [76][77][78][79][80][81][82][83][84][85]. Higher incidence of CAV is noted in heart transplant recipients with history of AMR than recipients without the history [76,77,84].…”

Section: Immunologic Factorsmentioning

confidence: 99%

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Cardiac Allograft Vasculopathy: A Review of Risk Factors and Pathogenesis

Munagala¹,

Phancao²

2018

obm.transplant

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Heart transplant remains the gold standard therapy for patients with end stage heart disease and offers improved survival and quality of life. Significant progress has been achieved in improving one-year mortality after heart transplantation. Nonetheless, longterm graft survival has not changed significantly over the past few decades. Long term survival of heart transplant recipients is limited by chronic rejection, cardiac allograft vasculopathy (CAV), and malignancy. CAV is a major contributor for graft failure and mortality after the first year of in heart transplant recipients. CAV is a proliferative vasculopathy characterized by diffuse myointimal hyperplasia and progressive narrowing of the graft vessels. Both immune dependent and independent factors have been shown to contribute to the pathogenesis of CAV. Understanding these risk factors is essential in developing preventative and therapeutic strategies. Angiography with Intravascular ultrasound has become the key diagnostic tool in the early detection of CAV as well as prognostication. Echocardiographic assessment of allograft function in conjunction with coronary angiographic findings are used in assessing the severity of CAV. Adjustment of immunosuppression and statins remain the initial steps in the management of CAV. Retransplantation is the definitive treatment for severe CAV, however, the paucity of organs along with increased mortality associated with retransplantation makes it a less desirable option. Remarkable progress has been achieved in the understanding of pathogenesis, risk factors for CAV and plaque morphology. Nevertheless, significant knowledge gaps persist in scientific understanding of risk factors, pathogenesis, prevention and treatment of CAV. Further research is warranted to fill these gaps, develop diagnostic modalities to facilitate early detection of CAV, and management strategies to Improve graft tolerance and immune modulation. This review focuses on summarizing the pathogenesis and risk factors for CAV.

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“…The most dangerous antibodies for cardiac transplantation would be the complementfixing ones [28][29][30][31] . Patients with episodes of humoral rejection are more exposed to CAV than those with no rejection, differently from the cellular rejection whose relationship with CAV is still controversial 32 .…”

Section: Chart 1 -Stanford Classification Of Intracoronary Lesions Asmentioning

confidence: 99%