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StatPearls
Continuing Education Activity
Transplant rejection can be classified as hyperađáng yêu, adễ thương, or chronic. Hyperacute rejection is usually caused by specific antibodies against the graft và occurs within minutes or hours after grafting. Axinh tươi rejection occurs days or weeks after transplantation & can be caused by specific lymphocytes in the recipient that recognize human leukocyte antigens in the tissue or organ grafted. Finally, chronic rejection usually occurs months or years after organ or tissue transplantation. Various mechanisms involving chronic inflammation, humoral, và cellular immune reactions play essential roles in the immunopathogenesis of chronic rejections. This activity đánh giá the evaluation và management of chronic transplant rejections và highlights the role of interprofessional team members in collaborating to lớn provide well-coordinated care và enhance outcomes for affected patients.
Objectives:
Identify the pathophysiology of chronic transplant rejection.
Describe the typical presentation of a patient with chronic transplant rejection.
Explain how to lớn manage chronic transplant rejection.
Explain the importance of improving coordination aước ao the interprofessional team lớn enhance care for patients affected by chronic transplant rejection.
Introduction
Transplant rejection can be classified as hyperađáng yêu, acute, or chronic. Hyperadễ thương rejection is usually caused by specific antibodies against the graft & occurs within minutes or hours after grafting. Ađáng yêu rejection occurs days or weeks after transplantation and can be caused by specific lymphocytes in the recipient that recognize HLA antigens in the tissue or organ grafted. Finally, chronic rejection usually occurs months or years after organ or tissue transplantation. Various mechanisms involving chronic inflammation, humoral, & cellular immune reactions play an essential role in the immunopathogenesis of chronic rejection.
Etiology
The etiology of chronic rejection is incompletely understood. Glinton et al. reported that a vital determinant of the complication of chronic solid organ allografts is by a vascular disease component of the transplanted graft. Their review, however, focused on cardiac transplantation only. In cardiac allograft vasculopathy, histoxúc tích evidence suggests that the accumulation & activation of phagocytes can be a contributing factor. Phagocytic cells such as macrophages, monocytes, và immature dendritic cell subsets are found in this type of chronic cardiac transplant rejection. Furthermore, myeloid phagocytes crosstalk with B and T lymphocytes while also signaling & activating vascular smooth muscle cells và fibroblasts, and these can cause fibrous intimal thickening.<1> Chronic renal allograft rejection has been labeled as interstitial fibrosis and tubular atrophy lớn help reflect the underlying histology & etiology. Chronic rejection is now cited as the leading cause of graft rejection.
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Epidemiology
The overall incidence & prevalence of chronic allograft nephropathy (CAN) in biopsies of renal allograft tissues depends on the timing và the indication of such graft biopsies. In protocol biopsies, in the first year post-transplantation, it has been reported that the prevalence can be as high as 94% (grade I) and up khổng lồ 100% after ten years.
In the United States, mortality in patients on chronic hemodialysis is significantly higher in winter months than in the summer. It is unknown whether a seasonal difference exists, however, for mortality or graft failure among muốn kidney transplant recipients. One report showed that there was a significant annual variation of deaths due to graft failures. <2>
Pathophysiology
Chronic allograft rejection can be caused by antibody-dependent complement activation lesions as well as cell arteritis leading to the development of interstitial fibrosis/tubular atrophy (IF/TA).<3> This injury can appear early after transplantation. At 1-year post-transplant, greater than 81% of the kidneys have sầu minimal lesions of IF/TA that tkết thúc to progress over time; these lesions affect greater than 50% of transplanted kidneys with severe lesions at five sầu years.
The 2011 Banff meeting focused on diagnostic criteria for late-antibody toàn thân mediated rejection. In this đánh giá, there was the recognition of CD4-negative antibody-mediated rejection, in which endothelial activation and NK cells were suggested as the primary causes of chronic reaction.<4> Other proposed pathophysioxúc tích và ngắn gọn mechanisms include:
Histopathology
The main histological finding in biopsies of rejected organs is arteriosclerosis that causes a progressive sầu luminal narrowing of graft vessels. This is typically referred to lớn as a vasculopathy or graft vascular disease. This entity is often accompanied by graft tissue (parenchymal) fibrosis.<5> For example, livers with chronic rejection show a decreased number of bile ducts on biopsy & obliteration of small arteries. Correspondingly, lung rejection is characterized by bronchiolitis obliterans. The presence of endothelial injury and subsequent inflammation has been suggested as the inciting cause of this vascular dysfunction.
History and Physical
Individuals presenting with chronic transplant rejection will have sầu had a previous history of organ or tissue transplantation (for example, kidney, liver, and lung) for any of many chronic medical conditions. The symptoms and signs of rejection depend on the organ transplanted; for instance, a chronic kidney rejection causes fatigue, fever, flu-lượt thích symptoms, anuria or decreased urine output, generalized edema, & pain or tenderness at the site of transplantation. Other signs & symptoms of organ rejection can include: