Renal and Transplant Department, Guy's and St Thomas' NHS Foundation Trust, London, UK; Duke Transplant Center, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Duke Transplant Center, Department of Surgery, Duke University Medical Center, Durham, NC 27710, USA.
Transplant Rev (Orlando). 2018 Jul;32(3):119-126. doi: 10.1016/j.trre.2018.01.001. Epub 2018 Feb 10.
Thrombotic microangiopathy (TMA) is a histological feature of antibody-mediated rejection and has the potential to cause problematic graft dysfunction, particularly for highly sensitized cross-match positive kidney transplant recipients. Prompt recognition of pertinent histopathological and systemic features of TMA in kidney transplantation is necessary. Underlying mechanisms of this process involve the activation of both complement and coagulation systems as a response to HLA antibody. As serine proteases, coagulation and complement cascades exhibit similar characteristics with respect to homeostatic function. Increasing evidence now exists for the interaction between these innate defenses in both activation and regulation, lending scope for intervention. Understanding the complexities of these interactions remains a challenge. This review provides an overview of the current understanding, particularly with respect to the activation of coagulation and complement by HLA antibody in the setting of highly sensitized kidney transplantation.
血栓性微血管病（TMA）是抗体介导排斥反应的组织学特征，有可能导致移植肾功能出现问题，尤其是对高度致敏交叉配型阳性的肾移植受者。因此，及时识别肾移植中 TMA 的相关组织病理学和系统性特征是必要的。这一过程的潜在机制涉及补体和凝血系统的激活，作为对 HLA 抗体的反应。作为丝氨酸蛋白酶，凝血和补体级联在稳态功能方面具有相似的特征。目前有越来越多的证据表明这些先天防御系统在激活和调节方面相互作用，为干预提供了可能。了解这些相互作用的复杂性仍然是一个挑战。本文综述了目前的认识，特别是在高度致敏肾移植中 HLA 抗体激活凝血和补体的机制。
