Abstract：
Delayed graft function is a manifestation of acute kidney injury unique to transplantation usually related to donor ischemia or recipient immunological causes. Ischemia also considered the most important trigger for innate immunity activation and production of non-HLA antibodies. While ischemia is inevitable after deceased donor transplantation, this complication is rare after living transplantation. Heterologous Immunity commonly used to describe the activation of T cells recognizing specific pathogen-related antigens as well unrelated antigens is common post-viral infection. In transplant-setting induction of heterologous immunity that cross-react with HLA-antigens and subsequent reactivation of memory T cells can lead to allograft rejection.
Here we describe a non-sensitized child with ESRD secondary to lupus nephritis and recent history of COVID-19 infection who experienced 17 days of anuria after first kidney living transplantation from her young HLA-haploidentical uncle donor. Graft histology showed acute cellular rejection, evidence of mild antibody-mediated rejection and vascular wall necrosis in some arterioles suggesting possibility of intraoperative graft ischemia. Both pre- and post-transplant sera showed very high level of several non-HLA antibodies.
The patient was treated for cellular and antibody-mediated rejection while maintained on hemodialysis before her graft function started to improve on day seventeen post transplantation.
The cellular rejection likely trigged by ischemia that activated T-cells-mediated immunity. The high level of non- HLA-antibodies further aggravated the damage and the rapid onset of rejection may be partly related to memory T-cell activation induced by heterologous immunity.
Here we describe a non-sensitized child with ESRD secondary to lupus nephritis and recent history of COVID-19 infection who experienced 17 days of anuria after first kidney living transplantation from her young HLA-haploidentical uncle donor. Graft histology showed acute cellular rejection, evidence of mild antibody-mediated rejection and vascular wall necrosis in some arterioles suggesting possibility of intraoperative graft ischemia. Both pre- and post-transplant sera showed very high level of several non-HLA antibodies.
The patient was treated for cellular and antibody-mediated rejection while maintained on hemodialysis before her graft function started to improve on day seventeen post transplantation.
The cellular rejection likely trigged by ischemia that activated T-cells-mediated immunity. The high level of non- HLA-antibodies further aggravated the damage and the rapid onset of rejection may be partly related to memory T-cell activation induced by heterologous immunity.
摘要：
背景：移植物功能延迟是移植特有的急性肾损伤的表现，通常与供体缺血或受体免疫原因有关。缺血也被认为是先天免疫激活和非HLA抗体产生的最重要的触发因素。虽然在死者移植后缺血是不可避免的，这种并发症在活体移植后很少见。通常用于描述识别特定病原体相关抗原以及无关抗原的T细胞的激活的异源免疫是病毒感染后常见的。在移植设置中，与HLA抗原交叉反应的异源免疫的诱导以及随后记忆T细胞的重新激活可导致同种异体移植排斥。
方法：在这里，我们描述了一名患有狼疮肾炎继发ESRD且最近有COVID-19感染史的非致敏儿童，她从年轻的HLA单倍体叔叔供者那里进行了首次肾脏活体移植后出现了17天的无尿。移植物组织学显示急性细胞排斥反应，在一些小动脉中存在轻度抗体介导的排斥反应和血管壁坏死,提示术中移植物缺血的可能性。移植前和移植后血清均显示出非常高水平的几种非HLA抗体。
结果：患者在移植后第17天移植功能开始改善之前，接受了细胞和抗体介导的排斥治疗，同时维持血液透析。
结论：细胞排斥反应可能由激活T细胞介导的免疫的缺血引发。高水平的非HLA抗体进一步加重了损伤,并且排斥反应的快速发作可能部分地与异源免疫诱导的记忆T细胞活化有关。
方法：在这里，我们描述了一名患有狼疮肾炎继发ESRD且最近有COVID-19感染史的非致敏儿童，她从年轻的HLA单倍体叔叔供者那里进行了首次肾脏活体移植后出现了17天的无尿。移植物组织学显示急性细胞排斥反应，在一些小动脉中存在轻度抗体介导的排斥反应和血管壁坏死,提示术中移植物缺血的可能性。移植前和移植后血清均显示出非常高水平的几种非HLA抗体。
结果：患者在移植后第17天移植功能开始改善之前，接受了细胞和抗体介导的排斥治疗，同时维持血液透析。
结论：细胞排斥反应可能由激活T细胞介导的免疫的缺血引发。高水平的非HLA抗体进一步加重了损伤,并且排斥反应的快速发作可能部分地与异源免疫诱导的记忆T细胞活化有关。
