Owing to an increasing shortage of donor organs, the majority of patients with end-stage kidney disease remains reliant on extracorporeal hemodialysis (HD) in order to counter the lifelong complications of a failing kidney. While HD remains a life-saving option for these patients, mounting evidence suggests that it also fuels a vicious cycle of thromboinflammation that can increase the risk of cardiovascular disease. During HD, blood-borne innate immune systems become inappropriately activated on the biomaterial surface, instigating proinflammatory reactions that can alter endothelial and vascular homeostasis. Complement activation, early during the HD process, has been shown to fuel a multitude of detrimental thromboinflammatory reactions that collectively contribute to patient morbidity. Here we discuss emerging aspects of complement's involvement in HD-induced inflammation and put forth the concept that targeted intervention at the level of C3 might constitute a promising therapeutic approach in HD patients.

由于供体器官的日益短缺，大多数患有终末期肾脏疾病的患者仍然依赖于体外血液透析（HD），以应对肾脏衰竭的终生并发症。尽管HD对这些患者而言仍然是挽救生命的选择，但越来越多的证据表明，HD还加剧了血栓炎症的恶性循环，从而增加了患心血管疾病的风险。在HD期间，血源性先天免疫系统会在生物材料表面上被不适当地激活，从而引发可改变内皮和血管动态平衡的促炎反应。在HD过程的早期，补体激活已被证明可引发多种有害的血栓炎症反应，这些反应共同导致患者发病。在这里，我们讨论补数的新兴方面”