Johnson R J
Baxter Healthcare Corporation, Corporate Research and Technical Services, Round Lake, Illinois 60073, USA.
Curr Opin Nephrol Hypertens. 1997 Mar;6(2):120-7. doi: 10.1097/00041552-199703000-00003.
The complement system is a critical element of innate immunity whose role in renal physiology and disease is illustrated by the following observations: (1) a deficiency or inhibition of a complement regulatory protein results in renal tissue damage; (2) inhibition of complement activation (with cobra venom factor or sCR1), or in C6-deficient rats, attenuates complement-mediated tissue destruction; and (3) ongoing glomerular disease has been associated with the deposition/expression of complement proteins in glomerular or tubular structures and the excretion of C5b-9 and CD59 proteins. Complement activation by cellulosic membranes results in the production of C5a, which has now been shown to provoke most of the same inflammatory responses observed during hemodialysis. Controlling the dose of C5a given during dialysis, by controlling blood flow rates or membrane types, may have an impact on patient health. Finally, lessons learned in the xenotransplant setting suggest that complement activation can be effectively controlled to limit inflammation (with sCR1 or anti-C5 monoclonal antibodies). Recent developments in this area may lead to new therapeutic approaches to deal with the complex etiology of renal disease.
补体系统是固有免疫的关键组成部分，以下观察结果表明了其在肾脏生理学和疾病中的作用：（1）补体调节蛋白的缺陷或抑制会导致肾组织损伤；（2）抑制补体激活（使用眼镜蛇毒因子或sCR1），或在C6缺陷大鼠中，可减轻补体介导的组织破坏；（3）进行性肾小球疾病与补体蛋白在肾小球或肾小管结构中的沉积/表达以及C5b-9和CD59蛋白的排泄有关。纤维素膜激活补体可产生C5a，现已证明C5a会引发血液透析期间观察到的大多数相同炎症反应。通过控制血流速度或膜类型来控制透析期间给予的C5a剂量，可能会对患者健康产生影响。最后，在异种移植环境中吸取的经验教训表明，补体激活可以通过sCR1或抗C5单克隆抗体有效地加以控制，以限制炎症。该领域的最新进展可能会带来新的治疗方法，以应对复杂的肾脏疾病病因。
