Hakim R M
Clin Nephrol. 1986;26 Suppl 1:S9-12.
During clinical hemodialysis, interactions between blood and dialysis membranes lead to the activation of several pathways such as the coagulation, kallikrein and complement pathways. The sum of these interactions defines the biocompatibility of the dialysis membrane; Cuprophane membranes, the most widely used dialysis membranes elicit intense blood-membrane interactions. Complement activation can be measured by determining the concentration of the activated third and fifth component of the complement cascade, namely C3a and C5a. These active products lead to the well known neutropenia seen during the early phase of dialysis. However, the neutropenia is only the most visible manifestation of the effects of complement activation. C5a-induced secretion of granule enzymes from neutrophils and their subsequent desensitization to further chemotaxis and phagocytosis may be an important factor in the incidence of infections in the dialysis patient. Endothelial cell damage by complement stimulated granulocytes mediated via superoxide anion may also play a role in the pulmonary dysfunction seen in dialysis patients, and recent evidence suggests that complement products may lead to cardiac dysfunction manifested by impaired ventricular contractility. Although some of these events may not be mediated directly by activated complement products, recent studies suggest that they play a role in the activation of several other pathways and pathophysiological process.
在临床血液透析过程中，血液与透析膜之间的相互作用会引发多种途径的激活，如凝血、激肽释放酶和补体途径。这些相互作用的总和决定了透析膜的生物相容性；铜仿膜是使用最广泛的透析膜，会引发强烈的血膜相互作用。补体激活可通过测定补体级联反应中活化的第三和第五成分，即C3a和C5a的浓度来衡量。这些活性产物会导致透析早期出现众所周知的中性粒细胞减少。然而，中性粒细胞减少只是补体激活效应最明显的表现。C5a诱导中性粒细胞分泌颗粒酶以及随后它们对进一步趋化作用和吞噬作用的脱敏可能是透析患者感染发生率的一个重要因素。补体刺激的粒细胞通过超氧阴离子介导的内皮细胞损伤也可能在透析患者出现的肺功能障碍中起作用，最近的证据表明补体产物可能导致以心室收缩功能受损为表现的心脏功能障碍。尽管其中一些事件可能并非直接由活化的补体产物介导，但最近的研究表明它们在激活其他多种途径和病理生理过程中发挥作用。
