Combe C, Pourtein M, de Précigout V, Baquey A, Morel D, Potaux L, Vincendeau P, Bézian J H, Aparicio M
Service d'Hémodialyse, Hôpital Pellegrin, Bordeaux, France.
Am J Kidney Dis. 1994 Sep;24(3):437-42. doi: 10.1016/s0272-6386(12)80900-0.
Hemodialysis with complement-activating membranes, such as cuprophane, induces neutropenia and expression of the granulocyte adhesion receptor Mac-1 (CD11b/CD18), while hemodialysis with noncomplement-activating membranes does not. Increased expression of CD11b by neutrophils may mediate cuprophane-induced leukopenia. However, the rebound granulocytosis that follows leukopenia is not fully understood. Ten patients on regular hemodialysis were included in a cross-over study. Hemodialysis was performed for 2 weeks with cuprophane and 2 weeks with polyamide, a high-flux noncomplement-activating membrane. At the end of each period, the following parameters were determined during a hemodialysis session: C5a concentration by enzyme immunoassay and the neutrophil expression of CD11b, LFA-1 (CD11a/CD18), and the antigen recognized by MoF11 (MoF11 Ag), a monoclonal antibody that recognizes activated neutrophils, by immunofluorescence flow cytometry. Hemodialysis with cuprophane induced an increase in C5a concentration and in the expression of CD11b and MoF11 Ag, which were maximal after 15 minutes of hemodialysis, at the nadir of neutropenia. CD11b expression was maintained throughout hemodialysis, despite the reversal of neutropenia. Conversely, after peak expression, C5a and MoF11 Ag decreased as the neutrophil count increased to baseline values. Polyamide hemodialysis did not induce variations in C5a concentration, nor in CD11b and MoF11 Ag expression. CD11a/CD18 expression remained stable during hemodialysis with both membrane types. Neutrophil activation, as determined by MoF11 Ag expression, was correlated with the evolution of neutrophil count and C5a concentration during cuprophane hemodialysis, while CD11b expression was not correlated with neutrophil count throughout dialysis. A decrease in neutrophil activation could explain in part the detachment of neutrophils previously bound to endothelium and, therefore, the reversal of neutropenia.(ABSTRACT TRUNCATED AT 250 WORDS)
使用补体激活膜（如铜仿膜）进行血液透析会导致中性粒细胞减少以及粒细胞黏附受体Mac-1（CD11b/CD18）的表达，而使用非补体激活膜进行血液透析则不会。中性粒细胞CD11b表达的增加可能介导了铜仿膜诱导的白细胞减少。然而，白细胞减少后出现的粒细胞增多反弹现象尚未完全明确。十名接受定期血液透析的患者被纳入一项交叉研究。分别使用铜仿膜进行2周血液透析，以及使用聚酰胺（一种高通量非补体激活膜）进行2周血液透析。在每个阶段结束时，在一次血液透析过程中测定以下参数：通过酶免疫测定法测定C5a浓度，通过免疫荧光流式细胞术测定中性粒细胞CD11b、LFA-1（CD11a/CD18）以及MoF11识别的抗原（MoF11 Ag，一种识别活化中性粒细胞的单克隆抗体）的表达。使用铜仿膜进行血液透析会导致C5a浓度以及CD11b和MoF11 Ag表达增加，在血液透析15分钟后达到峰值，此时中性粒细胞减少至最低点。尽管中性粒细胞减少情况有所逆转，但CD11b表达在整个血液透析过程中持续存在。相反，在表达峰值后，随着中性粒细胞计数增加至基线值，C5a和MoF11 Ag下降。聚酰胺血液透析未引起C5a浓度、CD11b和MoF11 Ag表达的变化。在两种膜类型的血液透析过程中，CD11a/CD18表达均保持稳定。通过MoF11 Ag表达确定的中性粒细胞活化与铜仿膜血液透析过程中中性粒细胞计数和C5a浓度的变化相关，而在整个透析过程中CD11b表达与中性粒细胞计数无关。中性粒细胞活化的降低可能部分解释了先前黏附于内皮的中性粒细胞的脱离，进而解释了中性粒细胞减少的逆转。（摘要截断于250字）
