Paul J L, Man N K, Roch-Arveiller M, Raichvarg D
Laboratoire de Biochimie A, Hôpital Cochin, Paris.
Nephrologie. 1987;8(6):287-92.
Clinical evidence indicates that infection is still a cause of morbidity and mortality in patients undergoing hemodialysis. The major role played by the polymorphonuclear cells in antimicrobial response by the host explained considerable study of several aspects of granulocyte functions in chronic hemodialysis patients. It is now well documented that hemodialysis induces the sequential activation of the complement components of the alternative pathway and may provide a mechanism for initiating leukoaggregation and sequestration of granulocytes. This complement activation could also explain the profound leukopenia observed shortly after the initiation of hemodialysis. It has been also assumed that the sequestration of granulocytes is dependent on a temporarily altered cell function and leads to a depressed chemotaxis, an impairment of phagocytic and bactericidal capacities. Moreover, a significant defect in the oxidative metabolism was observed before and during the course of the dialysis session. This article summarizes research that has been done on the function of neutrophils from chronic hemodialysis patients.
临床证据表明，感染仍是接受血液透析患者发病和死亡的一个原因。多形核细胞在宿主抗菌反应中发挥的主要作用，解释了对慢性血液透析患者粒细胞功能几个方面进行大量研究的原因。现已充分证明，血液透析会诱导替代途径补体成分的顺序激活，并可能提供一种引发白细胞聚集和粒细胞滞留的机制。这种补体激活也可以解释血液透析开始后不久观察到的严重白细胞减少。还有人认为，粒细胞的滞留取决于暂时改变的细胞功能，并导致趋化性降低、吞噬和杀菌能力受损。此外，在透析过程之前和期间观察到氧化代谢存在显著缺陷。本文总结了对慢性血液透析患者中性粒细胞功能所做的研究。
