ABSTRACT
Increased free radical activity during hemodialysis (HD) treatment has also been reported. During the dialysis session, some authors observed significant alterations in polymorphonuclear (PMN) cells’ chemiluminescence production, which is a well-established and sensitive means for measuring the production of ROS (24). Among the dialysis-related factors that can result in PMN alteration or activation, the cellulosic nature of the dialysis membrane has been incriminated (25,26), mainly via its capacity to activate complement system (27,28). These direct interactions of peripheral blood neutrophils with the dialysis membrane is known to induce degranulation, which invariably accompanied the increased oxidative metabolism of these cells. Moreover, recent studies support the hypothesis that both dialysis-and uremia-related factors contribute to monocyte activation and consequent interleukin-1 (IL-1) and tumor necrosis factor α (TNFα) production (29). Activation of immunocompetent cells was also demonstrated in the peritoneum of patients treated with continuous ambulatory peritoneal dialysis (CAPD) (30,31). These monokines act synergistically in a variety of biological processes; furthermore, the possibility that TNFα, when present at sufficient levels, could itself induce RLO production (32) must also be considered in long-term HD patients. It now becomes evident that increased generation of ROS triggered by incompatible dialysis membranes is indeed the reflection of an acute-phase inflammatory reaction and may participate in a large measure in the pathological changes and clinical symptoms observed in HD patients.
