Fig. 5
Working hypothesis. Our hypothesis is that not MPO but ROS may play a primary role for the development of HD-related fatigue. ROS itself cannot be measured at routine examinations, thus, the change of MDA-a level is employed as a surrogate marker for the intensity of ROS in the clinical setting. The result that ⊿MDA-a was identified as an independent risk factor for the presence of fatigue in CHD (Table 5), may well support this notion. In this regard, increases of MPO by E-HD does not necessarily reflect the enhanced oxidative stress and may be the result of improved neutrophil viability. The exact mechanisms leading to suppression of oxidative stress and enhancement of anti-oxidation have remained unclear. However, we suppose the following possibilities. Regarding the mechanisms underlying decreased MDA-a, H2 in the dialysis solution may directly quench radical oxygen species, thereby decreasing adduct production, or E-HD may increase the viability of cells that scavenge the MDA-a, thereby shortening the disappearance time. Regarding the increase in thioredoxin, decreased consumption/production of thioredoxin due to less oxidative stress, or increased viability of the cells producing thioredoxin, may be involved with the phenomenon. C-HD, standard hemodialysis; E-HD, hemodialysis employing electrolyzed water; MPO, myeloperoxidase; ROS, reactive oxygen species; MDA-a, malondialdehyde-protein adduct; TRX, thioredoxin-1