*2.4. Oxidative Stress*

Oxidative stress in CKD results from an imbalance in reactive oxygen species production and impaired antioxidant defense [35]. Various oxidation products have been shown to be overabundant in CKD. Increased ROS production has been reported to contribute to myocardial hypertrophy and fibrosis by lipid peroxidation, proinflammatory cytokines and DNA damage [35,36]. A marker of oxidative stress, 8-isoprostane, increases as CKD progresses [37]. Furthermore, NADPH oxidase generates reactive oxygen species, and this in turn leads to endothelial dysfunction [38]. Another e ffect of elevated oxidative stress is the oxidation of plasma proteins, which causes activation of phagocytes

and increases inflammation [39]. Advanced oxidation protein products promote cardiomyocyte apoptosis. This process is mediated by upregulation of c-Jun N-terminal kinase (JNK) signaling and enhanced endoplasmic reticulum stress [40].
