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Received Aug 14, 2017; Revised Nov 15, 2017; Accepted Dec 11, 2017
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1. Introduction
Oxidative stress (OS) is defined as the tissue injury and the systemic damage caused by disrupted balance between oxidative molecules and insufficient antioxidant defense mechanisms [1, 2]. Among the plethora of oxidative products, reactive oxygen species (ROS) and nitric oxide (NO) are the most common, while antioxidants can be molecules either endogenously synthesized or exogenously administered. The main targets of OS-induced damage are proteins, carbohydrates, lipids, and nucleic acids (DNA). Chronic kidney disease (CKD) is characterized by enhanced oxidation status of proteins, lipids and DNA, and subsequent tissue and organ injury. OS is evident even in the early stages of CKD, progresses along with the deterioration of renal function, and is further exacerbated in patients undergoing dialysis. There is a growing body of evidence showing that OS is a crucial promoter of atherosclerosis in end-stage renal disease (ESRD) [2–4]. Moreover, OS is of paramount relevance for the chronic inflammation state and ensuing fibrosis of the peritoneum in patients undergoing peritoneal dialysis (PD). It is also related to residual renal function (RRF). On the other hand, antioxidant supplementation is an emerging strategy to counteract OS with the potential to preserve peritoneal function. However, although OS in hemodialysis (HD) has been thoroughly studied during the past decade, the data regarding the pathogenesis, role, and predictive value of OS in PD patients is still limited but constantly growing.
2. OS Status in PD
2.1. Pathophysiological Mechanism
Both HD and PD are accompanied by enhanced OS, although underlying mechanisms are considered to differ. In HD, the formation of oxidative products is associated with the type of dialysis membranes, use of heparin, intravenous iron administration, and activation of platelets and leukocytes. In contrast, the composition of the PD solution (low pH, elevated osmolality, increased lactate concentration, and glucose degradation products) is responsible for accumulation of oxidative products [5]. In vitro studies showed that when cultured human mesothelial cells are exposed to dextrose or icodextrin dialysates for one hour, it produces ROS, increasing thus OS [6]. In...