Abstract
Peritoneal dialysis (PD) patients manifest excessive oxidative stress (OS) compared to the general population and predialysis chronic kidney disease patients, mainly due to the composition of the PD solution (high-glucose content, low pH, elevated osmolality, increased lactate concentration and glucose degradation products). However, PD could be considered a more biocompatible form of dialysis compared to hemodialysis (HD), since several studies showed that the latter results in an excess accumulation of oxidative products and loss of antioxidants. OS in PD is tightly linked with chronic inflammation, atherogenesis, peritoneal fibrosis, and loss of residual renal function. Although exogenous supplementation of antioxidants, such as vitamins E and C, N-acetylcysteine, and carotenoids, in some cases showed potential beneficial effects in PD patients, relevant recommendations have not been yet adopted in everyday clinical practice.
Highlights
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]
Terawaki et al showed that oxidized albumin—another marker of OS status—was significantly increased in 21 chronic continuous ambulatory peritoneal dialysis (CAPD) patients compared to healthy controls and was tightly associated with blood urea nitrogen but not with urine volume or serum concentration of β2-microglobulin
These results were confirmed by other investigators: Choi et al showed that the dialysate/plasma ratio of nitric oxide (NO) concentrations is a strong marker assessing the severity of peritonitis in CAPD patients as well as the effectiveness of treatment [91]
Summary
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]. 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) [2,3,4]. OS is of paramount relevance for the chronic inflammation state and ensuing fibrosis of the peritoneum in patients undergoing peritoneal dialysis (PD). 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
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