Oxidative stress, inflammation, and peritoneal dialysis: A molecular biology approach

The key role of oxidative stress (OxSt) and inflammation for the induction of cardiovascular disease, the leading cause of excess morbidity/mortality in chronic kidney disease and dialysis patients, is known and both the activations of NADPH oxidase and RhoA/Rho kinase (ROCK) pathway are pivotal for their effects. While specific hemodialysis procedures, such as hemodiafiltration with on‐line reinfusion of ultrafiltrate and/or the use of vitamin E‐coated dialyzers, are beneficial for OxSt and inflammation, studies in peritoneal dialysis (PD) are instead scarce and results seem not favorable. In nine patients under PD OxSt in terms of mononuclear cell protein level of p22phox (Western blot), subunit of NADPH oxidase, essential for the generation of OxSt, and MYPT‐1 phosphorylation state (Western blot), a marker of ROCK activity, have been measured at the beginning and after 3 and 6 months of PD. Blood levels of interleukin 6 (IL‐6), ferritin, and albumin have been considered for evaluating the inflammatory state. p22phox protein expression, MYPT‐1‐phosphorylation, and ferritin level were increased both at baseline vs healthy subjects (P = .02, P