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

Abstract

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 < .0001, P = .004, respectively) and vs baseline after 3 and 6 months of peritoneal dialysis (P = .007, P < .001, P = .004, respectively). Albumin was lower after 6 months of PD (P = .0014). IL‐6 was increased at baseline vs reference values and remained unchanged at 3 and 6 months. OxSt and inflammation increase during PD confirming via molecular biology approach a report at biochemical level. To improve OxSt state in PD, a multitarget approach is necessary. It might include the use of more physiologic pH, low glucose degradation products, low lactate and iso‐osmolar PD solutions, patients’ strict glycemic control, optimal volume management, and antioxidant administration, such as N‐acetylcysteine.

Nrf2 Protein Serum Concentration in Human CKD Shows a Biphasic Behavior

“…The significant interplay between inflammation and oxidative stress in CKD has been stressed [ 35 , 36 , 37 , 38 ]. Our analyses did not show a significant correlation between the inflammation marker C-reactive protein and Nrf2 protein concentration.…”

Paeoniflorin alleviates liver injury in hypercholesterolemic rats through the ROCK/AMPK pathway

“…Our previous studies showed that inhibiting hepatic ROCK could improve oxidative stress and the inflammatory response in hypercholesterolemia ( Ma et al, 2011a ; Ma et al, 2011c ). In this study, we used the p-MYPT-1 as a marker for ROCK activity ( Innico et al, 2021 ), and we showed that p-MYPT-1 is highly expressed in the liver of hypercholesterolemic rats, which indicates that hepatic ROCK pathway expression was increased. After PF treatment, we found that p-MYPT-1 expression was significantly reduced, which also showed that PF could reduce hepatic oxidative stress and the inflammatory response, and these results are consistent with our previous research.…”

The Pivotal Role of Oxidative Stress in the Pathophysiology of Cardiovascular-Renal Remodeling in Kidney Disease

“…In peritoneal dialysis, oxidative stress has been reported only in terms of increased AGEs, and other pro-oxidants derived by glucose [90]. Very recently, by using a molecular biology approach, we have observed in peritoneal dialysis patients that, oxidative stress is increased by peritoneal dialysis procedure as shown by the significantly increased levels of oxidative stress markers such as p22 phox , ROCK activity (MYPT1) and ferritin levels which all further increased after 6 months [91], therefore the use of more biocompatible dialysis solutions containing different glucose polymers such as icodestrin should be considered for their possible beneficial effects on oxidative stress and inflammation ( ).…”