2021
DOI: 10.1007/s00005-021-00638-1
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Peroxiredoxins as Markers of Oxidative Stress in IgA Nephropathy, Membranous Nephropathy and Lupus Nephritis

Abstract: IgA nephropathy (IgAN), membranous nephropathy (MN), and lupus nephritis (LN) represent important causes of chronic kidney disease. They belong to the immune-mediated glomerulonephritis (GNs), and have distinct pathogenesis, distinct clinical courses, and variable responses to treatment. Therefore, specific diagnostic procedures are necessary for more effective patient management. Recently, a role for oxidative stress has been proposed in various renal disorders. Thus, molecules related to oxidative stress, su… Show more

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Cited by 18 publications
(15 citation statements)
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“… 49 Elevated levels of F2 isoprostane have been attributed to tissue oxidation in SLE and therefore can be utilized as a marker to assess the relationship between mitochondrial function and oxidative stress in fatigued patients. 50 These metabolites establish covalent bonds to proteins, thereby enhancing their immunogenicity and prompting pathogenic autoantibodies to form. Taken together, current evidence suggests a positive correlation between elevated levels of lipid peroxidation and disease activity in SLE patients.…”
Section: Introductionmentioning
confidence: 99%
“… 49 Elevated levels of F2 isoprostane have been attributed to tissue oxidation in SLE and therefore can be utilized as a marker to assess the relationship between mitochondrial function and oxidative stress in fatigued patients. 50 These metabolites establish covalent bonds to proteins, thereby enhancing their immunogenicity and prompting pathogenic autoantibodies to form. Taken together, current evidence suggests a positive correlation between elevated levels of lipid peroxidation and disease activity in SLE patients.…”
Section: Introductionmentioning
confidence: 99%
“…Page 5 of 17 12 study Krata et al (2021) found different concentration of 2-Cys-peroxiredoxins, biomarkers of oxidative stress (Krata et al 2018), in different glomerular pathologies, including IgAN and their association with lower glomerular filtration rates. C3 glomerular deposits are detected in most biopsies and complement system activation, which can be done by serum IgA (Hiemstra et al 1987), causes glomerular damage via alternative and lectin pathways (Roos et al 2006;Ohsawa et al 2012).…”
Section: Proteomicsmentioning
confidence: 99%
“…During MN, complement activation and formation of the membrane attack complex C5b-9 target podocytes, causing the release of arachidonic acid, upregulation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) oxidase, and production of large amounts of ROS, leading to podocyte destruction and dysfunction. [42] The ROS generated by oxidative stress can also damage the GBM by triggering lipid peroxidation and degrading type IV collagen in the GBM. Oxygen radical scavengers effectively reduce micronutrient-induced proteinuria in MN.…”
Section: Podocyte Damage In Mnmentioning
confidence: 99%