Oxidative stress and non-enzymatic glycation in IgA nephropathy

Vas, Tibor; Wagner, Zoltán; Jenei, Viktória; Varga, Zoltán; Kovács, Tibor; Wittmann, István; Schinzel, Reinhard; Balla, György; Balla, József; Heidland, A.; Nagy, Judit

doi:10.5414/cnp64343

Cited by 17 publications

(8 citation statements)

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“…IgA nephropathy (IgAN), the most common glomerular disease globally, is a leading cause of CKD and renal failure. A systemic pro-oxidant environment—marked by increased serum levels of lipoperoxide or malondialdehyde and reduced activity of superoxide dismutase, catalase, and glutathione peroxidase, as detected in sera of patients with IgAN—has been associated with disease activity and progression [131,132,133]. Markedly, circulating AOPP have been shown to correlate with proteinuria and be a potent risk marker of decline in the renal function and disease progression since early in the clinical course of IgAN.…”

Section: Oxidative Stress and Clinical Models Of Ckdmentioning

confidence: 99%

Oxidative Stress in the Pathogenesis and Evolution of Chronic Kidney Disease: Untangling Ariadne’s Thread

Duni

Liakopoulos

Roumeliotis

et al. 2019

IJMS

237

177

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Amplification of oxidative stress is present since the early stages of chronic kidney disease (CKD), holding a key position in the pathogenesis of renal failure. Induction of renal pro-oxidant enzymes with excess generation of reactive oxygen species (ROS) and accumulation of dityrosine-containing protein products produced during oxidative stress (advanced oxidation protein products—AOPPs) have been directly linked to podocyte damage, proteinuria, and the development of focal segmental glomerulosclerosis (FSGS) as well as tubulointerstitial fibrosis. Vascular oxidative stress is considered to play a critical role in CKD progression, and ROS are potential mediators of the impaired myogenic responses of afferent renal arterioles in CKD and impaired renal autoregulation. Both oxidative stress and inflammation are CKD hallmarks. Oxidative stress promotes inflammation via formation of proinflammatory oxidized lipids or AOPPs, whereas activation of nuclear factor κB transcription factor in the pro-oxidant milieu promotes the expression of proinflammatory cytokines and recruitment of proinflammatory cells. Accumulating evidence implicates oxidative stress in various clinical models of CKD, including diabetic nephropathy, IgA nephropathy, polycystic kidney disease as well as the cardiorenal syndrome. The scope of this review is to tackle the issue of oxidative stress in CKD in a holistic manner so as to provide a future framework for potential interventions.

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Section: Oxidative Stress and Clinical Models Of Ckdmentioning

confidence: 99%

Oxidative Stress in the Pathogenesis and Evolution of Chronic Kidney Disease: Untangling Ariadne’s Thread

Duni

Liakopoulos

Roumeliotis

et al. 2019

IJMS

237

177

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“…These complexes stimulate cultured human mesangial cells (3)(4)(5), resulting in activation of oxidative stress pathways (6 -8). Evidence of increased oxidative stress has been noted in renal tissue of patients with IgAN (9) as well as in their sera and/or erythrocytes (i.e., increased levels of lipoperoxide or malondialdehyde and reduced activity of superoxide dismutase, catalase, and glutathione peroxidase) (10,11). Moreover, increased serum levels of another marker of oxidative stress, advanced oxidation protein products (AOPPs), have been recently associated with proteinuria and disease progression in patients with IgAN (12).…”

Section: Introductionmentioning

confidence: 99%

Oxidative Stress and Galactose-Deficient IgA1 as Markers of Progression in IgA Nephropathy

Camilla

Suzuki

Daprà

et al. 2011

Clinical Journal of the American Society of Nephrology

106

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Summary Background and objectives We assessed the activation of the oxidative stress pathway in patients with IgA nephropathy (IgAN), while evaluating the classic marker of the disease (galactose-deficient serum IgA1). Design, setting, participants, & measurements Sera from 292 patients and 69 healthy controls from Italy and the United States were assayed for advanced oxidation protein products (AOPPs), free sulfhydryl groups on albumin (SH-Alb), and IgA1 with galactose-deficient hinge-region O-glycans (Gd-IgA1). Gd-IgA1 was detected by binding to Helix aspersa agglutinin (HAA) and expressed as total Gd-IgA1 or as degree of galactose deficiency relative to a standard Gd-IgA1 myeloma protein (%HAA). Results Sera from IgAN patients showed higher levels of Gd-IgA1, %HAA, and AOPPs, but lower levels of SH-Alb in comparison to that from healthy controls. Serum levels of AOPPs significantly correlated with serum Gd-IgA1 and %HAA. The relationship between these biomarkers and clinical features at sampling and during follow-up was assessed in 62 patients with long-term follow-up. AOPPs and %HAA correlated with proteinuria at sampling and independently associated with subsequent proteinuria. Levels of AOPPs correlated with rate of decline in renal function after sampling. The combination of a high level of AOPPs and a high level of %HAA associated with decline in estimated GFR. Conclusions Serum levels of aberrantly glycosylated IgA1 are elevated and oxidative stress pathways are activated in patients with IgAN; the intensity of the stress correlated with expression and progression of the disease. We speculate that oxidative stress may modulate the nephrotoxicity of aberrantly glycosylated IgA1 in IgAN.

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“…Markers of oxidative stress, including increased levels of lipoperoxide or malondialdehyde and reduced activity of superoxide dismutase, catalase and glutathione peroxidase enzymes, have been shown in kidney tissue of patients with IgAN [12]. Similar findings were also described in serum and/or red blood cells of patients with IgAN [13,14]. Additionally, elevated levels of oxidative stress markers, advanced oxidation protein products (AOPPs), have been reported to be associated with proteinuria and disease progression in IgAN patients [15,16].…”

Section: Introductionmentioning

confidence: 66%

Oxidative stress and macrophage infiltration in IgA nephropathy

et al. 2021

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Background The aim of this study was to evaluate the interactions among serum levels of galactose-deficient IgA1 (Gd-IgA1), oxidative stress and macrophage infiltration and their clinical correlates in patients with IgA Nephropathy (IgAN). Methods A total of 47 patients with biopsy-proven primary IgAN, aged between 16 and 79 years, with a follow-up period ≥ 1 year or who showed progression to end stage kidney disease (ESKD) regardless the duration of follow-up were included. Study endpoint was the progression to ESKD. Serum Gd-IgA1 and advanced oxidation protein product (AOPP) levels were measured using ELISA assays. Kidney biopsies were evaluated according to the Oxford MEST-C scoring, with C4d and CD68 staining. Results Seventeen patients (36%) experienced ESKD during a median follow-up time of 6 years (IQR 3.7-7.5). Serum AOPP levels were correlated with the intensity of glomerular C3 deposition (r = 0.325, p = 0.026), glomerular (r = 0.423, p = 0.003) and interstitial CD68 + cell count (r = 0.298, p = 0.042) and Gd-IgA1 levels (r = 0.289, p = 0.049). Serum Gd-IgA1 levels were correlated with the intensity of C3 deposition (r = 0.447, p = 0.002). eGFR at biopsy (adjusted HR (aHR) 0.979 p = 0.011), and E score (aHR, 8.305, p = 0.001) were associated with progression to ESKD in multivariate analysis. 5-year ESKD-free survival rate was significantly lower in patients with higher E score compared to patients with E score 0 [p = 0.021]. Conclusions An increased number of macrophages in the glomerular and tubulointerstitial area may play a role in oxidative stress and complement system activation. Endocapillary hypercellularity is a predictive factor for poor prognosis in IgAN.

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Oxidative stress and non-enzymatic glycation in IgA nephropathy

Cited by 17 publications

References 0 publications

Oxidative Stress in the Pathogenesis and Evolution of Chronic Kidney Disease: Untangling Ariadne’s Thread

Oxidative Stress in the Pathogenesis and Evolution of Chronic Kidney Disease: Untangling Ariadne’s Thread

Oxidative Stress and Galactose-Deficient IgA1 as Markers of Progression in IgA Nephropathy

Oxidative stress and macrophage infiltration in IgA nephropathy

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