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Antioxidants
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Antioxidants in Chronic and End-Stage Kidney Disease: Defining Biological and...
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Antioxidants in Chronic and End-Stage Kidney Disease: Defining Biological and Clinical Plausibility

A Special Issue of Antioxidants (ISSN 2076-3921) belonging to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 20 February 2027 | Viewed by 1166

Editors

Dr. Stefanos Roumeliotis

E-Mail Website
Guest Editor
2nd Department of Nephrology, Medical School, AHEPA Hospital, Aristotle University, 54636 Thessaloniki, Greece
Interests: CKD; hemodialysis; oxidative stress; vitamin K; diabetic nephropathy; vascular calcification; CVD; matrix GLA protein
Special Issues, Collections and Topics in MDPI journals
Dr. Vassilios Liakopoulos

E-Mail Website
Guest Editor
2nd Department of Nephrology, AHEPA Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece
Interests: chronic kidney disease; cardiovascular disease; vascular calcification; diabetes mellitus; hemodialysis; peritoneal dialysis
Special Issues, Collections and Topics in MDPI journals

Special Issue Information

Dear Colleagues,

During recent years, oxidative stress has been at the center of scientific research in both chronic (CKD) and end-stage kidney disease (ESKD) patients. It has emerged as a novel risk factor for cardiovascular disease. These populations exhibit a marked deficiency of various antioxidants due to dietary restrictions, the intestine's incapacity to absorb vitamins and minerals, and the loss of antioxidants through dialysis membranes, which leads to increased oxidative stress.

Although it is known that oxidative stress occurs early in chronic kidney stage and is progressively increased with deterioration of kidney function, several questions remain unanswered regarding the possible clinical role of various exogenous supplemented antioxidants and the biological role of endogenous antioxidants, including Vitamins (B, C, D, E, K), N-acetylcysteine, Superoxide dismutase, catalase and glutathione. The data regarding the potential beneficial effects of antioxidants on diseases and clinical outcomes in these populations are scarce and primarily derived from experimental studies. Large, clinical studies in CKD and ESKD cohorts are still lacking.

We invite research (in vitro, in vivo, and clinical studies) and review articles to this Special Issue, on any of these topics: pathophysiology of antioxidants in CKD and ESKD, regulation, clinical roles of antioxidants in cardiovascular disease, longevity, kidney function, cognitive function, anemia, vascular calcification, and calcium-phosphate balance.

Dr. Stefanos Roumeliotis
Dr. Vassilios Liakopoulos
Guest Editors

Manuscript Submission Information

Manuscripts should be submitted online at www.mdpi.com by registering and logging in to this website. Once you are registered, click here to go to the submission form. Manuscripts can be submitted until the deadline. All submissions that pass pre-check are peer-reviewed. Accepted papers will be published continuously in the journal (as soon as accepted) and will be listed together on the special issue website. Research articles, review articles as well as short communications are invited. For planned papers, a title and short abstract (about 250 words) can be sent to the Editorial Office for assessment.

Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Antioxidants is an international peer-reviewed open access monthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2900 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • CKD
  • ESKD
  • cardiovascular disease
  • catalase
  • chronic kidney disease
  • end stage kidney disease
  • N-acetylcysteine
  • superoxide dismutase
  • vascular calcification
  • vitamin C
  • vitamin E

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Published Papers (2 papers)

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Research

17 pages, 4728 KB  
Article
N-Acetylcysteine Protects HPMCs from High-Glucose-Induced Oxidative DNA Damage
by Tina Oberacker, Tobias Leibold, Adrian Salega, Leonie Kraft, Moritz Schanz, Markus Ketteler, Jörg Latus and Severin Schricker
Antioxidants 2026, 15(8), 1032; https://doi.org/10.3390/antiox15081032 - 19 Aug 2026
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Abstract
Peritoneal dialysis (PD) is an effective renal replacement therapy; however, its long-term use is limited by the detrimental effects of glucose-based PD fluids on the peritoneal membrane, contributing to fibrosis and ultrafiltration failure. Previous studies have demonstrated that high-glucose exposure promotes oxidative DNA [...] Read more.
Peritoneal dialysis (PD) is an effective renal replacement therapy; however, its long-term use is limited by the detrimental effects of glucose-based PD fluids on the peritoneal membrane, contributing to fibrosis and ultrafiltration failure. Previous studies have demonstrated that high-glucose exposure promotes oxidative DNA damage through upregulation of thioredoxin-interacting protein (TXNIP) expression, resulting in reduced thioredoxin (Trx) activity. This study investigated strategies to reduce oxidative stress in human peritoneal mesothelial cells exposed to high glucose concentrations. TXNIP expression, Trx activity, intracellular oxidative stress levels, and oxidative DNA damage were analyzed. High-glucose exposure caused a dose-dependent increase in TXNIP expression, a 5–15% reduction in Trx activity, and increased intracellular oxidative stress levels and oxidative DNA damage. Pre-treatment with the ROS scavenger N-acetylcysteine (NAC) reduced these effects. These findings demonstrate that glucose-induced TXNIP upregulation disrupts cellular redox homeostasis, resulting in increased intracellular oxidative stress and oxidative damage. Antioxidant compounds may therefore represent promising therapeutic strategies to protect the peritoneal membrane and improve long-term outcomes in PD. Full article
(This article belongs to the Special Issue Antioxidants in Chronic and End-Stage Kidney Disease: Defining Biological and Clinical Plausibility)
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15 pages, 2649 KB  
Article
The Nephroprotective Efficacy of Omega-3 Fatty Acids Against Streptozotocin-Induced Diabetic Renal Injury: A Biochemical, Histopathological and Ultrastructural Study
by Emrah Zayman, Eda Nur Özsoy, Mehmet Erman Erdemli, Zeynep Erdemli, Nilüfer Bulut, Feyza İnceoğlu and Mehmet Gül
Antioxidants 2026, 15(8), 975; https://doi.org/10.3390/antiox15080975 - 6 Aug 2026
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Abstract
The present study was designed to evaluate the structural and biochemical efficacy of Omega-3 fatty acids in preventing renal injury in streptozotocin (STZ)-induced diabetic kidney injury and to correlate systemic oxidative stress parameters with histological and ultrastructural parameters. Twenty-eight male Wistar Albino rats [...] Read more.
The present study was designed to evaluate the structural and biochemical efficacy of Omega-3 fatty acids in preventing renal injury in streptozotocin (STZ)-induced diabetic kidney injury and to correlate systemic oxidative stress parameters with histological and ultrastructural parameters. Twenty-eight male Wistar Albino rats were randomly divided into four groups (n = 7) as follows: Control, Omega-3 (500 mg/kg, orally), Diabetes Mellitus (DM; 50 mg/kg STZ, i.p.), and DM+Omega-3 (STZ, followed by 500 mg/kg Omega-3 for 42 days). Biochemical analysis of renal function (blood urea nitrogen (BUN) and creatinine) and oxidative status (malondialdehyde (MDA), glutathione (GSH), superoxide dismutase (SOD), catalase (CAT), total antioxidant status (TAS), total oxidant status (TOS) and oxidative stress index (OSI)) was measured by ELISA. Histopathological scoring and Caspase-3 staining were performed by Hematoxylin and Eosin (H&E) and immunohistochemically, respectively. Transmission Electron Microscopy (TEM) was used to examine the renal tissues. Our results showed that the DM group presented with severe hyperglycemia, uremia, and a significant oxidative shift, as evidenced by increased MDA/TOS levels and depleted antioxidant defenses. Light microscopy showed extensive glomerular damage, tubular degeneration and inflammatory infiltration in the kidneys of diabetic rats. Immunohistochemical analysis revealed strong Caspase-3 expression in the tubular and glomerular compartments. TEM showed severe podocyte effacement and damage to the glomerular basement membrane (GBM). Notably, Omega-3 supplementation significantly reversed renal dysfunction, restored the pro-oxidant/antioxidant balance and reduced histopathological injury scores. Moreover, Omega-3 treatment efficiently blocked Caspase-3-mediated apoptotic signaling and preserved the ultrastructural integrity of the glomerular filtration barrier (GFB) and tubular mitochondria. Our results demonstrate the potent nephroprotective effects of Omega-3 fatty acids in reducing oxidative stress, preventing programmed cell death and maintaining the stability of the renal parenchyma’s microarchitecture. These findings suggest that Omega-3 fatty acids could be an effective adjuvant therapeutic agent for the management of diabetic nephropathy. Full article
(This article belongs to the Special Issue Antioxidants in Chronic and End-Stage Kidney Disease: Defining Biological and Clinical Plausibility)
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