Oxidative Stress and Inflammation in Kidney Diseases

A special issue of Antioxidants (ISSN 2076-3921). This special issue belongs to the section "Health Outcomes of Antioxidants and Oxidative Stress".

Deadline for manuscript submissions: 31 March 2026 | Viewed by 2300

Special Issue Editor


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Guest Editor
Unit of Nephrology, Dialysis and Transplantation and Laboratory of Molecular Nephrology, IRCCS Istituto Giannina Gaslini, 16147 Genoa, Italy
Interests: chronic renal failure; clinical nephrology; renal physiology; glomerulonephritis; diabetic nephropathy; renal disease; oxidative stress; kidney transplantation

Special Issue Information

Dear Colleagues,

Oxidative stress and inflammation are central mechanisms in the initiation and progression of kidney diseases. Excessive production of reactive oxygen species (ROS) and reactive nitrogen species (RNS) disrupts cellular redox balance, leading to lipid peroxidation, protein modification, DNA damage, and ultimately cell death. Beyond their direct cytotoxicity, ROS also amplify inflammatory pathways, creating a vicious cycle that promotes tissue injury and loss of renal function.

Increasing attention is being paid to the close interplay between oxidative stress and the immune system. Innate immunity, through leukocyte activation and complement, and adaptive responses, including humoral mechanisms, are recognized as key amplifiers of glomerular damage. This crosstalk between redox imbalance and immune activation drives persistent inflammation, which in turn leads to fibrosis. Importantly, fibrosis represents the final and largely irreversible outcome of many kidney diseases, while the upstream pathways that fuel oxidative stress and inflammation remain, at least in part, potentially reversible if identified and targeted early. This convergence of oxidative stress and immune activation is increasingly recognized as a major determinant of disease progression in all fields of nephrology, including chronic kidney disease (CKD), diabetic nephropathy, glomerulonephritis, and kidney transplant.

This Special Issue aims to collect original research and reviews exploring the mechanisms, biomarkers, and therapeutic approaches targeting oxidative stress, immunity, and inflammation in kidney diseases. We welcome contributions from basic science, translational research, and clinical studies.

Dr. Andrea Angeletti
Guest Editor

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Keywords

  • chronic renal failure
  • clinical nephrology
  • renal physiology
  • glomerulonephritis
  • diabetic nephropathy
  • renal disease
  • oxidative stress
  • kidney transplantation

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Published Papers (1 paper)

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Review

20 pages, 1294 KB  
Review
Stress Pathways in Chronic Kidney Disease: Linking Cortisol, Oxidative Stress, and Inflammation
by Maria Motrenikova, Krasimir Boyanov, Neli Bojinova and Anelia Bivolarska
Antioxidants 2025, 14(10), 1259; https://doi.org/10.3390/antiox14101259 - 20 Oct 2025
Viewed by 2123
Abstract
This review aims to synthesize current evidence on the role of chronic stress and hypothalamic–pituitary–adrenal (HPA) axis dysregulation in the pathogenesis of chronic kidney disease (CKD). The focus is on the interplay between cortisol, oxidative stress, inflammation, and metabolic risk factors within the [...] Read more.
This review aims to synthesize current evidence on the role of chronic stress and hypothalamic–pituitary–adrenal (HPA) axis dysregulation in the pathogenesis of chronic kidney disease (CKD). The focus is on the interplay between cortisol, oxidative stress, inflammation, and metabolic risk factors within the psycho-neuro-endocrine-immune (PNEI) system. CKD is a multifactorial disease characterized by oxidative stress, chronic low-grade inflammation, and neuroendocrine imbalance. These processes interact to accelerate renal injury and systemic complications. Pro-inflammatory mediators such as tumor necrosis factor-alpha (TNF-α), interleukin-1 beta (IL-1β), and interleukin-6 (IL-6), together with oxidative stress markers including malondialdehyde (MDA), advanced oxidation protein products (AOPPs), and 8-hydroxy-2′-deoxyguanosine (8-OHdG), are strongly associated with disease progression. Altered cortisol dynamics—assessed in serum, saliva, and hair—further reflect chronic HPA activation and contribute to immune dysfunction, metabolic disturbances, and cardiovascular risk. By integrating experimental and clinical findings, this review highlights how stress-induced dysregulation of the PNEI system amplifies CKD progression. Understanding these interconnected mechanisms underscores the potential of combining oxidative, inflammatory, and neuroendocrine biomarkers for improved risk stratification and targeted therapeutic interventions. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Kidney Diseases)
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