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 December 2026 | Viewed by 7492

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 (4 papers)

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Research

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15 pages, 2612 KB  
Article
Dynamic Regulation of Ferroptosis in a Neonatal Rat Model of Postnatal Hypoxia-Induced Acute Kidney Injury
by Tzu-Hao Liu, Bo-Hau Chen, Guan-Hong Lin, Hsin-Hung Chen, Hsiang-Chin Chiu, Chih-Chieh Yang, Yi-Ting Chu, Ching-Ming Lin and Wen-Hsien Lu
Antioxidants 2026, 15(5), 582; https://doi.org/10.3390/antiox15050582 - 4 May 2026
Viewed by 340
Abstract
Hypoxia during the postnatal period represents a significant risk factor for renal injury in neonates, yet the molecular mechanisms linking oxygen deprivation to kidney damage remain unclear. In this study, we explored whether ferroptosis serves as a key mediator in hypoxia-induced acute kidney [...] Read more.
Hypoxia during the postnatal period represents a significant risk factor for renal injury in neonates, yet the molecular mechanisms linking oxygen deprivation to kidney damage remain unclear. In this study, we explored whether ferroptosis serves as a key mediator in hypoxia-induced acute kidney injury (AKI). Using a neonatal rat model, we demonstrated that hypoxic exposure disrupts iron homeostasis, leading to iron accumulation and excessive lipid peroxidation in renal tissues. These alterations were associated with marked tubular injury, glomerular damage, and progressive fibrotic remodeling. Importantly, reoxygenation attenuated ferroptosis-related signaling pathways and improved renal structural and functional outcomes, although incomplete recovery was observed in fibrotic changes. Our findings suggest that ferroptosis is not only involved in the initiation of hypoxia-induced renal injury but may also contribute to its progression toward chronic kidney pathology. Targeting ferroptosis and iron metabolism may therefore represent a promising strategy for preventing or treating neonatal hypoxia-related AKI. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Kidney Diseases)
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Review

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15 pages, 4094 KB  
Review
Sialic Acids in Kidney Disease: Immune Regulation, Complement Activation and Glomerular Injury
by Agnese Spennacchio, Gianluca Caridi, Carolina Bigatti, Gabriele Gaggero, Katia Mazzocco, Maria Teresa Gambaudo, Roberta Musso, Valerio Gaetano Vellone, Andrea Angeletti and Xhuliana Kajana
Antioxidants 2026, 15(5), 626; https://doi.org/10.3390/antiox15050626 - 14 May 2026
Viewed by 197
Abstract
Oxidative stress and inflammation are key drivers of kidney injury and disease progression. In this context, the role of sialic acids emerged as a critical regulatory layer linking redox imbalance, immune activation, and tissue damage. Sialic acids are terminal negatively charged residues that [...] Read more.
Oxidative stress and inflammation are key drivers of kidney injury and disease progression. In this context, the role of sialic acids emerged as a critical regulatory layer linking redox imbalance, immune activation, and tissue damage. Sialic acids are terminal negatively charged residues that regulate complement activity, immune cell signaling, and the structural integrity of the glomerular filtration barrier. Alterations in sialylation, resulting from impaired biosynthesis or increased sialidase activity, disrupt immune homeostasis, enhance inflammatory responses, and promote complement-mediated injury. In the kidney, these mechanisms contribute to podocyte dysfunction, glomerular inflammation, and fibrosis and are implicated in glomerulopathies, transplantation, and plasma cell dyscrasias. Emerging evidence also highlights the therapeutic potential of targeting sialic acid metabolism through inhibition of desialylation or restoration of sialylation pathways. Overall, sialic acids represent dynamic modulators at the intersection of oxidative stress and immunity, offering novel opportunities for biomarker development and mechanism-based therapies in kidney disease. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Kidney Diseases)
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52 pages, 1669 KB  
Review
Oxidative Stress-Driven Mechanisms and Biomarkers of Drug-Induced Nephrotoxicity: Translational Insights and Therapeutic Implications
by Rizwan Ahamad, Nida Mubin, Mohammed Alnukhali, Mohd Akhtar, Mohd Aqil, Mohd Mujeeb and Anis Ahmad
Antioxidants 2026, 15(4), 412; https://doi.org/10.3390/antiox15040412 - 25 Mar 2026
Cited by 1 | Viewed by 1189
Abstract
Drug-induced kidney injury remains a major clinical challenge associated with diverse therapeutic agents and is an important cause of acute kidney injury, chronic renal dysfunction, and treatment-related morbidity. Growing evidence indicates that nephrotoxicity caused by anticancer, immunosuppressive, and anti-infective drugs is strongly driven [...] Read more.
Drug-induced kidney injury remains a major clinical challenge associated with diverse therapeutic agents and is an important cause of acute kidney injury, chronic renal dysfunction, and treatment-related morbidity. Growing evidence indicates that nephrotoxicity caused by anticancer, immunosuppressive, and anti-infective drugs is strongly driven by oxidative stress and redox homeostasis disruption. Excessive production of reactive oxygen species (ROS) in renal tubular cells overwhelms endogenous antioxidant defenses and triggers mitochondrial dysfunction, inflammatory signaling, and activation of stress-responsive pathways that culminate in tubular injury and renal functional decline. These processes promote apoptosis, necrosis, microvascular injury, and a reduction in the glomerular filtration rate, while dysregulation of redox-sensitive pathways involved in cell survival and repair further heightens renal vulnerability. This review summarizes current mechanistic insights into oxidative stress-mediated pathways of drug-induced nephrotoxicity, with emphasis on their translational relevance. In addition, it discusses emerging biomarkers for early detection and highlights recent advances in antioxidant-based and redox-modulating strategies that may help prevent renal injury and preserve kidney function. Full article
(This article belongs to the Special Issue Oxidative Stress and Inflammation in Kidney Diseases)
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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
Cited by 3 | Viewed by 5084
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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