Oxidative Stress and Inflammation in Kidney Diseases

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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