Oxidative Stress in Childhood Nephrotic Syndrome: A Narrative Review From Mechanisms to Clinical Implications

Pediatric nephrotic syndrome (NS) is a complex renal disorder characterized by proteinuria, hypoalbuminemia, edema, hyperlipidemia, and risk of chronic kidney disease. Oxidative stress (OS) is increasingly recognized as a central mechanism driving glomerular and tubular injury, inflammation, and progression of kidney injury. The aim of this review was to summarize the evidence on the role of OS in the pathophysiology and clinical implications of NS. A narrative review was conducted using PubMed, Scopus, Web of Science, and Google Scholar (2000-2025), focusing on recent studies. Keywords included "nephrotic syndrome," "oxidative stress," "reactive oxygen species," and "antioxidant enzymes." Data were synthesized to identify key oxidative mechanisms, biomarkers, and clinical relevance. The NS is characterized by excessive reactive oxygen species production via NADPH oxidase, xanthine oxidase, and mitochondrial pathways, accompanied by impaired antioxidant defenses such as glutathione and superoxide dismutase. Elevated malondialdehyde and advanced oxidation protein products correlate with proteinuria, podocyte injury, and steroid resistance. Reduced antioxidants indicate diminished cellular defense and redox imbalance. The OS contributes to podocyte effacement, tubulointerstitial apoptosis, fibrosis, and progressive nephron loss. Monitoring OS biomarkers can improve assessment of disease activity, predict relapse or steroid resistance, and guide possible antioxidant interventions.