Articles
| Open Access |
https://doi.org/10.55640/
OXIDATIVE STRESS IN CHRONIC KIDNEY DISEASE: MOLECULAR MECHANISMS, GENETIC DETERMINANTS, AND CLINICAL IMPLICATIONS
Sapayeva Z.A. , ¹Department of Internal Medicine and Dermatovenerology, Urgench State Medical Institute, Uzbekistan Karimova N.O.² , ²Department of Family Medicine, Urgench State Medical Institute, UzbekistanAbstract
Background: Chronic kidney disease (CKD) is characterized by progressive renal dysfunction and high morbidity, especially due to cardiovascular complications. Oxidative stress (OS), defined as imbalance between reactive oxygen/nitrogen species and antioxidant defenses, is increasingly recognized as a central pathogenic mechanism in CKD.
Objectives: This review critically evaluates evidence on molecular mechanisms, genetic determinants, clinical consequences, biomarkers, and therapeutic strategies targeting OS in CKD.
Methods: Literature from 2018–2025 was systematically reviewed using PubMed, Scopus, and Web of Science, focusing on reactive oxygen/nitrogen species, mitochondrial dysfunction, NADPH oxidases, uremic toxins, genetic polymorphisms, oxidative biomarkers, and antioxidant therapies.
Results: OS in CKD arises from mitochondrial dysfunction, eNOS uncoupling, NADPH oxidase activation, and accumulation of uremic toxins. Genetic variants in HLA, APOL1, and Nrf2 pathways influence susceptibility. OS promotes renal fibrosis, cardiovascular disease, anemia, and chronic inflammation. Biomarkers of lipid, protein, and DNA oxidation correlate with disease severity. Antioxidant and pharmacological interventions yield mixed clinical efficacy.
Conclusion: OS is a pivotal mediator of CKD progression and systemic complications. Integrating molecular and genetic insights into clinical practice may improve early diagnosis and guide targeted therapies.
Keywords
chronic kidney disease, oxidative stress, mitochondria, genetic polymorphism, cardiovascular complications, antioxidant therapy.
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