From Oxidative Stress to Genomic Instability: A Comparative Overview of Hemodialysis and Peritoneal Dialysis
DNA damage in Dialysis patients
Keywords:
Chronic kidney disease, hemodialysis , peritoneal dialysis, DNA damage ,genomic instability.
Abstract
Chronic kidney disease (CKD) is linked to elevated oxidative stress (OS) due to impaired renal function, inflammation, and uremic toxin accumulation. In end-stage renal disease, renal replacement therapies—hemodialysis (HD) and peritoneal dialysis (PD)—further increase oxidative burden, contributing to DNA damage and genomic instability. HD triggers acute oxidative bursts through blood contact with bio-incompatible membranes and complement activation, whereas PD causes sustained oxidative stress via continuous exposure to glucose-based dialysate and its degradation products. Excess reactive oxygen species induce DNA base oxidation, strand breaks, chromosomal alterations, and telomere shortening. Biomarkers such as 8-hydroxy-2′-deoxyguanosine (8-OHdG), comet assay, and micronucleus test consistently show higher DNA damage in individuals undergoing dialysis. Impaired DNA repair mechanisms and polymorphisms in base excision repair pathways exacerbate genomic instability. Long-term consequences include increased risk of cardiovascular disease, cancer, and cellular senescence. Preventive strategies, including antioxidant supplementation, biocompatible or vitamin E-coated membranes, lifestyle modifications, and optimization of dialysis modality and dialysate quality, may mitigate genotoxic risk. This review compares HD and PD in relation to oxidative DNA damage, highlighting mechanisms, biomarker evidence, and current preventive approaches
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Published
2026-03-02
How to Cite
1.
John F, Pillai A, John F. From Oxidative Stress to Genomic Instability: A Comparative Overview of Hemodialysis and Peritoneal Dialysis. jms [Internet]. 2026Mar.2 [cited 2026Aug.25];29(1):3-25. Available from: https://jmsskims.org/index.php/jms/article/view/1479
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Review Articles
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