DNA Damage Analysis with Oxidative Stress Index and 8-Hydroxy 2'-Deoxy Guanosine Level in Patients Developing Contrast Nephropathy After Coronary Angiography
ANATOLIAN JOURNAL OF CARDIOLOGY, 2026 (SCI-Expanded, Scopus, TRDizin)
- Yayın Türü: Makale / Tam Makale
- Basım Tarihi: 2026
- Doi Numarası: 10.14744/anatoljcardiol.2026.6059
- Dergi Adı: ANATOLIAN JOURNAL OF CARDIOLOGY
- Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, CINAHL, EMBASE, MEDLINE, Directory of Open Access Journals, TR DİZİN (ULAKBİM), Academic Search Ultimate (EBSCO), Biomedical Reference Collection: Corporate Edition (EBSCO), Health Research Premium Collection (ProQuest)
- Eskişehir Osmangazi Üniversitesi Adresli: Evet
Özet
Background: Contrast-induced nephropathy (CIN) is a common cause of hospital-acquired acute kidney injury, and oxidative stress is thought to play a crucial role in its pathogenesis. Evidence regarding DNA damage after contrast exposure remains limited. This study aimed to evaluate oxidative stress and DNA damage in patients developing CIN by assessing total antioxidant status (TAS), total oxidant status (TOS), oxidative stress index (OSI), and 8-hydroxy-2 '-deoxyguanosine (8-OHdG) levels as well as clinical factors associated with CIN. Methods: A total of 191 patients undergoing coronary angiography were prospectively evaluated. Blood samples were obtained before the procedure and at 72 hours afterward. CIN was defined as >= 25% or >= 0.5 mg/dL increase in serum creatinine. Patients were classified into CIN (n = 85) and control groups (n = 106). Results: Advanced age and heart failure were the strongest predictors of CIN. Hypertension, anemia, chronic kidney disease, and hyperuricemia were also more frequent in the CIN group. After angiography, TAS increased and TOS decreased in both groups; however, the reduction in TOS reached significance only in controls. Post-procedure TAS levels were higher in the CIN group (P = .033). Baseline 8-OHdG levels were higher in patients who later developed CIN, whereas the post-procedure decline in 8-OHdG was significant only in controls (P = .02). No significant differences in TOS, OSI, or post-procedure 8-OHdG were observed between groups. Conclusion: This study isamongthefirstto investigate DNAdamage in CIN using 8-OHdG levels. The higher baseline DNA damage in CIN patients and the greater reduction in controls suggest a possible link between DNA injury and CIN. Oxidative stress markers did not differ significantly, which may reflect the use of modern low-toxicity contrast agents or the involvement of multifactorial mechanisms. Further studies are needed to clarify the role of oxidative stress and DNA damage in CIN.