Dose–response associations between dietary antioxidant capacity and prevalent chronic kidney disease: NHANES 2003–2018

Background Oxidative stress plays an important role in the development and progression of chronic kidney disease (CKD). Dietary antioxidants may help counteract oxidative damage; however, the dose–response associations between overall dietary antioxidant capacity, assessed by the composite dietary antioxidant index (CDAI), and prevalent CKD remain unclear. Methods Data were obtained from the National Health and Nutrition Examination Survey (NHANES) 2003–2018. Adults aged ≥ 45 years were included in this cross-sectional analysis. Dietary intakes of antioxidant nutrients (vitamins A, C, and E, selenium, zinc, carotenoids, and niacin) were assessed using 24-hour dietary recall data, and the CDAI was calculated based on energy-adjusted standardized intakes. Survey-weighted multivariable logistic regression models were applied to examine associations between continuous antioxidant exposures and quartiles of antioxidant intake and prevalent CKD. Restricted cubic spline models were used to explore potential nonlinear dose–response associations. Results Compared with participants without CKD, those with CKD had lower intakes of vitamin C, vitamin E, selenium, zinc, niacin, as well as lower CDAI values. After full adjustment for potential confounders, higher intake categories of vitamin E (OR = 0.50, 95% CI: 0.43–0.80), selenium (OR = 0.58, 95% CI: 0.44–0.78), niacin (OR = 0.64, 95% CI: 0.47–0.88), zinc (OR = 0.60, 95% CI: 0.49–0.84), and CDAI (OR = 0.73, 95% CI: 0.55–0.97) were associated with lower odds of prevalent CKD. Restricted cubic spline analyses suggested nonlinear associations, with lower odds of prevalent CKD observed at higher intake levels, followed by a plateau. Conclusion Higher overall dietary antioxidant capacity was inversely associated with prevalent CKD, with evidence of nonlinear dose–response patterns. These findings suggest that the associations between antioxidant intake and CKD prevalence may be more pronounced at higher intake levels. Given the cross-sectional design, causal inference cannot be established, and prospective studies are warranted to further clarify these relationships.