Background <p>The long-term renal effects of electronic cigarette (e-cigarette) use remain poorly understood, despite its global rise as a nicotine delivery system. This study investigates the association between e-cigarette use and chronic kidney disease (CKD), with emphasis on dose-response relationships, subgroup heterogeneity, and adjustment for cigarette smoking.</p> Methods <p>We analyzed data from 872 adults in NHANES (2017–2020). E-cigarette use was categorized by self-reported frequency (non-users, 1–2 days/week, ≥ 3 days/week). CKD was defined as urinary albumin-to-creatinine ratio ≥ 30&#xa0;mg/g. Weighted multivariable logistic regression models adjusted for age, gender, race, BMI, diabetes, hypertension, and current cigarette smoking. Propensity score matching (PSM, 1:1) balanced baseline covariates, including current smoking. Dose-response trends were assessed via restricted cubic splines (RCS).</p> Results <p>Among 188 e-cigarette users and 684 non-users, users were significantly younger and had higher serum cotinine. In fully adjusted models (Model 3), e-cigarette use was associated with a 2.50-fold higher odds of CKD (95% CI: 1.80–3.48, <i>P</i> &lt; 0.001). A significant dose-response relationship existed: adjusted ORs for CKD were 1.80 (95% CI: 1.20–2.70) for 1–2 days/week and 2.60 (95% CI: 1.70–4.00) for ≥ 3 days/week use (P-trend = 0.002). This association was significantly stronger in non-diabetics (OR = 2.40, 95% CI: 1.65–3.50) vs. diabetics (P-interaction = 0.032) and in current smokers (OR = 2.35, 95% CI: 1.55–3.56) vs. non-smokers (P-interaction = 0.021). Sensitivity analyses confirmed robustness: PSM yielded OR = 1.89 (95% CI: 1.18–3.01, <i>P</i> = 0.009); excluding dual users yielded OR = 1.98 (95% CI: 1.28–3.06, <i>P</i> = 0.003); and cotinine-based exposure yielded OR = 2.25 (95% CI: 1.43–3.54, <i>P</i> = 0.001).</p> Conclusion <p>E-cigarette use is independently associated with CKD in a dose-dependent manner, particularly among non-diabetic individuals. Notably, NHANES data limitations include lack of past e-cigarette use or smoking history records, which may introduce residual confounding. These findings highlight vaping as a modifiable risk factor for kidney disease, urging targeted public health interventions.</p>

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Electronic cigarette use and risk of chronic kidney disease: a dose-response analysis with propensity score matching in a nationally representative cohort

  • Song Li,
  • Ruoxuan Liu,
  • Jianhua Zhang,
  • Weidong Pei,
  • Junqing Hou

摘要

Background

The long-term renal effects of electronic cigarette (e-cigarette) use remain poorly understood, despite its global rise as a nicotine delivery system. This study investigates the association between e-cigarette use and chronic kidney disease (CKD), with emphasis on dose-response relationships, subgroup heterogeneity, and adjustment for cigarette smoking.

Methods

We analyzed data from 872 adults in NHANES (2017–2020). E-cigarette use was categorized by self-reported frequency (non-users, 1–2 days/week, ≥ 3 days/week). CKD was defined as urinary albumin-to-creatinine ratio ≥ 30 mg/g. Weighted multivariable logistic regression models adjusted for age, gender, race, BMI, diabetes, hypertension, and current cigarette smoking. Propensity score matching (PSM, 1:1) balanced baseline covariates, including current smoking. Dose-response trends were assessed via restricted cubic splines (RCS).

Results

Among 188 e-cigarette users and 684 non-users, users were significantly younger and had higher serum cotinine. In fully adjusted models (Model 3), e-cigarette use was associated with a 2.50-fold higher odds of CKD (95% CI: 1.80–3.48, P < 0.001). A significant dose-response relationship existed: adjusted ORs for CKD were 1.80 (95% CI: 1.20–2.70) for 1–2 days/week and 2.60 (95% CI: 1.70–4.00) for ≥ 3 days/week use (P-trend = 0.002). This association was significantly stronger in non-diabetics (OR = 2.40, 95% CI: 1.65–3.50) vs. diabetics (P-interaction = 0.032) and in current smokers (OR = 2.35, 95% CI: 1.55–3.56) vs. non-smokers (P-interaction = 0.021). Sensitivity analyses confirmed robustness: PSM yielded OR = 1.89 (95% CI: 1.18–3.01, P = 0.009); excluding dual users yielded OR = 1.98 (95% CI: 1.28–3.06, P = 0.003); and cotinine-based exposure yielded OR = 2.25 (95% CI: 1.43–3.54, P = 0.001).

Conclusion

E-cigarette use is independently associated with CKD in a dose-dependent manner, particularly among non-diabetic individuals. Notably, NHANES data limitations include lack of past e-cigarette use or smoking history records, which may introduce residual confounding. These findings highlight vaping as a modifiable risk factor for kidney disease, urging targeted public health interventions.