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Purpose <p>Biological aging was found to be associated with the higher prevalence of several diseases, but it is unclear in the prevalence of chronic kidney disease (CKD). This study investigated the effect of aging phenotypes, characterized by PhenoAge (PA), Klemera–Doubal Method (KDM), allostatic load (AL), homeostatic dysregulation (HD), and telomere length (TL) on CKD from the perspective of both clinical relevance and genetic susceptibility.</p> Method <p>From the clinical perspective, the study analyzed data from 7482 participants in the National Health and Nutrition Examination Survey 2006–2015. Logistic regression and restricted cubic spline (RCS) models were employed to evaluate both linear and nonlinear associations between aging phenotypes and the prevalence of CKD. From the genetic susceptibility perspective, Mendelian randomization analyses were conducted to establish causality between telomere length and CKD outcomes.</p> Result <p>Multivariate logistic regression revealed that PA, KDM, AL, and HD were associated with an increased prevalence of CKD, with PA remaining a significant risk factor after adjusting for covariates (OR = 1.0714, 95% CI = 1.0558–1.0872). RCS curves further indicated a nonlinear relationship between PA, AL, HD, and CKD prevalence (<i>P</i> &lt; 0.001). Besides, inflammation indicators were found to mediate this association. Mendelian randomization analysis demonstrated a significant causal relationship between telomere length and CKD risk across multiple datasets. The results were as follows: Discovery Group (OR = 0.892, 95% CI = 0.832–0.956, <i>P</i> = 0.001) and (OR = 0.896, 95% CI = 0.836–0.961, <i>P</i> = 0.002); Replication Group (OR = 0.872, 95% CI = 0.808–0.940, <i>P</i> &lt; 0.001) and (OR = 0.909, 95% CI = 0.854–0.967, <i>P</i> = 0.003).</p> Conclusion <p>These findings underscore the strong connection between aging phenotypes and CKD risk, with the mediated effect of inflammatory markers, contributing to the early disease prevention and therapeutic strategy development.</p>

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Association between aging phenotypes and chronic kidney disease: evidence from the NHANES and Mendelian randomization

  • 期刊论文

  • 发表日期：

    2025年4月10日

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  • Yukai Zhang,
  • Chenwei Zhang,
  • Peiyun He,
  • Xinling Tian,
  • Yuzhe Kong,
  • Yun Zhou

摘要

Purpose

Biological aging was found to be associated with the higher prevalence of several diseases, but it is unclear in the prevalence of chronic kidney disease (CKD). This study investigated the effect of aging phenotypes, characterized by PhenoAge (PA), Klemera–Doubal Method (KDM), allostatic load (AL), homeostatic dysregulation (HD), and telomere length (TL) on CKD from the perspective of both clinical relevance and genetic susceptibility.

Method

From the clinical perspective, the study analyzed data from 7482 participants in the National Health and Nutrition Examination Survey 2006–2015. Logistic regression and restricted cubic spline (RCS) models were employed to evaluate both linear and nonlinear associations between aging phenotypes and the prevalence of CKD. From the genetic susceptibility perspective, Mendelian randomization analyses were conducted to establish causality between telomere length and CKD outcomes.

Result

Multivariate logistic regression revealed that PA, KDM, AL, and HD were associated with an increased prevalence of CKD, with PA remaining a significant risk factor after adjusting for covariates (OR = 1.0714, 95% CI = 1.0558–1.0872). RCS curves further indicated a nonlinear relationship between PA, AL, HD, and CKD prevalence (P < 0.001). Besides, inflammation indicators were found to mediate this association. Mendelian randomization analysis demonstrated a significant causal relationship between telomere length and CKD risk across multiple datasets. The results were as follows: Discovery Group (OR = 0.892, 95% CI = 0.832–0.956, P = 0.001) and (OR = 0.896, 95% CI = 0.836–0.961, P = 0.002); Replication Group (OR = 0.872, 95% CI = 0.808–0.940, P < 0.001) and (OR = 0.909, 95% CI = 0.854–0.967, P = 0.003).

Conclusion

These findings underscore the strong connection between aging phenotypes and CKD risk, with the mediated effect of inflammatory markers, contributing to the early disease prevention and therapeutic strategy development.