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RESEARCH PAPER / 2024-12-24

Associations of clinical parameter-based accelerated aging, genetic predisposition with risk of chronic kidney disease and associated life expectancy: A prospective cohort study.

Gang Zheng, Qing Chang, Yixiao Zhang, Yashu Liu, Chao Ji, Honghao Yang, Liangkai Chen, Yang Xia, Yuhong Zhao

Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, China Medical University, Shenyang, China.Department of Clinical Epidemiology, Shengjing Hospital of China Medical University, China Medical University, Shenyang, China. · pubmed

Abstract

Little evidence exists regarding the associations between clinical parameter-based biological aging and the incidence and outcome of chronic kidney disease (CKD). Thus, we aimed to assess the associations between biological aging, genetic risk, and the risk of CKD, as well as investigate the impact of accelerated biological aging on life expectancy. 281,363 participants free of kidney diseases from the UK Biobank were included in this prospective study. Biological age was measured from clinical traits using the KDM-BA and PhenoAge algorithms, and the discrepancies from chronological age were defined as biological age accelerations. A polygenic score was calculated to indicate the genetic predisposition of the estimated glomerular filtration rate (eGFR). A cause-specific competing risk model was used to estimate hazard ratios (HRs) and the corresponding confidence intervals (CIs) of incident CKD. We found that individuals with more pronounced accelerations in biological age exhibited an elevated risk of developing CKD (HR

The following analysis is generated by AI and may contain errors. It is separate from the authors’ abstract and is not peer review.

Research summary

The paper investigates the associations between biological aging, genetic predisposition, and chronic kidney disease (CKD), which are relevant to the broader context of aging research. However, while it provides solid research on the relationship between accelerated biological aging and CKD risk, it does not address the root causes of aging or propose interventions for lifespan extension. Thus, its impact is limited, making it a solid contribution but not a groundbreaking one.

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