Chen Yushu, Zhang Jiahao, Li Zhibiao, Zhan Yihua, Tang Zhicheng, Wang Juan, He Zhaohui, Tang Fucai
Department of Urology, The Eighth Affiliated Hospital of Sun Yat-sen University, Shenzhen, Guangdong, China.
Department of Urology, Sun Yat-sen Memorial Hospital of Sun Yat-sen University, Guangzhou, Guangdong, China.
Int J Surg. 2025 Jun 10;111(9):6063-74. doi: 10.1097/JS9.0000000000002658.
Our previous genome-wide association study (GWAS) suggested a potential negative causal relationship between basal metabolic rate (BMR) and kidney stone disease (KSD) from a genetic standpoint. This study aimed to further investigate their association from a clinical etiological perspective across diverse global populations and to elucidate their dose-response relationship.
A total of 21 140 adults from the US NHANES (2007-2020) and 289 007 participants without a prior history of KSD from the UK Biobank (2006-2014) were analyzed using cross-sectional and prospective cohort study designs, respectively. Data were collected through questionnaires and physical examinations. Multivariable logistic regression models and restricted cubic spline (RCS) analyses were employed to assess the relationship between BMR and the risk of KSD, adjusting for potential confounders. Subgroup and sensitivity analyses were conducted to explore gender- and age-related differences and evaluate the robustness of the results.
In the NHANES cohort, the fully adjusted odds ratio (OR) for the highest BMR quartile (Q4) compared to the lowest quartile (Q1) was 0.49 (95% CI: 0.35, 0.70; P for trend < 0.001). During the follow-up period in the UK Biobank cohort, 3620 participants ultimately developed KSD, and the relevant analysis further confirmed this negative causal association, with an OR of 0.72 (95% CI: 0.59, 0.89; P for trend = 0.003). In both cohorts, higher BMR was associated with a decreased risk of KSD, with consistent trends observed across sex and age subgroups. Sensitivity analyses validated the robustness of these findings.
In conclusion, a higher BMR appears to be a protective factor against KSD, with a negative causal association identified. Lifestyle interventions aimed at increasing BMR may help prevent the development of kidney stones.
我们之前的全基因组关联研究(GWAS)从遗传学角度表明基础代谢率(BMR)与肾结石病(KSD)之间可能存在负向因果关系。本研究旨在从临床病因学角度进一步调查不同全球人群中它们之间的关联,并阐明它们的剂量反应关系。
分别采用横断面研究和前瞻性队列研究设计,对来自美国国家健康与营养检查调查(NHANES,2007 - 2020年)的21140名成年人以及来自英国生物银行(2006 - 2014年)的289007名无KSD既往史的参与者进行分析。数据通过问卷调查和体格检查收集。采用多变量逻辑回归模型和受限立方样条(RCS)分析来评估BMR与KSD风险之间的关系,并对潜在混杂因素进行调整。进行亚组分析和敏感性分析以探讨性别和年龄相关差异,并评估结果的稳健性。
在NHANES队列中,最高BMR四分位数(Q4)与最低四分位数(Q1)相比,完全调整后的比值比(OR)为0.49(95%置信区间:0.35,0.70;趋势P值<0.001)。在英国生物银行队列的随访期间,3620名参与者最终患上了KSD,相关分析进一步证实了这种负向因果关联,OR为0.72(95%置信区间:0.59,0.89;趋势P值 = 0.003)。在两个队列中,较高的BMR与较低的KSD风险相关,在性别和年龄亚组中观察到一致的趋势。敏感性分析验证了这些发现的稳健性。
总之,较高的BMR似乎是预防KSD的保护因素,已确定存在负向因果关联。旨在提高BMR的生活方式干预可能有助于预防肾结石的发生。