目的:已知膳食钠摄入过多对血管内液量和全身血压有不良影响,这可能会影响眼内压(IOP)和青光眼风险。本研究旨在评估尿钠排泄的相关性,饮食摄入的生物标志物,青光眼及相关特征,并确定这种关系是否被疾病的遗传易感性所改变。
方法:在基于人群的英国生物库研究中进行横断面观察和基因-环境相互作用分析。
方法:多达103634人(平均年龄57岁,51%的女性)完全排尿,眼,和协变数据。
方法:从中段尿液样本计算尿钠:肌酐比值(UNa:Cr;mmol:mmol)。作为全面眼科检查的一部分,测量了眼部参数,并通过自我报告和相关的国家医院记录相结合来确定青光眼病例。基于包括2673种常见遗传变异的青光眼多基因风险评分(PRS)计算青光眼的遗传易感性。多变量线性和逻辑回归,根据关键的社会人口统计学进行调整,medical,人体测量学,和生活方式因素,用于建模关联和基因-环境相互作用。
方法:角膜补偿眼压,光学相干断层扫描来源于黄斑区视网膜神经纤维层(mRNFL)和神经节细胞内网状层(GCIPL)的厚度,和普遍的青光眼。
结果:在最大调整回归模型中,UNa:Cr的一个标准偏差增加与更高的IOP(0.14mmHg;95%CI,0.12至0.17;P<0.001)和更高的青光眼患病率(OR,1.11;95%CI,1.07至1.14;P<0.001),但不是mRNFL或GCIPL厚度。与UNA:Cr处于最低五分之一的水平相比,处于最高五分之一的患者的眼压(0.45mmHg;95%CI,0.36至0.53,P<0.001)和青光眼患病率(OR,1.30;95%CI,1.17~1.45;P<0.001)。在青光眼PRS较高的参与者中,发现与青光眼的相关性更强(P交互作用=0.001)。
结论:尿钠排泄,饮食摄入的生物标志物,可能是青光眼的一个重要的可改变的危险因素,尤其是在具有高潜在遗传风险的个体中。这些发现值得进一步调查,因为它们可能具有重要的临床和公共卫生意义。
OBJECTIVE: Excessive dietary sodium intake has known adverse effects on intravascular fluid volume and systemic blood pressure, which may influence intraocular pressure (IOP) and glaucoma risk. This study aimed to assess the association of urinary sodium excretion, a biomarker of dietary intake, with glaucoma and related traits, and determine whether this relationship is modified by genetic susceptibility to disease.
METHODS: Cross-sectional observational and gene-environment interaction analyses in the population-based UK Biobank study.
METHODS: Up to 103 634 individuals (mean age: 57 years; 51% women) with complete urinary, ocular, and covariable data.
METHODS: Urine sodium:creatinine ratio (UNa:Cr; mmol:mmol) was calculated from a midstream urine sample. Ocular parameters were measured as part of a comprehensive eye examination, and glaucoma case ascertainment was through a combination of self-report and linked national hospital records. Genetic susceptibility to glaucoma was calculated based on a glaucoma polygenic risk score comprising 2673 common genetic variants. Multivariable linear and logistic regression, adjusted for key sociodemographic, medical, anthropometric, and lifestyle factors, were used to model associations and gene-environment interactions.
METHODS: Corneal-compensated IOP, OCT derived macular retinal nerve fiber layer and ganglion cell-inner plexiform layer (GCIPL) thickness, and prevalent glaucoma.
RESULTS: In maximally adjusted regression models, a 1 standard deviation increase in UNa:Cr was associated with higher IOP (0.14 mmHg; 95% confidence interval [CI], 0.12-0.17; P < 0.001) and greater prevalence of glaucoma (odds ratio, 1.11; 95% CI, 1.07-1.14; P < 0.001) but not macular retinal nerve fiber layer or ganglion cell-inner plexiform layer thickness. Compared with those with UNa:Cr in the lowest quintile, those in the highest quintile had significantly higher IOP (0.45 mmHg; 95% CI, 0.36-0.53, P < 0.001) and prevalence of glaucoma (odds ratio, 1.30; 95% CI, 1.17-1.45; P < 0.001). Stronger associations with glaucoma (P interaction = 0.001) were noted in participants with a higher glaucoma polygenic risk score.
CONCLUSIONS: Urinary sodium excretion, a biomarker of dietary intake, may represent an important modifiable risk factor for glaucoma, especially in individuals at high underlying genetic risk. These findings warrant further investigation because they may have important clinical and public health implications.
BACKGROUND: Proprietary or commercial disclosure may be found in the Footnotes and Disclosures at the end of this article.