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早产在年轻人应激性钠排泄中的作用。

The role of preterm birth in stress-induced sodium excretion in young adults.

机构信息

Wake Forest University School of Medicine.

Department of Surgery-Hypertension and Vascular Research.

出版信息

J Hypertens. 2024 Jun 1;42(6):1086-1093. doi: 10.1097/HJH.0000000000003705. Epub 2024 Feb 28.

Abstract

BACKGROUND

Early-life programming due to prematurity and very low birth weight (VLBW, <1500 g) is believed to contribute to development of hypertension, but the mechanisms remain unclear. Experimental data suggest that altered pressure natriuresis (increased renal perfusion pressure promoting sodium excretion) may be a contributing mechanism. We hypothesize that young adults born preterm will have a blunted pressure natriuresis response to mental stress compared with those born term.

METHODS

In this prospective cohort study of 190 individuals aged 18-23 years, 156 born preterm with VLBW and 34 controls born term with birth weight at least 2500 g, we measured urine sodium/creatinine before and after a mental stress test and continuous blood pressure before and during the stress test. Participants were stratified into groups by the trajectory at which mean arterial pressure (MAP) increased following the test. The group with the lowest MAP trajectory was the reference group. We used generalized linear models to assess poststress urine sodium/creatinine relative to the change in MAP trajectory and assessed the difference between groups by preterm birth status.

RESULTS

Participants' mean age was 19.8 years and 57% were women. Change in urine sodium/creatinine per unit increase in MAP when comparing middle trajectory group against the reference group was greater in those born preterm [β 5.4%, 95% confidence interval (95% CI) -11.4 to 5.3] than those born term (β 38.5%, 95% CI -0.04 to 92.0), interaction term P = 0.002.

CONCLUSION

We observed that, as blood pressure increased following mental stress, young adults born preterm exhibited decreased sodium excretion relative to term-born individuals.

摘要

背景

早产儿和极低出生体重(VLBW,<1500g)的早期生活编程被认为会导致高血压的发展,但机制尚不清楚。实验数据表明,压力利钠作用(增加肾脏灌注压促进钠排泄)的改变可能是一个促成机制。我们假设,与足月出生的人相比,早产儿在心理压力下的压力利钠反应会减弱。

方法

在这项对 190 名 18-23 岁个体的前瞻性队列研究中,156 名早产儿 VLBW 和 34 名出生体重至少为 2500g 的足月对照组,我们在心理应激测试前后测量了尿钠/肌酐,在应激测试前后测量了连续血压。根据测试后平均动脉压(MAP)升高的轨迹,将参与者分为不同的组。MAP 轨迹最低的组为参考组。我们使用广义线性模型来评估应激后尿钠/肌酐相对于 MAP 轨迹变化的相对值,并根据早产出生状况评估组间差异。

结果

参与者的平均年龄为 19.8 岁,57%为女性。与足月出生者相比,中轨迹组与参考组相比,MAP 每增加一个单位,尿钠/肌酐的变化更大[β 5.4%,95%置信区间(95%CI)-11.4 至 5.3],而早产儿出生者[β 38.5%,95%CI -0.04 至 92.0],交互项 P=0.002。

结论

我们观察到,随着心理应激后血压的升高,与足月出生的个体相比,早产儿表现出相对较低的钠排泄。

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本文引用的文献

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