Graudal Niels, Hubeck-Graudal Thorbjørn, Jurgens Gesche
Lupus and Vasculitis Clinic VRR4242, Copenhagen University Hospital Rigshospitalet, Blegdamsvej 9, Copenhagen DK-2100, Denmark.
Department of Nuclear Medicine & PET-Centre, Aarhus University Hospital, Palle Juul-Jensens Boulevard 99, Aarhus DK 8200, Denmark.
EClinicalMedicine. 2021 Feb 4;33:100750. doi: 10.1016/j.eclinm.2021.100750. eCollection 2021 Mar.
Low sodium intake stimulates the production and activity of renin. The aim is to analyse the association between a large range of sodium intake and the plasma renin activity (PRA).
We performed electronic searches for articles published between January 1st 1946 and March 18th 2020 and updated on January 21st 2021. Randomized controlled trials (RCTs) allocating participants to different sodium diets were included. Data were extracted from published reports. Meta-regression analyses of mean PRA versus mean sodium intake estimated by 24-hour urinary sodium excretion were performed. PROSPERO Registration number is CRD42020150355.
93 RCTs (102 interventions) were identified. In populations with usual/high sodium intake PRA was not associated with sodium intake. In populations with low sodium intake this association was mean -2·91 ng/ml/h per 100 mmol sodium (95% CI: -5·41- -0·42) in 60 studies of normotensive populations ( = 1769) and -1·91 ng/ml/h per 100 mmol sodium (-3·24 - -0·58) in 42 studies of hypertensive populations ( = 1267). The association of the change in PRA with the change in sodium intake was 1·32 ng/ml/h per 100 mmol sodium (0·47-2·18) in normotensive populations and 0·82 ng/ml/h per 100 mmol sodium (0·39-1·24) in hypertensive populations. Contrasting over-all bias assessments and potential effect modifiers had no independent impact on the sodium-PRA relationship. The variability between studies was considerable (I > 90%).
The accelerating effect of sodium reduction on PRA towards a sodium intake of zero mmol/24 h probably explains the interstudy variability. Further studies are needed to test whether this stimulating effect on PRA reflects a physiological disadvantage potentially associated with increased mortality.
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低钠摄入会刺激肾素的产生和活性。目的是分析大范围钠摄入与血浆肾素活性（PRA）之间的关联。
我们对1946年1月1日至2020年3月18日发表且于2021年1月21日更新的文章进行了电子检索。纳入了将参与者分配到不同钠饮食的随机对照试验（RCT）。数据从已发表的报告中提取。对通过24小时尿钠排泄估计的平均PRA与平均钠摄入量进行了Meta回归分析。PROSPERO注册号为CRD42020150355。
共识别出93项RCT（102项干预措施）。在钠摄入量正常/高的人群中，PRA与钠摄入无关。在钠摄入量低的人群中，在60项正常血压人群研究（n = 1769）中，这种关联为每100 mmol钠平均-2.91 ng/ml/h（95%CI：-5.41--0.42），在42项高血压人群研究（n = 1267）中为每100 mmol钠-1.91 ng/ml/h（-3.24--0.58）。在正常血压人群中，PRA变化与钠摄入变化的关联为每100 mmol钠1.32 ng/ml/h（0.47 - 2.18），在高血压人群中为每100 mmol钠0.82 ng/ml/h（0.39 - 1.24）。对比总体偏倚评估和潜在效应修饰因素对钠-PRA关系没有独立影响。研究之间的变异性相当大（I²> 90%）。
钠减少对PRA向零mmol/24小时钠摄入量的加速作用可能解释了研究间的变异性。需要进一步研究来检验这种对PRA的刺激作用是否反映了可能与死亡率增加相关的生理劣势。
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