Influence of sodium intake and change in sodium intake on plasma-renin in man. (March 2021)

• Record Type: Journal Article
• Authors: Graudal, Niels; Hubeck-Graudal, Thorbjørn; Jurgens, Gesche
• Is Part Of: EClinicalMedicine. Volume 33(2021)
• Publication Date: 2021-03
• Subjects: Medicine -- Research -- Periodicals; Medical policy -- Periodicals; Clinical Medicine; Health Policy; Public Health; Medical policy; Medicine -- Research; Periodical; Electronic journals; Periodicals; 613
• DOI: 10.1016/j.eclinm.2021.100750
• Languages: English
• ISSNs: 2589-5370

Abstract

Abstract: Background: 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). Methods: 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. Findings: 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 ( n = 1769) and -1·91 ng/ml/h per 100 mmol sodium (-3·24 – -0·58) in 42 studies of hypertensive populations ( n = 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 2 > 90%). Interpretation: 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 Funding: None