SynthesisScientific reports2023
A low dietary sodium dose is associated with a more pronounced aldosterone response in normotensive than in hypertensive individuals.
Synthesis in Scientific reports, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
4 citing papers in PubMed.
- Guidelines for daily sodium intake: a counterpoint to the current recommendation for low sodium intake.Sleep advances : a journal of the Sleep Research Society · 2026Review
- The Burden, Outcomes, and Management of Patients with Aldosterone Dysregulation: A Targeted Literature Review.Advances in therapy · 2026Review
- Sodium, potassium intake, and all-cause mortality: confusion and new findings.BMC public health · 2024Observational
- Correlation of renal biomarkers, electrolyte imbalances and vitamin D levels in hypertensive subjects.Medicine internationalArticle
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this comprehensive meta-regression analysis encompassing 79 randomized controlled trials, we observed that in populations assigned to a high sodium intake level exceeding 94 mmol, there was no discernible link between plasma aldosterone levels and sodium intake. However, among populations with normal blood pressure subjected to a lower sodium intake, falling below 111 mmol (N = 1544), the association between sodium intake and plasma aldosterone levels manifested as a decrease of 192 pg/ml per 100 mmol of sodium (95% CI - 303 to - 81). In hypertensive populations (N = 1145), this association was less pronounced, with a reduction of 46 pg/ml per 100 mmol sodium, (95% CI - 112 to 20). Furthermore, in normotensive populations the plasma aldosterone increase associated with a decrease in sodium intake was 70 pg/ml per 100 mmol sodium (95% CI 27 to 113). In hypertensive populations, the observed increase was more modest, at 30 pg/ml per 100 mmol sodium, (95% CI 6.8 to 54). A limitation of this study lies in the absence of individual participant data. Our analysis included adjustments for potential effect-modifiers, encompassing bias estimation, which did not substantially alter these associations. One perspective of the present results may be to prompt a reconsideration of current sodium reduction recommendations.
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