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Effects of potassium supplementation on plasma aldosterone: a systematic review and meta-analysis in humans
Ryan J McNally1, Bushra Farukh, Philip J Chowienczyk
1King's College London British Heart Foundation Centre, Department of Clinical Pharmacology, St. Thomas' Hospital, Westminster Bridge, London, UK.
Objectives:
Effects of potassium supplementation on blood pressure (BP) may be offset by an increase in plasma aldosterone. The magnitude of potassium-dependent regulation of aldosterone secretion in humans is not fully characterized; it is not clear whether this is mediated by activation of the renin-angiotensin-aldosterone system (RAAS), as a result of a reduction in BP or other mechanisms. We performed a systematic review and meta-analysis of clinical trials assessing effects of potassium on plasma aldosterone and renin in adult individuals.
Methods:
This was carried out in accordance with PRISMA guidelines. Three databases were searched: MEDLINE, EMBASE and CENTRAL. Titles were firstly screened by title and abstract for relevance before full-text articles were assessed for eligibility. The keywords used included "aldosterone", "potassium" and "RAAS".
Results:
6395 articles were retrieved and after title/abstract screening, 123 full-text articles were assessed for eligibility. Thirty-six met the prespecified inclusion/exclusion criteria (of which 18/36 also reported systolic BP). Potassium supplementation caused a significant decrease in systolic BP (mean difference [95% CI] -3.69 mmHg [-4.91, -2.46], P < 0.001) and increase in serum potassium (+0.37 [0.23, 0.52] mmol/l, P < 0.001). There was an increase in plasma aldosterone (standardized difference 0.426 [0.299, 0.553], P < 0.001) but not in plasma renin activity. Meta-regression showed a significant positive correlation between change in plasma aldosterone and change in serum potassium ( P < 0.001).
Conclusions:
Potassium supplementation increases plasma aldosterone concentrations, which correlates with the increase in serum potassium concentration which does not appear to be mediated by an increase in plasma renin activity.
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