Expert FAQs - Hypertension and Aldosterone | Think Aldo

Aldosterone, part of the renin–angiotensin–aldosterone system (RAAS), regulates sodium reabsorption, water retention and blood pressure (BP) control.¹ In normal physiology, low sodium concentration, low BP and low renal perfusion lead to an increase in renin production, increasing aldosterone production.² Conversely, elevated BP and increased sodium inhibit renin release, lowering aldosterone.^3,4

Aldosterone dysregulation refers to the abnormal production of the hormone, despite excess sodium and fluid balance, leading to elevated BP and increased cardiovascular and kidney risk.^1,3,5

Inoue K, et al. Hypertension 2020; 76:113–120
Scott JH, et al. StatPearls Publishing; May 1, 2023. https://www.ncbi.nlm.nih.gov/books/NBK470339. Last accessed: August 2025
Vaidya A, et al. Endocr Rev 2018; 39(6):1057–1088
Schweda F, et al. Hypertension 2005; 46:780–786
Brown JM, et al. Ann Intern Med 2020; 173:10–20

Emerging evidence shows that aldosterone dysregulation exists on a continuum, with biochemically overt primary aldosteronism (PA) at one extreme.^1,2 Even modestly elevated aldosterone levels, below conventional biochemical PA thresholds, are linked to higher blood pressure (BP) and increased cardiovascular and kidney risk.²

Across a broad range of aldosterone–renin ratio values, aldosterone plays an important role to influence BP.³ Studies also demonstrate that aldosterone elevations below primary aldosterone thresholds are independently associated with adverse cardiovascular and kidney outcomes, highlighting the need to reassess what constitutes ‘normal’.²

Brown JM, et al. Ann Intern Med 2020;173:10–20
Vaidya A, et al. Am J Hypertens 2022;35:967-988
Tomaschitz A, et al. J Am Coll Cardiol 2010;55(19):2171–2180

Aldosterone plays a central role in blood pressure (BP) control and can contribute to cardiovascular, kidney, cerebrovascular and metabolic disease.¹

Independent of its effects on BP, excess aldosterone leads to inflammation and fibrosis across blood vessels, the heart and kidneys, driving vascular and cardiac remodelling, heart failure and kidney injury.²

Compared with patients with essential hypertension, patients with aldosterone dysregulation have higher risks of coronary artery disease, stroke and atrial fibrillation.³ In chronic kidney disease (CKD), patients with elevated aldosterone are at increased risk of CKD progression and end-stage kidney disease.⁴

Otsuka H, et al. Int J Mol Sci 2023;24:5370
Verhovez A, et al. Curr Signal Transduct Ther 2012;7:132–141
Monticone S, et al. Lancet Diabetes Endocrinol 2018;6:41–50
Verma A, et al. Eur Heart J 2022;43(38):3781–3791

Guidelines recommend measurement of renin and aldosterone (e.g. aldosterone–renin ratio) in patients with hypertension to screen for primary aldosteronism (PA), the most severe form of aldosterone dysregulation.^1,2

Evidence suggests that aldosterone dysregulation exists on a continuum, where even modest amounts of aldosterone production (relative to the sodium and fluid in the body) lead to blood pressure (BP) elevation and independently drive adverse cardiovascular and kidney outcomes.^2,3 However, there is currently insufficient evidence to screen for patients across this broader continuum of aldosterone dysregulation using aldosterone and/or renin.^1,3

Clinical decisions should instead be guided by the need to prioritise BP control for all patients, recognising aldosterone as a likely cause of poor control in those on multiple antihypertensive medications.^1,4

Adler GK, et al. J Clin Endocrinol Metab 2025;110:2453–2495
Vaidya A, et al. Endocr Rev 2018;39:1057–1088
Brown JM, et al. Ann Intern Med 2020;173:10–20
Vaidya A, et al. Am J Hypertens 2022;35:967-988
Cannone V, et al. Mayo Clin Proc 2018;93:980–990

Aldosterone dysregulation may be a pathological driver in those whose hypertension is not at goal, despite taking multiple antihypertensive medications.¹ In addition, patients with hypokalaemia, obstructive sleep apnoea, obesity or type 2 diabetes may also have dysregulated aldosterone production.^2–5

Cannone V, et al. Mayo Clin Proc 2018;93:980–990
Pratt-Ubunama MN, et al. Chest 2007;131:453–459
Ruiz-Sánchez JG, et al. J Clin Endocrinol Metab 2023;109(1):e379–e388
Tyfoxylou E, et al. Biomedicines 2022;10(9):2308
Burrello J, et al. Hypertension 2020;75(4):1025–1033

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