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Practice Easily Missed?

Primary aldosteronism

BMJ 2022; 377 doi: https://doi.org/10.1136/bmj-2021-065250 (Published 20 April 2022) Cite this as: BMJ 2022;377:e065250
  1. Kay Weng Choy, chemical pathologist1,
  2. Peter J Fuller, professor and consultant endocrinologist234,
  3. Grant Russell, professor of primary care research and general practitioner5,
  4. Qifu Li, professor and consultant endocrinologist6,
  5. Marianne Leenaerts, patient and advocate7,
  6. Jun Yang, head of endocrine hypertension group, senior research fellow, consultant endocrinologist234
  1. 1Department of Pathology, Northern Health, Epping, Australia
  2. 2Centre for Endocrinology and Metabolism, Hudson Institute of Medical Research, Clayton, Australia
  3. 3Department of Endocrinology, Monash Health, Clayton, Australia
  4. 4Department of Medicine, Monash University, Clayton, Australia
  5. 5Department of General Practice, Monash University, Clayton, Australia
  6. 6Department of Endocrinology, First Affiliated Hospital of Chongqing Medical University, Chongqing, China
  7. 7Governing Board, Primary Aldosteronism Foundation (primaryaldosteronism.org)
  1. Correspondence to: J Yang jun.yang{at}hudson.org.au

What you need to know

  • Aldosterone excess can cause cardiovascular, cerebrovascular, and renal disease

  • Consider primary aldosteronism in patients with moderate to severe hypertension, resistant hypertension, hypertension with an adrenal mass, or hypokalaemia

  • A minority of patients have hypokalaemia: most cases resemble essential hypertension, leading to missed or delayed diagnosis

  • The screening test of choice is plasma aldosterone-to-renin ratio (ARR) but testing may not be accurate (due to interfering medications) or available (in less resourced settings)—consider temporary medication changes before screening or a therapeutic trial of a mineralocorticoid receptor antagonist in these contexts

  • Unilateral disease is treated with adrenalectomy; bilateral disease is treated with a mineralocorticoid receptor antagonist

A 57 year old woman presented for a routine health check. She had an elevated blood pressure of 150/100 mm Hg. Her average blood pressure had remained above 140/90 mm Hg over three years, despite the introduction and up-titration of perindopril, amlodipine, and moxonidine. She has no other relevant medical history or family history of hypertension. Routine investigations were unremarkable, including serum potassium of 3.7 mmol/L (reference range 3.5-5.2 mmol/L) and estimated glomerular filtration rate (eGFR) of 90 mL/min/1.73 m2.

What is primary aldosteronism?

Primary aldosteronism, also known as Conn’s syndrome, is characterised by inappropriate aldosterone production despite suppressed renin secretion and, commonly, hypertension.1 Normally, in response to intravascular volume depletion, renin stimulates aldosterone secretion to increase sodium reabsorption and facilitate volume expansion.1 In primary aldosteronism, however, aldosterone is autonomously produced independent of renin (for example, aldosterone-producing adenomas or hyperplasia involving one or both adrenal glands).1 Renin levels are suppressed while unchecked aldosterone levels increase sodium reabsorption and lead to hypertension, the main presenting complaint (fig 1). As potassium excretion is paired with renal sodium reabsorption, patients may experience hypokalaemia and associated muscle cramps, weakness, or cardiac arrhythmia.2

Fig 1

The pathophysiology of primary aldosteronism (original created with BioRender.com)

How common is it?

Primary aldosteronism is the most common …

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