Primary aldosteronism is the most common specifically treatable and potentially curable form of hypertension. It accounts for at least 5% of hypertensive patients, with most patients normokalemic.
Approximately 30% have unilateral forms correctable by unilateral laparoscopic adrenalectomy, and 70% have bilateral forms in which hypertension responds well to aldosterone antagonist medications.
Optimal detection involves screening all hypertensive patients using the plasma aldosterone/renin ratio, after controlling for factors (including medications) that may confound results.
In patients with repeatedly elevated aldosterone/renin ratios, definitive confirmation or exclusion of diagnosis involves careful suppression testing with measurement of aldosterone response to fludrocortisone or to salt loading.
Subtype differentiation for optimal treatment involves genetic testing for familial forms where suspected. If genetic testing is not performed or negative, adrenal CT and adrenal venous sampling should be performed to differentiate unilateral from bilateral forms.
In primary aldosteronism (PA), aldosterone production exceeds the body's requirements and is relatively autonomous with regard to its normal chronic regulator, the renin-angiotensin II system. This results in excessive sodium reabsorption via amiloride-sensitive epithelial sodium channels within the distal nephron, leading to hypertension and suppression of renin-angiotensin II. Urinary loss of potassium and hydrogen ions, exchanged for sodium at the distal nephron, may result in hypokalemia and metabolic alkalosis if severe and prolonged.
History and exam
- fludrocortisone suppression test
- saline infusion testing
- oral salt loading
- genetic testing
- adrenal CT
- adrenal venous sampling
- adrenal MRI
- adrenal selenocholesterol scanning
- posture stimulation testing
- angiotensin II infusion testing
- 24-hour urinary hybrid steroids (18-hydroxy- and 18-oxo-cortisol)
- dexamethasone suppression testing
Michael Stowasser, MBBS, FRACP, PhD
Endocrine Hypertension Research Centre
University of Queensland School of Medicine
Greenslopes and Princess Alexandra Hospitals
MS is an author of references cited in this monograph.
Professor Michael Stowasser would like to gratefully acknowledge Professor Richard D. Gordon, a previous contributor to this monograph.
Paolo Mulatero, MD
Department of Medicine and Experimental Oncology
Division of Medicine and Hypertension
San Giovanni Battista Hospital
PM declares that he has no competing interests.
Wail Malaty, MD
Department of Family Medicine
University of North Carolina
Assistant Program Director
MAHEC Rural Family Medicine Residency
WM declares that he has no competing interests.
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