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Primary aldosteronism: the case against screening

Nature Clinical Practice Nephrology volume 3, pages 580–581 (2007)Cite this article

Hypertension is common, conveys considerable health risks and is amenable to drug therapy that saves lives. These facts do not necessarily translate into success in clinical practice, however: detection and control of hypertension remain inadequate. If a correctable cause of hypertension could be discovered, the need for long-term drug use in millions of individuals could be reduced. The list of diseases that cause raised blood pressure is long, but it is the possibilities of detecting underlying renal artery stenosis (which is not usually amenable to surgical cure) or primary aldosteronism (PA) that have captured most attention in recent years. The index case of PA was a young woman, described by Jerome Conn in 1955, who had severe hypertension and profound hypokalemic alkalosis. Both abnormalities resolved after removal of a 13 mm adrenal tumor. Although it is both intellectually and clinically satisfying to discover patients such as this, it is far from certain whether such satisfaction would justify the potentially enormous cost of screening the entire hypertensive population for what remains a rare disease.

The phenotype of 'Conn's syndrome' was defined as elevated production of aldosterone, resulting in sodium retention with renin suppression, potassium loss, and, of course, hypertension. Not all patients with PA have an aldosterone-secreting adenoma, however. Approximately two-thirds of these individuals have nodular hyperplasia of the adrenal glands, a condition that is not amenable to surgical cure and has been given the label idiopathic adrenal hyperplasia (IHA).1 It is questionable whether IHA is a true form of PA because production of aldosterone in this condition seems to be driven by an increased adrenal sensitivity to endogenous angiotensin II.2 Up to one-quarter of patients with primary hypertension have a low level of plasma renin, with normal plasma aldosterone levels and without hypokalemia; these individuals have been described as having low-renin hypertension (LRH).2 Patients with LRH are older and more sensitive to diuretic therapy than are those with normal renin levels. They can be considered quantitatively rather than qualitatively different from those with IHA, and perhaps form part of a continuum of hypertensive disease.2

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  1. Department of Medicine, 3rd floor, Alexander Donald Building, Western General Hospital, Crewe Road, Edinburgh EH4 2XU, UK paul.padfield@luht.scot.nhs.uk

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  1. P Padfield is a Consultant Physician at the Western General Hospital, and a Reader in Medicine at the University of Edinburgh, Edinburgh, UK.,

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Padfield, P. Primary aldosteronism: the case against screening. Nat Rev Nephrol 3, 580–581 (2007). https://doi.org/10.1038/ncpneph0625

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