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Endocrine Hypertension pp 33–50Cite as

Syndromes of Mineralocorticoid Excess

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Part of the book series: Contemporary Endocrinology ((COE))

Abstract

In addition to obesity, diabetes type 2, and the metabolic syndrome, hypertension represents a major public and global health problem, most of which can be improved by lifestyle changes, including changing dietary habits with less consumption of processed and preserved foods, which generally contain higher amounts of salt than freshly prepared food items. Amongst causes for endocrine hypertension are syndromes of mineralocorticoid excess typically resulting from overactive amiloride-sensitive sodium channels located in the distal convoluted tubules and collecting ducts of the kidney, as well as other tissues, including vascular smooth muscle. The net effect of such an overactivation, which occurs mostly in primary aldosteronism is sodium and water retention with volume expansion and hypertension that is exacerbated by a diet high in salt. Biochemically, plasma renin activity is suppressed and hypokalemia may be present. Aldosterone mediates its action through the mineralocortoid receptor (MR), which regulates salt homeostasis in the kidneys and plays a range of other roles in the vasculature, heart, brain, and adipose tissue.

Excessive MR activation can promote inflammation, fibrosis, and heart disease as well as psychiatric illness, including anxiety and depression, through key modulators, including the glucocorticoid receptor and the 11β-hydroxysteroid dehydrogenases.

Apart from aldosterone, the MR is also activated by products of abnormal ­adrenal steroid biosynthesis, dysregulated metabolism of cortisol in cells that are targets of mineralocorticoids, and activating mutations of the MR or of ion channels that are inducible by the MR. We provide here an overview of mineralocorticoid excess caused by congenital adrenal hyperplasia due to mutations of the 11beta-­hydroxylase and 17alpha-hydroxylase genes, by mutations of the 11beta-hydroxysteroid dehydrogenase type 2 gene (apparent mineralocorticoid excess (AME)), mutations of the epithelial sodium channel genes (Liddle syndrome), mutations of the ­mineralocorticoid receptor gene (Geller syndrome), and pseudohypoaldosteronism type 2 or Gordon syndrome.

Most of these conditions are treated by restricted dietary salt intake. However, some require special therapies, including hydrocortisone (CAH), spironolactone/eplerenone, thiazide diuretics (Liddle and Gordon syndrome), while in others spironolactone and other MR antagonists may be contraindicated (Geller syndrome). Understanding the pathophysiology of these rare conditions may help designing future molecular-targeted therapies. Naturally, the mainstay of antihypertensive therapy continues to be reducing the overconsumption of salt in addition to increasing compliance and adherence of patients to currently available indicated therapies.

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  1. Division of Endocrinology, University of Mississippi Medical Center, 2500 N State Street Clin Sci Building, Room 512, Jackson, MS, 39216, USA

    Eugen Melcescu & Christian A. Koch

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  1. Eugen Melcescu
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  2. Christian A. Koch
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  1. Dept. Medicine, Div. Endocrinology, Diabetes &, University of Mississippi Medical Center, N. State Street 2500, Jackson, 39216, Mississippi, USA

    Christian A Koch

  2. UNESCO Chair on Adolescent Health Care, Division of Endocrinology, University of Athens Medical School, Aghia Sophia Children's Hospital, Athens, 11527, Greece

    George P Chrousos

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Melcescu, E., Koch, C.A. (2013). Syndromes of Mineralocorticoid Excess. In: Koch, C., Chrousos, G. (eds) Endocrine Hypertension. Contemporary Endocrinology. Humana Press, Totowa, NJ. https://doi.org/10.1007/978-1-60761-548-4_2

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