Published online before print October 1, 2007, doi: 10.1161/HYPERTENSIONAHA.107.097303
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(Hypertension. 2007;50:837.)
© 2007 American Heart Association, Inc.
Editorial Commentaries |
Will the Lessons From Primary Aldosteronism Change the Treatment of Hypertension and Left Ventricular Hypertrophy?
From the Divisions of Endocrinology and Metabolism (R.J.A.) and Cardiology (M.H.D.), Department of Internal Medicine, and the Donald W. Reynolds Cardiovascular Clinical Research Center, University of Texas Southwestern Medical Center, Dallas.
Correspondence to Richard J. Auchus, Division of Endocrinology and Metabolism, Department of Internal Medicine, University of Texas Southwestern Medical Center, 5323 Harry Hines Blvd, Dallas, TX 75390-8857. E-mail Richard.auchus@utsouthwestern.edu
An extract of the first 250 words of the full text is provided, because this article has no abstract. |
The renin-angiotensin-aldosterone system effectively defends against volume depletion, but in most developed nations, dietary sodium is high, and aldosterone production should be suppressed. The syndrome of primary aldosteronism demonstrates the consequences of autonomous aldosterone production in a sodium-replete society. For many years, primary aldosteronism was thought to be an esoteric disorder only diagnosed by academicians at a handful of institutions worldwide. Conn, Biglieri, Bravo, and others characterized the syndrome and developed diagnostic strategies circa 1960–1980. Most clinicians, however, could not execute these algorithms, and management was unsatisfactory because of poor methods for localizing aldosterone production and limited options for medical management. Interest shifted to other mechanisms of hypertension, but during the last 20 years, the advent of commercial assays for renin and aldosterone, the broader use of adrenal vein sampling, and the development of selective aldosterone antagonists have rejuvenated interest in primary aldosteronism.1 Furthermore, end-organ damage is more severe in primary aldosteronism than in essential hypertension, and considerable evidence implicates the activation of mineralocorticoid receptors in these tissues as the mechanism.
Implicit in this aldosterone renaissance is the importance of making the diagnosis of primary aldosteronism to allow implementation of tailored therapy. Proteinuria is more prevalent in patients with primary aldosteronism than in those with essential hypertension,2 and the excess proteinuria largely reverses after treatment with surgery or spironolactone.3 Thus, the benefits reaped from the detection of primary aldosteronism and the implementation of targeted therapy extend beyond optimal control of blood pressure.
Another malady associated with primary aldosteronism is left
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Hypertension 2007 50: 911-918.
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  B Rayner Primary aldosteronism and aldosterone-associated hypertension J. Clin. Pathol., July 1, 2008; 61(7): 825 - 831. [Abstract] [Full Text] [PDF]
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