This Article Full Text Full Text (PDF) Submit a related Letter to the Editor Alert me when this article is cited Alert me when eLetters are posted Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Copyright Permission Google Scholar Articles by Stowasser, M. PubMed PubMed Citation Articles by Stowasser, M. Related Collections Adrenal and Hypertension Cardiovascular Endocrinology Endocrine Oncology

Update in Primary Aldosteronism

Endocrine Hypertension Research Center, University of Queensland School of Medicine, Greenslopes and Princess Alexandra Hospitals, Brisbane 4102, Australia

Address all correspondence and requests for reprints to: Michael Stowasser, Hypertension Unit, University of Queensland School of Medicine, Princess Alexandra Hospital, Ipswich Road, Woolloongabba Brisbane 4102, Australia. E-mail: m.stowasser{at}uq.edu.au.

It is now widely recognized that primary aldosteronism (PA) is much more common than previously thought, accounting for up to 5–10% of hypertensives, and that aldosterone excess has adverse cardiovascular consequences that go above and beyond hypertension development. These findings have precipitated a marked resurgence of research activity, most of which has supported the concept that PA plays an important role in cardiovascular disease states and should be systematically sought and specifically treated, and the development of an Endocrine Society clinical guideline for the case detection, diagnosis, and management of this common, specifically treatable, and potentially curable condition. Areas of recent, topical research include: 1) the demonstration of excess morbidity in patients with PA compared with other forms of hypertension, confirming the clinical relevance of non-blood pressure-dependent adverse effects of aldosterone excess; 2) the further demonstration that this excess morbidity and mortality are ameliorated with specific (but not nonspecific antihypertensive) therapy directed against aldosterone excess, confirming the importance of detection and diagnosis of PA to enable optimal specific management; 3) the development of new treatment strategies; 4) an ongoing appraisal and refinement of diagnostic approaches including screening, subtype differentiation, and new assay development; and 5) further insights into the importance and nature of genetic factors related to the development of PA.