Endocrine Abstracts (2015) 38 PL7 | DOI: 10.1530/endoabs.38.PL7

Confronting the last frontiers of endocrine hypertension

Richard J Auchus


Division of Metabolism, Endocrinology, and Diabetes, University of Michigan, Ann Arbor, Michigan, USA.


In the 60 years since primary aldosteronism (PA) was described, our understanding of its pathophysiology and approaches to diagnosis and treatment has improved remarkably. Despite this progress, <1% of patients with PA are ever screened for this condition, which accounts for 5–8% of hypertension (HTN). The resistance to screening for PA probably derives primarily from the complexities and uncertainties inherent in its evaluation and management. How many types of PA exist, and how do these various forms develop? What is idiopathic hyperaldosteronism? Is our approach to PA the best we can do? How can we encourage broader screening? I will explore some recent developments in PA that challenge some long-held concepts, raise new questions, and suggest alternate strategies.

Besides PA, other more rare forms of mineralocorticoid-mediated HTN exist, in which cortisol, corticosterone, or 11-deoxycorticosterone act on the mineralocorticoid receptor (MR) to cause HTN. Generously assuming that 10% of HTN is due to a well-defined state of mineralocorticoid excess, then why do 60–80% of unselected patients with HTN demonstrate good blood pressure responses to MR antagonists? In chronically salt-loaded societies, how much MR activation is enough to cause hypertension? How do we know if MR activation is responsible for HTN in a given individual? I will review some of these rare genetic and acquired forms of HTN, new disease mechanisms, and additional forms of HTN that might be related to MR and its ligands.

Finally, it is important to consider the mild phenotypes. As our ability to dissect and to characterize abnormalities in steroid biosynthesis improve, we now understand that some diseases are more common than previously assumed and that patients with milder defects can have different clinical manifestations than those that characterize the ‘classic’ syndromes. Because MR-mediated HTN exerts greater end-organ damage than other forms of HTN, the identification and characterization of patients with these milder phenotypes looms as a strategic frontier for endocrinology to conquer.

Generously supported by Clinical Endocrinology Trust.

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