title: The renaissance of primary aldosteronism: what has it taught us?
abstract: The growing realisation since the early 1990s that primary aldosteronism (PA) is a much more common cause of hypertension than previously thought, and that aldosterone excess has adverse effects that are at least partly independent of blood pressure, has been the main driving force for a renaissance in clinical and research interest in PA. This has generated a wealth of new knowledge regarding (1) PA's high prevalence, (2) the extent of non-BP dependent cardiovascular and renal organ damage and morbidity and reduced quality of life associated with PA, all of which appear to be at least partly ameliorated by specific treatment (especially surgical) directed against excessive aldosterone action, (3) the diversity of adrenal histopathology associated with PA and the need to subdivide patients based on glucocorticoid remediability (by genetic testing for the hybrid gene mutation causing familial hyperaldosteronism type I, FH-I) and lateralisation on adrenal venous sampling in order to ensure optimal treatment, (4) the value of elucidating genetic bases for PA in terms of improving detection, understanding of pathogenesis and treatment, as illustrated by the determination of the genetic basis of FH-I, and (5) the genetic basis of more common forms including aldosterone-producing adenoma. From the clinical perspective, the principal lesson learnt is that PA, being a common cause of cardiovascular morbidity and reduced quality of life reversible by specific treatment, is worth looking for.
authors: Endocrine Hypertension Research Centre, Greenslopes and Princess Alexandra Hospitals, University of Queensland School of Medicine, Brisbane, Australia. m.stowasser@uq.edu.au
authors: Michael
authors: M
authors: Stowasser
authors: Richard Douglas
authors: RD
authors: Gordon
mesh_terms: D000311:Adrenal Glands / Q000503:physiopathology; D006801:Humans; D006929:Hyperaldosteronism / Q000097:blood / Q000150:complications / Q000453:epidemiology / Q000235:genetics / Q000628:therapy; D006973:Hypertension / Q000097:blood / Q000453:epidemiology / Q000209:etiology / Q000503:physiopathology / Q000628:therapy; D009154:Mutation; D015995:Prevalence