Primary Aldosteronism: New Answers, New Questions

Horm Metab Res. 2015 Dec;47(13):935-40. doi: 10.1055/s-0035-1565182. Epub 2015 Nov 20.

Abstract

There have been 2, and possibly 3, major questions for primary aldosteronism (PA) answered at least in principle over the past 5 years. The first is that of somatic mutations underlying the majority of aldosterone producing adenomas. The second is the extension of our knowledge of the genetics of familial hypertension, and the third the role of renal intercalated cells in sodium homeostasis. New questions for the next 5 years include a single accepted confirmatory/exclusion test; standardisation of assays and cut-offs; alternatives to universal adrenal venous sampling; reclassification of 'low renin hypertension'; recognition of the extent of 'occult' PA; inclusion of low-dose mineralocorticoid receptor antagonist in first-line therapy for hypertension; and finally, possible resolution of the aldosterone/inappropriate sodium status enigma at the heart of the cardiovascular damage in PA.

Publication types

  • Review

MeSH terms

  • Adenoma / drug therapy
  • Adenoma / genetics
  • Humans
  • Hyperaldosteronism / complications
  • Hyperaldosteronism / drug therapy
  • Hyperaldosteronism / pathology*
  • Hyperaldosteronism / physiopathology
  • Hypertension / complications
  • Mineralocorticoid Receptor Antagonists / therapeutic use
  • Mutation / genetics
  • Renin / metabolism

Substances

  • Mineralocorticoid Receptor Antagonists
  • Renin