Syndromes that Mimic an Excess of Mineralocorticoids

High Blood Press Cardiovasc Prev. 2016 Sep;23(3):231-5. doi: 10.1007/s40292-016-0160-5. Epub 2016 Jun 1.


Pseudohyperaldosteronism is characterized by a clinical picture of hyperaldosteronism with suppression of renin and aldosterone. It can be due to endogenous or exogenous substances that mimic the effector mechanisms of aldosterone, leading not only to alterations of electrolytes and hypertension, but also to an increased inflammatory reaction in several tissues. Enzymatic defects of adrenal steroidogenesis (deficiency of 17α-hydroxylase and 11β-hydroxylase), mutations of mineralocorticoid receptor (MR) and alterations of expression or saturation of 11-hydroxysteroid dehydrogenase type 2 (apparent mineralocorticoid excess syndrome, Cushing's syndrome, excessive intake of licorice, grapefruits or carbenoxolone) are the main causes of pseudohyperaldosteronism. In these cases treatment with dexamethasone and/or MR-blockers is useful not only to normalize blood pressure and electrolytes, but also to prevent the deleterious effects of prolonged over-activation of MR in epithelial and non-epithelial tissues. Genetic alterations of the sodium channel (Liddle's syndrome) or of the sodium-chloride co-transporter (Gordon's syndrome) cause abnormal sodium and water reabsorption in the distal renal tubules and hypertension. Treatment with amiloride and thiazide diuretics can respectively reverse the clinical picture and the renin aldosterone system. Finally, many other more common situations can lead to an acquired pseudohyperaldosteronism, like the expansion of volume due to exaggerated water and/or sodium intake, and the use of drugs, as contraceptives, corticosteroids, β-adrenergic agonists and FANS. In conclusion, syndromes or situations that mimic aldosterone excess are not rare and an accurate personal and pharmacological history is mandatory for a correct diagnosis and avoiding unnecessary tests and mistreatments.

Keywords: 11 Hydroxysteroid dehydrogenase type 2; Aldosterone; Apparent mineralocorticoid excess syndrome; Deoxycorticosterone; Hypertension; Licorice; Mineralocorticoid receptor; Pseudohyperaldosteronism.

Publication types

  • Review

MeSH terms

  • Aldosterone / blood*
  • Biomarkers / blood
  • Cushing Syndrome / blood
  • Cushing Syndrome / drug therapy
  • Cushing Syndrome / etiology
  • Dexamethasone / therapeutic use
  • Diet / adverse effects
  • Genetic Predisposition to Disease
  • Glucocorticoids / therapeutic use
  • Humans
  • Hyperaldosteronism / blood*
  • Hyperaldosteronism / drug therapy
  • Hyperaldosteronism / etiology
  • Hyperaldosteronism / genetics
  • Hypertension / blood*
  • Hypertension / drug therapy
  • Hypertension / etiology
  • Hypertension / genetics
  • Liddle Syndrome / blood
  • Liddle Syndrome / drug therapy
  • Liddle Syndrome / genetics
  • Mineralocorticoid Receptor Antagonists / therapeutic use
  • Phenotype
  • Renin-Angiotensin System* / drug effects
  • Risk Factors
  • Sodium Chloride Symporter Inhibitors / therapeutic use
  • Up-Regulation


  • Biomarkers
  • Glucocorticoids
  • Mineralocorticoid Receptor Antagonists
  • Sodium Chloride Symporter Inhibitors
  • Aldosterone
  • Dexamethasone