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Related Experiment Videos

Pseudohyperaldosteronism: pathogenetic mechanisms.

Decio Armanini1, Lorenzo Calò, Andrea Semplicini

  • 1Department of Medical and Surgical Sciences-Endocrinology, University of Padua, via Ospedale 105, 35100 Padua, Italy.

Critical Reviews in Clinical Laboratory Sciences
|August 2, 2003
PubMed
Summary
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Pseudohyperaldosteronism mimics hyperaldosteronism by increasing mineralocorticoid effects. Causes include direct hormone action, enzyme inhibition of 11-hydroxysteroid-dehydrogenase type 2 (11HSD2), or genetic mutations affecting hormone receptors or sodium channels.

Area of Science:

  • Endocrinology
  • Genetics
  • Nephrology

Background:

  • Pseudohyperaldosteronism presents with clinical signs of hyperaldosteronism, including suppressed plasma renin activity and aldosterone levels.
  • It arises from conditions causing excessive mineralocorticoid activity, distinct from primary hyperaldosteronism.
  • Understanding the diverse etiologies is crucial for accurate diagnosis and management.

Purpose of the Study:

  • To elucidate the various mechanisms underlying pseudohyperaldosteronism.
  • To categorize the genetic and acquired causes of this condition.
  • To highlight the role of enzyme activity and receptor function.

Main Methods:

  • Review of existing literature on pseudohyperaldosteronism.
  • Analysis of etiological factors including direct mineralocorticoid effects, enzyme inhibition, and genetic mutations.

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  • Categorization based on the underlying molecular mechanisms.

    • Main Results:

    • Identified direct mineralocorticoid effects from substances like desoxycorticosterone, estrogens, and glycyrrhetinic acid.
    • Highlighted the role of 11-hydroxysteroid-dehydrogenase type 2 (11HSD2) deficiency, both inherited (apparent mineralocorticoid excess syndrome) and acquired (e.g., carbenoxolone, grapefruit juice).
    • Included activating mineralocorticoid receptor mutations and genetic defects in sodium channels (Liddle syndrome) as causes.

    Conclusions:

    • Pseudohyperaldosteronism results from diverse pathways leading to mineralocorticoid excess.
    • Mechanisms involve direct stimulation, impaired cortisol inactivation by 11HSD2, or altered mineralocorticoid receptor/sodium channel function.
    • Differential diagnosis requires consideration of these varied etiologies, encompassing genetic and exogenous factors.