Hyperaldosteronism

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Hyperaldosteronism Main page

Patient Information

Overview

Classification

1- Primary hyperaldosteronism
2- Secondary hyperaldosteronism
3- Pseudohyperaldosteronism causes (low renin)

Differentiating diagonsis

History and symptoms

Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Mehrian Jafarizade, M.D [2]

This page contains general information about Hyperaldosteronism. For more information on specific types, please visit the pages on Primary hyperaldosteronism, and Secondary hyperaldosteronism.

Synonyms and keywords: Aldosteronism

Overview

Classification

Aldosteronism and mineralocorticoid excess may be classified into two types, primary hyperaldosteronism (conn's syndrome) and secondary hyperaldosteronism. The different types of aldosteronism described in the below table:

Cause Laboratory
Renin activity Aldosterone levels urinary free cortisone
Renin-producing tumors
Apparent mineralocorticoid excess ↓↓
Licorice ingestion Moderate ↑
Ectopic ACTH production Markedly ↑↑
Primary hyperaldosteronism
Familial hyperaldosteronism
Cushing syndrome Markedly ↑↑
Renal artery stenosis
Liddle's syndrome
Diuretic use Nl
17 alpha hydroxylase deficiency
11 beta hydroxylase deficiency
Coarctation of aorta

Pseudohyperaldosteronism causes:

Pseudohyperaldosteronism causes Disease Cause Labratory
Elevated mineralocorticoid Renin Aldosterone Treatment
Endogenous causes Deficiency of 17a-hydroxylase Deoxycorticosterone (DOC)
11b-hydroxylase
Apparent mineralocorticoid excess syndrome (AME) Genetic or acquired defect of 11-HSD dexamethasone and/or MR-blockers
Liddle’s syndrome Mutation of the epithelial sodium channels (ENaC) gene in the distal renal tubules amiloride or triamterene can reverse the clinical picture reactivating the renin aldosterone
Cushing’s syndrome The main pathogenetic mechanism is linked to the excess

of cortisol which saturates 11-HSD2 activity, allowing cortisol to bind MR. A similar picture is also related to over secretion of cortisol by adrenocortical carcinomas. In some cases the disease is associated with secondary hyperaldosteronism due to a direct activation of the renin angiotensin system by glucocorticoids.

Insensitivity to glucocorticoids (Chrousos syndrome) mutations in glucocorticoid receptor (GR) gene Deoxycorticosterone (DOC) dexamethasone
Aldosterone-secreting adrenocortical carcinoma
Geller’s syndrome mutation of MR that alters its specificity and allows progesterone to bind MR severe hypertension particularly during pregnancy
Gordon’s syndrome or pseudohypoaldosteronism type 2 due to different mutations correlated to different phenotypes. Mutations of at least four genes have been identified, including WNK1 and WNK4 hypertension, characterized by hyperkalemia, normal renal function thiazide diuretics and/or dietary sodium restriction
Exogenous causes Corticosteroids with mineralocorticoid activity
Hypersodic diets
Water intossications
Licorice
grapefruit
Contraceptives
Some progestins
Particular causes of hypertension Sclerosis of juxtaglomerular apparatus (diabetic microangiopathy and/or of the elderly)
FANS
B-Adrenergic agonists
Aging
Low-renin essential hypertension
Autonomic dysfunction
Partial/total nephrectomy or removal of renal tissue


Differentiating Diagnosis

Hyperaldosteronism should be differentiated from other diseases causing hypertension and hypokalemia for example:

 
 
 
 
 
 
 
 
Hypertension and Hypokalemia
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Plasma renin activity
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Normal or High (Plasma Renin/Aldosterone ratio <10
 
 
 
 
 
 
 
 
 
 
 
Suppressed (Plasma Renin/Aldosterone ratio >20
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
*Renin-secreting tumors
*Diuretic use
*Renovascular hypertension
*Coarctation of aorta
*Malignant phase hypertension
 
 
 
 
 
 
 
 
 
 
 
Urinary aldosterone
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Elevated
 
Normal
 
 
Low
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Conn's syndrome (Primary aldosteronism)
 
Profound K+ depletion
 
 
• 17 alpha hydroxylase deficiency
• 11 beta hydroxylase deficiency
• Liddle's syndrome
• Licorice ingestion
• Deoxycortisone producing tumor
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Add Mineralocrticoid antagonist for 8 weeks
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
BP response
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
No BP response
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
• Deoxycorticosterone excess( Tumor, 17 alpha hydroxylase and 11 beta hydroxylase deficiency)
• Licorice ingestion
•Glucocorticoid resistance
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
 
Liddle's syndrome)

History and symptoms

de:Hyperaldosteronismus it:Iperaldosteronismo


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