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:

• Renal artery stenosis
• Cushing's syndrome
• Congenital adrenal hyperplasia (CAH)
  • 17 alpha hydroxylase deficiency
  • 11 beta hydroxylase deficiency
• Liddle's syndrome
• Diuretic use
• Licorice ingestion
• Renin-secreting tumors

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

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