How to Cite This Chapter: Rodríguez-Gutiérrez R, Contreras-Garza B, Rodriguez-Tamez G, Słowińska-Srzednicka J, Płaczkiewicz-Jankowska E. Hypoaldosteronism. McMaster Textbook of Internal Medicine. Kraków: Medycyna Praktyczna. https://empendium.com/mcmtextbook/chapter/B31.II.11.4.?utm_source=nieznany&utm_medium=referral&utm_campaign=social-chapter-link Accessed December 02, 2021.
Last Updated: January 26, 2018
Last Reviewed: August 7, 2019
Chapter Information

Etiology, PathogenesisTop

Hypoaldosteronism can be caused by defective stimulation of aldosterone secretion, primary defects in adrenal synthesis or secretion of aldosterone, and aldosterone resistance. The major clinical manifestations are hyperkalemia and mild hyperchloremic metabolic acidosis. When hyponatremia is present, primary adrenal insufficiency should be suspected. Most frequent causes include:

1) Primary aldosterone deficiency should be suspected in persons who have hyperkalemia despite normal renal function and lack of potassium supplementation or treatment with potassium-sparing diuretics; this may be caused by primary adrenal insufficiency, bilateral adrenalectomy, 21-hydroxylase deficiency (leading to hypersecretion of adrenal androgens with reduced production of cortisol and aldosterone), or aldosterone synthase deficiency (leading to isolated hypoaldosteronism). Causes of hyperkalemia other than endocrine disorders should also be considered, including drugs inhibiting adrenal steroid synthesis (eg, ketoconazole) and, although infrequently, heparin, which reduces the number of angiotensin II receptors in the zona glomerulosa of the adrenal cortex and results in suppression of aldosterone synthesis and hyperkalemia.

2) Renin-angiotensin-aldosterone system suppression: Hyporeninemic hypoaldosteronism (diabetic nephropathy, advanced age), drugs inhibiting renin secretion (nonsteroidal anti-inflammatory drugs, beta-blockers, ciclosporin [INN cyclosporine]), angiotensin-converting enzyme inhibitors, angiotensin receptor blockers.

3) Aldosterone resistance: Type I and type II pseudohypoaldosteronism, potassium-sparing diuretics that compete for the aldosterone receptor (eg, spironolactone and eplerenone) or that close the sodium channels in the luminal membrane (eg, amiloride and triamterene), and certain antibiotics that inhibit the collecting tubule sodium channel (trimethoprim and pentamidine).


Diagnosis is based on clinical history, focusing primarily on the use of medications or presence of diseases that could interfere with aldosterone metabolism and on laboratory findings. The different causes of hypoaldosteronism can be differentiated by measurement of plasma renin activity (PRA), serum aldosterone levels, and serum cortisol concentrations (Table 6.1-1).


Treatment depends on etiology:

1) Primary hypoaldosteronism: see Primary Adrenal Insufficiency.

2) Hyporeninemic hypoaldosteronism: Potassium restriction, fludrocortisone 0.2 to 1 mg/d. In case of hypertension or edema, consider furosemide or a thiazide diuretic. Monitor serum potassium levels.

3) Drug-induced hypoaldosteronism: Attempt to discontinue or reduce the dose of the offending drug. Correct electrolyte abnormalities.


Table 6.1-1. Differential diagnosis of different causes of hypoaldosteronism


Plasma renin activity

Serum aldosterone

Serum cortisol

Hyporeninemic hypoaldosteronism


Primary adrenal insufficiency


Adrenal enzyme deficiency



­↑, increased; ↓, decreased.

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