How to Cite This Chapter: Rodríguez-Gutiérrez R, Prebtani APH, 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. Accessed July 15, 2024.
Last Updated: January 10, 2022
Last Reviewed: January 10, 2022
Chapter Information

DEFINITION, Etiology, PathogenesisTop

Hypoaldosteronism is defined as insufficient secretion or ineffective action of aldosterone. It can be caused by defective stimulation of aldosterone secretion, primary defects in adrenal synthesis or secretion of aldosterone, and aldosterone resistance or blockade. 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, due to decreased synthesis or release of aldosterone from the adrenal gland, 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, classic 21-hydroxylase deficiency (leading to hypersecretion of adrenal androgens with reduced production of cortisol and aldosterone), severe illness, transient hypoaldosteronism following surgical cure of hyperaldosteronism, 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 leading to decreased aldosterone stimulation/secretion: Hyporeninemic hypoaldosteronism/type IV renal tubular acidosis (RTA) (diabetic nephropathy, advanced age with chronic tubulointerstitial disease), drugs inhibiting renin secretion (nonsteroidal anti-inflammatory drugs, beta-blockers, calcineurin inhibitors (INN cyclosporine), angiotensin-converting enzyme inhibitors, angiotensin receptor blockers.

3) Aldosterone resistance or blockade: Type I 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 levels of plasma renin, serum aldosterone, serum cortisol, and sometimes androgens (Table 1).


Treatment depends on etiology:

1) Primary hypoaldosteronism: see Primary Adrenal Insufficiency.

2) Hyporeninemic hypoaldosteronism: Potassium restriction, fludrocortisone 0.05 to 0.2 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


Normal or ↓

­↑, increased; ↓, decreased.

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