Version May 2024
| Reduced aldosterone production |
| Hyporeninemic hypoaldosteronism |
| Kidney disease, most often diabetic nephropathy |
| Nonsteroidal antiinflammatory drugs |
| Calcineurin inhibitors |
| Volume expansion, as in acute glomerulonephritis |
| Angiotensin inhibitors, such as ACE inhibitors, angiotensin II receptor blockers, and direct renin inhibitors |
| Chronic heparin therapy (impairs aldosterone synthesis) |
| Primary adrenal insufficiency |
| Severe illness |
| Inherited disorders |
| Congenital hypoaldosteronism (21-hydroxylase deficiency and isolated hypoaldosteronism) |
| Pseudohypoaldosteronism type 2 (Gordon's syndrome) |
| Aldosterone resistance |
| Inhibition of the epithelial sodium channel |
| Potassium-sparing diuretics, such as spironolactone, eplerenone, amiloride, and triamterene |
| Antibiotics, trimethoprim, and pentamidine |
| Pseudohypoaldosteronism type 1 |
| Voltage defects |
| Markedly reduced distal sodium delivery |
| Acquired or congenital defects in sodium reabsorption by the distal tubule principal cells (obstructive uropathy), SLE, and sickle cell disease |
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