Mineralocorticoid Replacement Therapy

Aldosterone is the body’s principal mineralocorticoid. In the distal nephron, it directs the kidneys to retain sodium; water follows sodium, supporting extracellular fluid volume and blood pressure. In exchange, the kidneys excrete potassium and hydrogen ions. This explains the clinical pattern of aldosterone deficiency. Sodium loss pulls water out of the circulation, producing volume depletion, salt craving, postural hypotension, and sometimes hyponatremia. Potassium is retained, so hyperkalemia may develop. The patient may describe dizziness when standing long before a markedly low seated blood pressure appears. Mineralocorticoid excess produces the mirror image: sodium and water retention, hypertension, edema, and potassium wasting. This opposite physiology determines whether the patient needs fludrocortisone replacement or a mineralocorticoid-receptor antagonist.