A 70-year-old man is found to have serum sodium of 122 mEq/L. He is on a thiazide diuretic for hypertension. His urine osmolality is 480 mOsm/kg, urine sodium is 55 mEq/L, and he appears euvolaemic. Thyroid and adrenal function are normal. What is the likely mechanism and first-line treatment?
- A Thiazide-induced SIADH-like hyponatraemia; stop thiazide and restrict fluid to 500–800 mL/day ✓
- B Cerebral salt wasting; treat with hypertonic saline and fludrocortisone
- C Psychogenic polydipsia; restrict fluid intake only
- D Reset osmostat; no treatment needed
Explanation
Thiazide diuretics cause euvolaemic hyponatraemia by impairing urinary dilution (blocking NaCl transport in the distal convoluted tubule) while ADH is appropriately released; the mechanism mimics SIADH. The features here (concentrated urine, high urinary Na, euvolaemia, normal TSH/cortisol) confirm thiazide-induced hyponatraemia. Stopping the thiazide is mandatory; fluid restriction augments correction. Hypertonic saline is reserved for severe symptomatic hyponatraemia.
Reference: Harrison's Principles of Internal Medicine, 21st ed.
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