A 78-year-old woman on hydrochlorothiazide for three months presents with fatigue and serum sodium of 124 mEq/L with normal volume status. The most important contributor to her hyponatremia is:

• A Osmotic diuresis from glycosuria induced by the drug
• B Increased proximal tubular sodium reabsorption causing obligatory water loss
• C Direct stimulation of aquaporin-2 channels by the thiazide molecule
• D Impaired diluting ability with non-suppressible antidiuretic hormone secretion ✓

Explanation

Thiazides preserve medullary concentration gradient and concentrating ability but abolish cortical diluting capacity in the distal nephron, so any ingested water cannot be excreted maximally and vasopressin release driven by mild volume contraction further retains free water. Elderly women are the highest risk group, typically after weeks to months of therapy. Loops spare the diluting defect relatively better, which is why they are preferred if diuresis is needed in hyponatremic patients.

Reference: Harrison's Principles of Internal Medicine, 21st ed.

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Written and medically reviewed by the StethoPrep medical team.