A patient on long-term lithium therapy for bipolar disorder is started on hydrochlorothiazide for hypertension. One week later, he develops tremors, confusion, and nausea. Serum lithium levels are elevated. The increase in lithium levels is primarily because thiazides:

• A Increase lithium reabsorption in the proximal tubule ✓
• B Inhibit lithium metabolism by cytochrome P450
• C Increase lithium absorption from the gastrointestinal tract
• D Decrease lithium reabsorption in the distal tubule

Explanation

Thiazide diuretics cause sodium depletion, which triggers compensatory upregulation of sodium reabsorption in the proximal tubule. Lithium, which is handled similarly to sodium, is passively reabsorbed along with sodium, leading to elevated serum lithium levels and toxicity. Lithium is not metabolized by cytochrome P450, and thiazides do not affect its GI absorption.

Reference: Katzung and Trevor's Pharmacology, 12th ed.

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