Lithium is filtered freely at the glomerulus and is reabsorbed in which segment of the nephron?

Explanation

## Lithium Renal Handling **Key Point:** Lithium is freely filtered at the glomerulus and undergoes significant reabsorption in the proximal convoluted tubule (PCT), competing with sodium for reabsorption via the Na⁺-K⁺-ATPase pump. ### Mechanism of Reabsorption Lithium ions are treated by the kidney similarly to sodium ions: - Freely filtered across the glomerular filtration barrier - Reabsorbed in the PCT alongside sodium via active transport - Approximately 80% of filtered lithium is reabsorbed in the PCT - The remaining 20% is reabsorbed in the loop of Henle and distal tubule ### Clinical Significance **High-Yield:** Sodium depletion (from diuretics, low-salt diet, or dehydration) reduces lithium clearance by increasing PCT reabsorption, leading to lithium accumulation and toxicity. **Clinical Pearl:** Thiazide diuretics increase lithium levels by causing volume depletion and enhanced proximal tubular reabsorption, whereas loop diuretics (furosemide) and osmotic diuretics (mannitol) increase lithium clearance. ### Therapeutic Implications - Adequate sodium and fluid intake is essential to maintain lithium clearance - Renal function monitoring (serum creatinine, eGFR) is mandatory during chronic lithium therapy - Lithium has a narrow therapeutic window (0.5–1.2 mEq/L); toxicity begins above 1.5 mEq/L