A patient with bipolar I disorder has been stable on lithium for 3 years. He develops polyuria (3.5 L/day), polydipsia, and urine specific gravity of 1.003 that does not concentrate after water deprivation but partially responds to desmopressin. Serum lithium is in the therapeutic range. What is the most likely complication?
- A Lithium-induced nephrogenic diabetes insipidus ✓
- B Lithium-induced central diabetes insipidus
- C Lithium toxicity causing SIADH
- D Primary polydipsia secondary to lithium-induced thirst
Explanation
Lithium-induced nephrogenic diabetes insipidus (NDI) is the most common renal tubular effect of long-term lithium therapy, occurring in 20–40% of patients. Lithium blocks aquaporin-2 (AQP2) insertion in collecting duct principal cells, impairing ADH responsiveness. Key features: urine specific gravity <1.010, inability to concentrate urine after water deprivation (confirms NDI), only partial response to desmopressin (partial, as some residual AQP2 function exists). Treatment includes adequate fluid intake, lowest effective lithium dose, amiloride (blocks ENaC, reducing lithium entry into collecting duct cells), and if severe, switching to an alternative mood stabiliser.
Reference: Kaplan & Sadock's Synopsis of Psychiatry, 11th ed.
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Written and medically reviewed by the StethoPrep medical team.