Case Reports in Nephrology · Published 2026-01-01 · DOI 10.1155/crin/9998067
Lithium is an effective mood stabilizer but may cause nephrogenic diabetes insipidus (NDI) by impairing the renal collecting duct response to arginine vasopressin (AVP). We report a 52-year-old woman on long-term lithium therapy who presented with diarrhea, fatigue, polyuria, and confusion. Initial evaluation showed hypernatremia (serum sodium 156–159 mmol/L), low urine osmolality (101 mOsm/kg) despite serum osmolality of 286 mOsm/kg, daily urine output of 6.5–7.5 L, and a lithium level of 1.65 mmol/L. Renal function was preserved. Intravenous 5% dextrose was administered for free-water replacement. Bicarbonate and potassium supplementation were initiated based on blood gas and biochemical findings consistent with metabolic acidosis (pH: 7.33 and serum bicarbonate: 22.1 mmol/L) and hypokalemia, requiring potassium supplementation. Lithium was discontinued, and a thiazide-containing regimen was initiated. Without desmopressin, serum sodium normalized to 140 mmol/L within 72 h, urine output decreased to approximately 2 L/day, and mental status fully recovered. This case demonstrates that timely recognition and management of lithium-induced NDI may allow recovery of urinary concentrating ability.
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