Lithium-Induced Nephrogenic Diabetes Insipidus Reversed with Timely Intervention: Case Report
Written By : Medha Baranwal
Medically Reviewed By : Dr. Kamal Kant Kohli
Published On 2026-05-01 16:00 GMT | Update On 2026-05-01 16:01 GMT
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Turkey: A recent case report published in Case Reports in Neurology by Sevil Uygun İlikhan from the Department of Internal Medicine, Ankara Bilkent City Hospital, Turkey, and colleagues highlights a reversible form of nephrogenic diabetes insipidus (NDI) triggered by long-term lithium therapy, highlighting the importance of early recognition and timely intervention.
Lithium remains a widely used and effective mood stabilizer, particularly in patients with chronic psychiatric disorders. However, its long-term use is known to affect renal function, particularly by impairing the kidney’s ability to respond to arginine vasopressin (AVP), which can result in NDI. This condition is characterized by the kidneys' inability to concentrate urine, resulting in excessive urination and disturbances in fluid and electrolyte balance.
The authors describe the case of a 52-year-old woman with paranoid schizophrenia who had been on prolonged lithium therapy along with other antipsychotic medications, including clozapine, quetiapine, and aripiprazole. She presented to the emergency department with a 10-day history of diarrhea, fatigue, excessive urination, and altered mental status.
On examination, the patient appeared moderately dehydrated, with dry oral mucosa, low-normal blood pressure, and tachycardia. Laboratory investigations revealed marked hypernatremia, with serum sodium levels ranging between 156 and 159 mmol/L. Despite elevated serum osmolality, her urine osmolality remained inappropriately low, confirming impaired urinary concentration. The patient was producing large volumes of urine daily, between 6.5 and 7.5 liters. Notably, her serum lithium level was elevated, while kidney function remained within normal limits.
Management focused on correcting fluid and electrolyte imbalances and addressing the underlying cause. The patient received intravenous 5% dextrose to replenish free water. Additional treatment included bicarbonate and potassium supplementation to correct metabolic acidosis and hypokalemia. Crucially, lithium therapy was discontinued. To control excessive urine output, a thiazide-based regimen was initiated.
The patient showed rapid clinical improvement. Within 72 hours, her serum sodium levels normalized to 140 mmol/L without the need for desmopressin, a medication commonly used in diabetes insipidus. Urine output decreased significantly to around 2 liters per day, and her mental status returned to baseline.
This case demonstrates that lithium-induced NDI, although potentially severe, can be reversible if identified early and managed appropriately. The findings emphasize that clinicians should maintain a high index of suspicion for NDI in patients on lithium who present with polyuria and electrolyte abnormalities.
The authors conclude that regular monitoring of patients receiving lithium therapy is essential to detect renal complications at an early stage. Prompt discontinuation of lithium, along with supportive care, can lead to recovery of renal concentrating ability and prevent further complications.
Reference:
İlikhan, S. U., Dilken, G., Hazıroğlu, G., Ülke, S., & Karaahmetoğlu, S. (2025). Reversible Nephrogenic Diabetes Insipidus Induced by Lithium: A Case Report. Case Reports in Nephrology, 2026(1), 9998067. https://doi.org/10.1155/crin/9998067
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