MON-869 - A Race Against Hypernatremia : Lithium-Induced Nephrogenic Diabetes Insipidus Developing within 24 Hours

Background: Nephrogenic diabetes insipidus (NDI) affects up to 40% of lithium-treated patients and typically develops gradually over weeks to years of chronic therapy.[1-3] Acute lithium overdose rarely precipitates severe NDI with life-threatening hypernatremia. We report a case of rapid-onset NDI following accidental lithium overdose, demonstrating dramatic electrolyte derangements and response to desmopressin therapy.

Case Presentation: A 51-year-old female with bipolar disorder on chronic lithium therapy presented with altered mental status and agitation after accidental overdose. one day prior, her lithium level was therapeutic at 1.3 mmol/L. On admission, lithium was 2.8 mmol/L (therapeutic 0.6-1.2 mmol/L), sodium 141 mmol/L, creatinine 1.12 mg/dL, urine osmolality 398 mOsm/kg, and urine sodium 122 mEq/L. Lithium was discontinued and IV lactated Ringer's initiated.
Within 24 hours, severe hypernatremia developed (sodium 148→152→157 mmol/L) despite aggressive fluid resuscitation. Urine osmolality plummeted from 398 to 143 mOsm/kg, indicating acute NDI. Creatine kinase peaked at 922 U/L. Nephrology recommended D5W infusion (150 mL/hour) and intranasal desmopressin. Lithium levels declined progressively (2.8→2.1→1.8→1.7→1.5→1.2→1.1 mmol/L).
Outcome: Combined hypotonic fluid replacement and desmopressin therapy resulted in gradual normalization of serum sodium and restoration of renal concentrating ability. The patient achieved complete recovery with normalized electrolytes and renal function. Following psychiatric evaluation, lithium was cautiously reintroduced at reduced dosing with close monitoring. She was discharged with multidisciplinary nephrology and psychiatry follow-up.

Conclusion: This case demonstrates acute lithium toxicity can precipitate severe NDI within hours, contrasting with the typical gradual onset over weeks to years.[1-2][4] The dramatic decline in urine concentrating ability (osmolality 398→143 mOsm/kg in 24 hours) and severe hypernatremia (141→157 mmol/L) despite aggressive hydration underscore the potential for acute supratherapeutic levels to cause rapid renal dysfunction. While standard NDI treatment involves thiazide diuretics, NSAIDs, and amiloride, desmopressin may provide benefit in acute settings despite theoretical vasopressin resistance.[3][5-6] This case highlights the critical importance of early recognition, aggressive hypotonic fluid management, and multidisciplinary care to prevent irreversible complications. Patient education regarding lithium dosing and regular therapeutic monitoring remain essential preventive strategies.

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