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Central Diabetes Insipidus in the Background of Lithium Use: Consider Central Causes Despite Nephrogenic as the Most
Jeffrey J Li1, Shirley Tan1, Takumi Kawashita2
1Department of Internal Medicine, California University of Science and Medicine, Colton, CA, USA.
Insights
Lithium use can rarely cause central diabetes insipidus (CDI), a condition affecting water balance. This case highlights CDI as a potential diagnosis in patients experiencing excessive urination and high sodium levels during long-term lithium treatment.
Area of Science:
- Endocrinology
- Nephrology
- Psychiatry
Background:
- Lithium is a common treatment for bipolar disorder.
- Nephrogenic diabetes insipidus is a known side effect of lithium.
- Central diabetes insipidus (CDI) is a rare but documented adverse effect of lithium.
Observation:
- A 31-year-old woman on long-term lithium therapy presented with polyuria and polydipsia.
- Lab results revealed hypernatremia, elevated serum osmolality, and low urine osmolality.
- Brain MRI showed no pituitary abnormalities, and desmopressin challenge confirmed CDI.
Findings:
- Despite subtherapeutic lithium levels, chronic lithium use was identified as the cause of CDI.
- Other common causes of CDI were excluded.
- This case represents a rare instance of lithium-induced CDI.
Implications:
- CDI should be considered in the differential diagnosis of polyuria and hypernatremia in patients on long-term lithium.
- Clinicians should assess for both nephrogenic and central diabetes insipidus in patients with these symptoms.
- This case underscores the importance of monitoring for rare adverse effects of lithium therapy.
Abstract:
BACKGROUND Nephrogenic diabetes insipidus is a well-known adverse effect of lithium use. Albeit rare, there have also been documented cases of central diabetes insipidus (CDI) associated with lithium use. CASE REPORT A 31-year-old woman with a past medical history of bipolar disorder, managed with lithium 300 mg by mouth every day for 3 years, was assessed for a 1-year history of polyuria with accompanying polydipsia. During her initial hospital stay, her estimated urine output was more than 4 L per day. Initial labs showed elevated serum sodium (149 mmol/L; reference range 135-145), elevated serum osmolality (304 mOsm/kg; reference range 275-295), urine osmolality of 99 mOsm/kg (reference range 50-1200), and urine specific gravity (1.005; reference range 1.005-1.030). Lithium was at a subtherapeutic level of 0.05 mEq/L (reference range 0.6-1.2). Magnetic resonance imaging of the brain revealed no abnormalities of the pituitary gland. Two different occasions of desmopressin administration resulted in >50% increase in urine osmolality, confirming the diagnosis of CDI. Common causes of CDI, including trauma, tumors, and familial CDI, were ruled out and chronic lithium use was determined as the most probable cause for the patient's CDI. CONCLUSIONS CDI in the background of chronic lithium use is rarely reported. We present this case to consider CDI as a differential diagnosis when evaluating polyuria and hypernatremia in patients with long-term lithium use. These presentations warrant the consideration of both types of diabetes insipidus in the differential diagnoses.
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