SUN-283 Lithium Induced Partial Nephrogenic Insipidus: An Unusual Presentation

• Published in: Journal of the Endocrine Society Vol. 4; no. Supplement_1
• Main Authors: Akagi, Roberto Kenji Mitsui, Olajide, Omolola Bolaji
• Format: Journal Article
• Language: English
• Published: US Oxford University Press 08.05.2020
• Subjects: Neuroendocrinology and Pituitary
• ISSN: 2472-1972; 2472-1972
• DOI: 10.1210/jendso/bvaa046.962

Abstract Background: Diabetes insipidus (DI) is characterized by hypotonic polyuria and polydipsia. Nephrogenic DI is the result of an inadequate response of the kidneys to arginine vasopressin (AVP), either due to hereditary causes or acquired from various drugs, most commonly lithium. Clinical case: A 30 year old male with past medical history of Hashimoto’s thyroiditis, severe mental impairment was admitted to the hospital for abdominal pain. Medical history was difficult to obtain since the patient was nonverbal. His thyroid function tests, electrolytes including sodium, potassium were all normal on admission. During the hospital course, he was made NPO for both an upper and lower GI endoscopy. He notably had a mild increase in sodium level with subsequent improvement after restitution of diet. Two days after the procedure, he was found to be drinking out of the toilet and also attempting to drink from the urine jug. Due to this odd behavior, he had to be put on physical restraints. The day after, he was found to have a serum sodium of 158 mEq/L. Hypotonic saline was started and urine output was notably ranging from 6-10 L/day with a negative balance. Desmopressin (DDAVP) test was done with a resultant urine osmolality of 170, 237, 257 and 264 mOsm/kg after 30, 60, 90 and 180 mins. Subcutaneous DDAVP was started with some improvement of serum sodium and decrease in urine output. Endocrinology service was consulted for the evaluation of hypernatremia and polyuria. Initial review of his medications did not show any potential cause of DI. Further inquiry of his prior medication history revealed that he had taken Lithium for over 10 years and stopped 4 months prior to the admission due to polyuria. After excluding other causes of polyuria, with partial improvement of urine osmolality to a level <300 mOsm/kg and a clinical history of prior Lithium therapy, a diagnosis of partial nephrogenic DI was made. Patient was started on HCTZ and given adequate water intake with subsequent improvement of his serum sodium back to normal. Conclusion: Nephrogenic DI due to Lithium use usually recovers after treatment is stopped but could be persistent for several years after. In our case, the patient compensated for his polyuria with increased water intake. When his water intake was restricted due to physical restraints, polyuria and subsequently hypernatremia became evident. A thorough medication history including past drug use is essential as it can help unravel the offending agent which was Lithium in our case. There needs to be an increased awareness that the effect of Lithium in the kidneys could be persistent even after stopping the drug for up to many years. References: Thompson CJ. Persistent nephrogenic diabetes insipidus following lithium therapy. Scott Med J 1997; 42:16-17.