Abstract: PUB185
Partial Nephrogenic Diabetes Insipidus Secondary to Lithium Use
Session Information
Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders
- 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical
Authors
- Nassar, Sameh, St. Barnabas Hospital, Bronx, New York, United States
- Kashfi, Simon Adam, The City College of New York CUNY School of Medicine, New York, New York, United States
- Sanchez, Maria C., St. Barnabas Hospital, Bronx, New York, United States
- Flores Chang, Bessy Suyin, St. Barnabas Hospital, Bronx, New York, United States
- Ibrahim, Jamil, St. Barnabas Hospital, Bronx, New York, United States
Introduction
Nephrogenic diabetes insipidus (NDI) is caused by reduced renal response to vasopressin. NDI affects up to 40% of patients on lithium. We present a case of partial NDI secondary to lithium use.
Case Description
A 66 year old male with bipolar disorder on lithium presented with shortness of breath, chest tightness and cough. On exam he was cachectic, lethargic, tremulous with decreased skin turgor and dry mucous membranes found to have COVID-19 with initial unremarkable blood work. Received treatment for COVID and subsequently developed worsening encephalopathy, follow up blood work revealed elevated serum sodium of 168 mg/dl, with urine osmolality of 382 and lithium level was elevated at 1.6 mEq/L. He received adequate IV fluid hydration with hypotonic fluids and free water. Serum sodium remained elevated with polyuria. Follow up labs showed urine osmolality decrease to 94 mosml/L therefore nephrogenic diabetes insipidus was suspected. A desmopressin stimulation test was performed and hourly urine osmolality was obtained [Table 1] confirming the diagnosis of nephrogenic diabetes insipidus with a partial response to desmopressin compatible with lithium-induced partial diabetes insipidus. Treatment was started initially with chlorthalidone with inappropriate response, then dose increased to 100mg daily with further addition of amiloride 10mg twice daily with subsequent response and decrease of sodium level from 167 to 147 mEq/L.
Discussion
Lithium-induced NDI is explained by downregulation of aquaporin 2 channel expression in the principal cells due to accumulation of toxic concentrations of lithium and reduction of the kidneys’ ability to preserve water in response to vasopressin. NDI usually presents with polyuria, polydipsia, severe dehydration, and electrolyte imbalance. A less than 50% increase in urine osmolality following desmopressin administration proves NDI. Treatment options include high doses of desmopressin, low sodium diet, thiazide diuretics, amiloride, and NSAIDs.
Urine osmolalities during the desmopressin stimulation test
| Hour | Urine Osmolality (mosm/kg) |
| Before desmopressin | 90 |
| 1 | 113 |
| 2 | 113 |
| 3 | 113 |
| 4 | 118 |