Abstract: FR-PO0628
A Case of Osmotic Diuresis Obfuscating Arginine Vasopressin Deficiency
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 2
November 07, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Authors
- Choi, Jeongwon, Carilion Clinic, Roanoke, Virginia, United States
- Gordon, Douglas J, Carilion Clinic, Roanoke, Virginia, United States
- Hu, Dennis, Valley Nephrology Associates, Roanoke, Virginia, United States
- Roman, Renato Marcelino B., Valley Nephrology Associates, Roanoke, Virginia, United States
Introduction
Osmotic diuresis is an underrecognized cause of polyuria and hypernatremia the intensive care setting. Arginine Vasopressin Deficiency (AVPD) can be the main cause of polyuria in cases of neurosurgery involving the hypothalamus. However, glucocorticoids can cause urea excretion and osmotic diuresis through downregulation of urea transporters and protein catabolism – confounding the diagnosis of AVPD. This case highlights the pivotal role of urine studies in accurate workup of hypernatremia.
Case Description
A 20-year-old female with a third ventricular tumor with obstructive hydrocephalus was admitted for tumor resection. She received mannitol, iodinated contrast, and daily dexamethasone. She underwent a transcallosal resection of the tumor that was adherent to bilateral A1 segment of anterior cerebral arteries and posterior communicating arteries. Neurosurgeons noted high risk of hypothalamic involvement during the procedure.
Within 24 hours after surgery, she became polyuric and her sodium level increased from 138 to 164 mEq/L. AVPD was suspected, and desmopressin was started. Workup showed urine osmolality of 917mOsm/kg, urine sodium of 244 mmol/L, urine potassium of 24.8 mmol/L, serum osmolality 309mOsm/kg, urine urea above 1700 mg/dL, and BUN of 7mg/dL. Free water clearance was -8.2 liters, indicating that osmotic diuresis rather than AVPD was the predominant cause of polyuria. Given the normal BUN and high urine osmolality, dexamethasone was suspected to be the cause of osmotic diuresis.
Patient remained polyuric while dexamethasone was weaned. Urine urea peaked at day 6 at above 1700 mg/dL and urine osmolality peaked on day 7 at 1564 mOsm/kg. Patient’s polyuria resolved as the urine osmolality decreased and the urine electrolytes eventually normalized on desmopressin alone.
Discussion
This case underscores glucocorticoids as a cause of polyuria and hypernatremia in a neurosurgical patient. Glucocorticoids are frequently used post-op and are known to downregulate urea transporters of the inner medullary collecting duct (UT-A1, UT-A3) and promote protein catabolism, - leading to increased urine urea excretion and consequently osmotic diuresis. Differentiating the cause of polyuria is essential because it changes the patient’s clinical management. Early evaluation of urine osmolality, electrolytes, and urea nitrogen can help avoid diagnostic pitfalls.