Abstract: PUB107
Idiopathic Arginine Vasopressin Deficiency: A Case of Polyuria-Polydipsia Syndrome in a 38-Year-Old Active Duty Soldier
Session Information
Category: Fluid, Electrolytes, and Acid-Base Disorders
- 1102 Fluid, Electrolyte, and Acid-Base Disorders: Clinical
Author
- Gaeta, Robert M., Womack Army Medical Center, Fort Bragg, North Carolina, United States
Group or Team Name
- Womack Army Medical Center
Introduction
A 38-year-old active-duty White male US Army Soldier presented with a two-month history of progressive polyuria (documented 6.2L for 24h urine collection) and compensatory polydipsia (>8L daily). Renal function was preserved (steady-state serum creatinine 0.9-1.1 mg/dL over past several years) without albuminuria or hypertension. Clinical history was unremarkable for neurosurgery, traumatic brain injury, or lithium exposure although does have a history of anxiety disorder for which he is not prescribed any medication. He has no history of bilateral urinary obstruction, hypercalcemia, diabetes, recent azotemia, glucocorticoid therapy, high protein supplements or mannitol administration.
Case Description
Differential diagnosis focused on differentiating primary polydipsia from AVP deficiency (central DI) and AVP resistance (nephrogenic DI). A standard water 12h deprivation test was inconclusive; serum osmolality (SOsm) was initially low (153 mOsm/kg), likely due to chronic medullary washout from prolonged polydipsia. Subsequent 2mcg dDAVP challenge demonstrated a 91% increase in urine osmolality (UOsm 228 to 436 mOsm/kg) over 2 hours. Diagnosis was confirmed by a stimulated copeptin of 1.7 pmol/L (Reference: <4.9 pmol/L), excluding primary polydipsia and AVP resistance.
Contrast-enhanced MRI brain demonstrated an absent posterior pituitary "bright spot" without stalk thickening. Secondary workup for infiltrative or autoimmune etiologies (IgG4-related disease, Sarcoidosis, LCH, and germ cell tumors) remains ongoing, including serum ACE, AFP, β-hCG, and IgG4 levels. In the setting of a negative serological workup, PET/CT and CSF analysis for cytology and tumor markers are planned.
Discussion
Initial management prioritized the prevention of iatrogenic hyponatremia. Desmopressin was withheld until biochemical confirmation of AVP deficiency was established to mitigate seizure risk from continued volitional intake. Treatment was initiated with oral desmopressin 0.1 mg nightly, hydrochlorothiazide, and a low-solute/low-sodium (<2g/d) diet. Fluid intake was restricted to 2–3 L/d. NSAIDs were strictly contraindicated due to synergistic hyponatremia risk.