Abstract: FR-PO0886
Severe Cerebral Salt Wasting in Autoimmune Glial Fibrillary Acidic Protein (GFAP) Astrocytopathy
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 1
October 23, 2026 | Location: Exhibit Hall A, 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
- Santamaria Garcia, Cristofer Francisco, University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
- Flood, Ryan P., University of Colorado Anschutz Medical Campus, Aurora, Colorado, United States
Introduction
Cerebral salt wasting (CSW) is an underrecognized cause of hyponatremia in intracranial disease. Distinguishing CSW from SIADH is essential because fluid restriction may worsen hypovolemia and cerebral injury. We report severe natriuretic polyuria attributed to GFAP astrocytopathy.
Case Description
A 35-year-old woman with no medical history presented with one week of headache, nausea, vomiting, fever, and intermittent diplopia. Initial sodium was 138 mmol/L. CSF showed 860 nucleated cells/μL with 90% lymphocytes, protein 215 mg/dL, and glucose 36 mg/dL; empiric antimicrobials were started. One week later, sodium fell to 124 mmol/L with serum osmolality 258 mOsm/kg, urine osmolality 810 mOsm/kg, and urine sodium 273 mmol/L. Urine output rose from 1.1 to 9.7 L/day with orthostasis, negative fluid balance, hypokalemia requiring up to 60 mEq potassium every 6 hours, and FE uric acid 24.6%. TSH and cortisol were normal. CT showed cerebral edema, prompting hypertonic saline, but she required up to 200 mL/hour for several days to maintain sodium. Given natriuresis, polyuria, hypovolemia, and persistent uricosuria, CSW was favored over SIADH. Fludrocortisone 0.2 mg twice daily improved sodium to 145–150 mmol/L despite urine sodium in the 300s. Hypertonic saline was weaned as cerebral edema improved, although natriuresis and polyuria persisted. Infectious studies and initial autoimmune evaluation were unrevealing. She later developed progressive leg weakness; MRI showed longitudinally extensive myelitis with a trident sign. Repeat testing showed CSF GFAP-IgG positivity by IFA at 1:16, confirming GFAP astrocytopathy. She received corticosteroids and rituximab 1000 mg, with a second dose planned in two weeks followed by maintenance every six months. Neurologic status improved, and sodium was 137 mmol/L at discharge, though high urine output recurred requiring fludrocortisone during rehabilitation.
Discussion
This case highlights severe CSW as a rare nephrologic manifestation of autoimmune GFAP astrocytopathy. In meningoencephalitis, high urine sodium and concentrated urine may be misattributed to SIADH. Hypovolemia, polyuria, negative fluid balance, severe natriuresis, hypokalemia, persistent uricosuria, and response to saline/fludrocortisone supported CSW. Treatment requires aggressive sodium and volume repletion rather than fluid restriction.