Abstract: FR-PO0900
Therapy Targets for Secondary Hyperaldosteronism in a Patient with Gastrointestinal Sodium Wasting
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
- Thomson, Holly, Oregon Health & Science University, Portland, Oregon, United States
- Rope, Rob, Oregon Health & Science University, Portland, Oregon, United States
Introduction
This case highlights ileostomy as a cause of secondary hyperaldosteronism and treatment strategies for similar patients.
Case Description
A 67-year-old woman with Crohn’s disease requiring total colectomy and ileostomy presented to hypertension clinic for persistently elevated serum aldosterone. She reported headaches and anxiety. Due to chronically high ileostomy output associated with cramping and fatigue, she was receiving weekly 1 L normal saline infusions. Crohn’s symptoms were otherwise well controlled on azathioprine. She was taking various nutritional supplements, but no antihypertensives. Spironolactone and eplerenone had not been well tolerated. Physical exam was unremarkable. Blood pressure (BP) was 107/64 mmHg, similar to home readings. BMI was 20.48 kg/m2. Serial chemistry panels were normal; no hypokalemia or metabolic alkalosis. Serum aldosterone was 1064 ng/dL (reference 4.0-31.0 ng/dL) and plasma renin activity was 11.2 ng/mL/hr (reference 0.5-4.0 ng/mL/hr). Serial aldosterone renin ratios in the preceding 2 years showed aldosterone invariably >700 ng/dL and renin never suppressed to <1 ng/mL/hr. Labs were repeated the day after her weekly saline infusion to understand volume impact, showing reductions in both aldosterone at 635 ng/dL and renin at 3.2 ng/mL/hr. A 24-hour urine collection starting directly after saline infusion showed 1.2 L volume and undetectably low sodium. Renal ultrasound with Doppler was without stones or arterial stenosis. Findings were consistent with secondary hyperaldosteronism due to chronic gastrointestinal sodium loss. She was prescribed oral rehydration solutions in escalating doses, in addition to ongoing intravenous expansion, targeting detectable urine sodium.
Discussion
Commonly referenced causes of secondary hyperaldosteronism include reduced renal perfusion, sodium-wasting tubulopathies, and renin-producing tumors. This case highlights another, underrecognized cause: sodium and volume loss in ileostomy patients. Secondary hyperaldosteronism treatments target the underlying pathology. In this situation, we emphasized volume expansion to restore urine sodium. Ideally, this would be achieved with enteral therapy alone, reducing the cost and lifestyle burden of parenteral therapy. The end goal is kidney function preservation, as ileostomy is associated with increased chronic kidney disease risk thought due to persistent hypovolemia.