Kidney Week

Abstract: SA-PO0598

Flow-Dependent Intestinal Hydrogen Ion Loss Causing Severe Metabolic Alkalosis in High-Output Jejunostomy

Session Information

• Fluid, Electrolyte, and Acid-Base Disorders: Case Reports - 2
  October 24, 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

• Gill, Mohammad Danial, The University of Texas Southwestern Medical Center, Dallas, Texas, United States

Mohammad Danial Gill, MD

• Balakrishnan, Naveen Kishore, The University of Texas Southwestern Medical Center, Dallas, Texas, United States

Naveen Kishore Balakrishnan, MD

• Sambandam, Kamalanathan Kolandavelu, The University of Texas Southwestern Medical Center, Dallas, Texas, United States

Kamalanathan Kolandavelu Sambandam, MD

• Moe, Orson W., The University of Texas Southwestern Medical Center, Dallas, Texas, United States

Orson W. Moe, MD

• Davidson, Taylor, The University of Texas Southwestern Medical Center, Dallas, Texas, United States

Taylor Davidson, MS

Introduction

Diarrhea is classically associated with metabolic acidosis due to lower intestinal alkali loss. Based on this pathophysiology, the development of metabolic alkalosis is unexpected with high gastrointestinal losses distal to the stomach. We present a case of severe metabolic alkalosis in the setting of a high-output jejunostomy and impaired renal bicarbonate elimination.

Case Description

A 60-year-old man with heart failure with reduced ejection fraction (35%), atrial fibrillation, and prior mesenteric ischemia requiring extensive small-bowel resection with end jejunostomy (~85 cm remaining) presented with pre-renal acute kidney injury and severe metabolic alkalosis during periods of high ostomy output.

During episodes of massive jejunostomy output (~6 L/day), laboratory evaluation demonstrated severe hypochloremic metabolic alkalosis (serum chloride 77 mEq/L, bicarbonate 40–46 mEq/L) with hypokalemia. Urine pH remained ≤7, suggesting impaired bicarbonaturia in the setting of acute kidney injury.

To investigate the mechanism of alkalosis, jejunostomy effluent was analyzed. Stool pH was markedly acidic at 4.9 despite upstream pancreaticobiliary bicarbonate secretion. Sodium hydroxide titration demonstrated 54 mEq/L of titratable acid, corresponding to approximately 324 mEq/day of hydrogen ion loss. Following reduction of ostomy output to ~2 L/day using tincture of opium and antimotility therapy, stool pH increased to 5.7 and titratable acidity decreased to 28 mEq/L (~56 mEq/day), accompanied by parallel improvement in metabolic alkalosis.

Discussion

The relationship between luminal flow, stool acidity, titratable acid loss, and serum bicarbonate supports flow-stimulated jejunal proton secretion as the mechanism underlying this patient’s alkalosis. Analogous to the renal proximal tubule, increased luminal flow may augment sodium–hydrogen exchanger activity and luminal acid secretion within the proximal small bowel. In the setting of end jejunostomy, absence of distal bowel limits downstream buffering of proximal hydrogen ion secretion. Concurrent renal dysfunction further impaired bicarbonate excretion, permitting sustained alkalosis.

This case demonstrates that high-output jejunostomy can rarely produce severe metabolic alkalosis through substantial, flow-dependent intestinal hydrogen ion loss.