Kidney Week

Abstract: PO1183

Proton Pump Inhibitor (PPI) for the Treatment of Metabolic Alkalosis due to Gastric Losses

Session Information

• Mineral Homeostasis and Acid-Base Disorders: Clinical
  November 04, 2021 | Location: On-Demand, Virtual Only
  Abstract Time: 10:00 AM - 12:00 PM

Category: Fluid, Electrolyte, and Acid-Base Disorders

• 902 Fluid, Electrolyte, and Acid-Base Disorders: Clinical

Authors

• Rosen, Raphael Judah, Columbia University Irving Medical Center, New York, New York, United States

Raphael Judah Rosen, MD

• Han, Heedeok, Columbia University Irving Medical Center, New York, New York, United States

Heedeok Han,

• Prakash-Polet, Sindhuri, Columbia University Irving Medical Center, New York, New York, United States

Sindhuri Prakash-Polet,

• Peleg, Yonatan A., Columbia University Irving Medical Center, New York, New York, United States

Yonatan A. Peleg,

Introduction

Gastric losses of hydrochloric acid can result in severe metabolic alkalosis (met alk). We describe two cases where patients with significant losses of gastric secretions presented with severe met alk and AKI. In both cases, PPI therapy was used to reduce the volume of the gastric secretions with excellent effect.

Case Description

Patient 1:
A 44 year-old woman with Gardner Syndrome with near-total enterectomy and colectomy on total parenteral nutrition with a venting gastric tube (G-tube), presented with met alk (HCO₃ 50 meq/L) and AKI (Scr 4 mg/dL from baseline 1.3 mg/dL). Met alk persisted despite normal saline (NS) administration and gastric tube losses ranged from 4-8 liters per day. Twice daily intravenous PPI was started with immediate decrease of gastric losses and normalization in HCO₃. This patient was admitted one year later (off PPI therapy) with a similar derangements and resuming PPI therapy caused similar improvement.

Patient 2:
A 59 year-old man with gastric outlet obstruction and venting G-tube presented with met alk (HCO₃ 47 meq/L) and acute kidney injury (SCr 4.5 mg/dL from 1.3 mg/dL). Met alk persisted despite NS administration and his gastric tube losses ranged from 4-11 liters per day. Daily intravenous PPI was started with decrease of gastric losses and normalization of HCO₃. This patient presented again to the hospital one month later with normal HCO₃, on PPI therapy.

Both patients’ bicarbonate and gastric fluid output trend relative to PPI therapy is detailed in figure 1.

Discussion

There are few reported cases of PPI therapy for metabolic alkalosis due to gastric losses. Generally, met alk that occurs due to gastric losses is readily rectified by increased renal bicarbonate excretion, but this compensatory mechanism is limited in the setting of AKI. We report two cases in which PPI therapy successfully decreased the quantity of gastric fluid losses and rapidly improved metabolic alkalosis.