Abstract: SA-PO0602
Rapid Severe Metabolic Acidosis from Triple Mechanism Bicarbonate Loss
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
- Ali, Huzair, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Moraes, Cinthia Esbrile, The University of Texas Southwestern Medical Center, Dallas, Texas, United States
- Moe, Orson W., The University of Texas Southwestern Medical Center, Dallas, Texas, United States
Introduction
Medication-induced metabolic acidosis can be attributed to either renal or gastrointestinal bicarbonate loss. Combined pharmacologic effects involving both pathways are less well recognized and may lead to rapid and severe acidosis.
Case Description
We report a patient with neurofibromatosis type 1 and gastrointestinal dysmotility status-post colectomy with ileosigmoid anastomosis who presented with lower extremity weakness. Chronic medications included topiramate and tenapanor; plecanatide was initiated after admission. Vitals were normal and serum creatinine was 0.58 mg/dL. MRI was negative and weakness gradually improved. Following plecanatide initiation, serum bicarbonate rapidly declined from 24 to 9 mEq/L within 5 hours. Urinary studies showed a markedly negative urinary anion gap (−71.5). Discontinuation of plecanatide with parenteral bicarbonate normalized serum bicarbonate within 3 hours.
Discussion
The severe metabolic acidosis observed in this case reflects synergistic disruption of acid-base homeostasis in renal and intestinal pathways. Topiramate induces renal bicarbonate wasting and impaired ammonia trapping through carbonic anhydrase inhibition, impairing luminal acidification and bicarbonate reabsorption. Plecanatide, a guanylate cyclase-C uroguanylin mimic, enhances chloride and bicarbonate secretion into the proximal small intestine, adding to pancreatic bicarbonate secretion. Tenapanor inhibits the intestinal sodium/hydrogen exchanger-3, impairing bicarbonate absorption from the small intestine. The markedly negative urinary anion gap suggests a dominant gastrointestinal contribution. Discontinuation of plecanatide combined with bicarbonate repletion resulted in rapid correction of acidosis. This case highlights drug-induced metabolic acidosis caused by combined renal and gastrointestinal bicarbonate depletion. Recognition of additive pharmacologic effects on acid-base physiology is critical.
Figure 1. Rapid severe metabolic acidosis following plecanatide initiation with prompt correction after drug discontinuation and bicarbonate replacement.