Kidney Week

Abstract: FR-PO0904

Sodium Zirconium Cyclosilicate (SZC) Intoxication: A New Cause of Metabolic Alkalosis and Severe Hypokalemia with Insight into Mechanisms

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

• Vega, Melissa Mia, University of Massachusetts Chan Medical School TH Chan School of Medicine, Springfield, Massachusetts, United States

Melissa Mia Vega, MD

• Greco, Barbara A., University of Massachusetts Chan Medical School TH Chan School of Medicine, Springfield, Massachusetts, United States

Barbara A. Greco, MD

• Sarwat, Ahmed, University of Massachusetts Chan Medical School TH Chan School of Medicine, Springfield, Massachusetts, United States

Ahmed Sarwat, MD

• Tarasaria, Twara Karan, University of Massachusetts Chan Medical School TH Chan School of Medicine, Springfield, Massachusetts, United States

Twara Karan Tarasaria, MD

• Braden, Gregory Lee, University of Massachusetts Chan Medical School TH Chan School of Medicine, Springfield, Massachusetts, United States

Gregory Lee Braden, MD

Introduction

Standard doses of SZC to treat hyperkalemia can lead to a small increase in serum bicarbonate of 0.3-2.0 mEq/L after 48 hours. We now report a patient who was ingesting 7-8 packets of 10 gms SZC twice weekly for 4 weeks who presented with metabolic alkalosis with a serum bicarbonate of 38 mEq/L & a serum potassium of 1.9 mEq/L.

Case Description

An 84 yr ol woman with a serum creatinine of 1.4 mg/dL & serum HCO3 of 24 mEq/L had hyperkalemia of 6.4 mEq/L despite a low potassium diet. She developed congestive heart failure, severe weakness & a bigeminal rhythm with runs of ventricular tachycardia. She had been given SZC 10 gm bid for 2 weeks but she took 7-8 10 gm packets twice weekly for 4 weeks. Labs showed in mEq/L: Na 136, K 1.9, Cl 86 HCO3 36, BUN of, 16 mg/dL, creatinine 1.7 mg/dL, Ca 7.7 mg/dL, Mg 2.2 mg/dL An ABG showed a ph of 7.48, PO2 79 mmHg, PCO2 49 mmHg & a HCO3 of 38 mEq/L She received 2 doses of IV furosemiede for CHF & 600 mEq of potassium over the first 3 days. Her plasma renin activity was < 0.57 ng /ml/hr & serum aldosterone < 1.0 ng/dL. BUN dropped daily from 16 to 10 mg/dL. Urinary electrolytes showed : Na of 126 mEq/l, Choride 58 mEq/L and K of 10.3 mEq/L with a positive anion gap of 78 mEq/l.After 6 daysof oral and IV potassium a serum potassium was 4.8 mEq/L with a serum bicarbonate of 27 mEq/L.

Discussion

SZC in the GI tract exchanges K+ and NH4+ for Na+ and H+ ions.. In mice SZC markedly increases stool NH4+ losses by 6 fold over control. .SZC binds NH4+ ions generated from gut microbiome urease preventing ammonia absorption and lowering the BUN while at the same time increasing fecal excretion of H+ ions leading to metabolic alkalosis. Indeed in our patient, the BUN decreased daily as the serum bicarbonate rose daily to 38 mEq/l. Although it has been speculated that severe hypokalemia could increase urinary ammoniagenesis that may contribute to urinary losses of H+ ions our patient had a markededly positive urinary anion gap of 78 mEq/l showing renal ammoniagenesis is not a factor in SZC- induced metabolic alkalosis.
We conclude that SZC intoxication can not only cause severe hypokalmia but it can also cause unrecognized severe metabolic alkalosis due to increased GI NH4+ excretion. Anyone starting SZC should have electrolytes drawn 1-2 weeks after initiation to prevent severe hypokalemia and metabolic alkalosis.