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Abstract: PO1182

Pseudohypobicarbonatemia in a Patient with Paraproteinemia

Session Information

Category: Fluid, Electrolyte, and Acid-Base Disorders

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


  • Bukhari, Marvi Manzoor, UPMC Mercy, Pittsburgh, Pennsylvania, United States
  • Boyd-Shiwarski, Cary R., University of Pittsburgh Renal-Electrolyte Division, Pittsburgh, Pennsylvania, United States
  • Abramovitz, Blaise William, University of Pittsburgh Renal-Electrolyte Division, Pittsburgh, Pennsylvania, United States

The first step in acid-base disorders’ diagnosis is obtaining measurement of blood bicarbonate (HCO3-), pH and partial pressure of carbon dioxide (pCO2) levels. Blood HCO3- levels are estimated via two methods: direct measurement of serum total carbon dioxide (TCO2), or via Henderson-Hasselbalch equation using arterial blood and directly measuring pH and pCO2 levels. With the enzymatic method, there have been reported cases of falsely low serum HCO3- due to interference by elevated triglyceride levels, but only two cases have been reported of spuriously low serum HCO3- due to interference by paraproteins.

Case Description

A 74-year-old male with a history of bladder carcinoma in situ and hypertension presented with complaints of malaise after a recent bladder irrigation. Basic metabolic panel (BMP) was unremarkable except for a HCO3- of 8 mmol/L measured using a Siemens Vista (SV) enzymatic chemistry analyzer. He was hospitalized for high anion gap metabolic acidosis with anion gap of 22. He was started on intravenous NaHCO3 (150 mEq/L) after nephrology was consulted. Repeat serum HCO3- was 11 mmol/L the next day with transition to oral NaHCO3 650 mg therapy thrice daily. On outpatient follow-up, he had low serum HCO3- ranging from 8-11 mmol/L (using SV analyzer) despite his reported compliance with NaHCO3. He was evaluated by another nephrologist with repeat BMP and an arterial blood gas (ABG). The results revealed a serum HCO3- of 8 mmol/L in contrast with ABG pH of 7.41 and HCO3- of 25 mmol/L. Due to the discrepancy, his serum HCO3- was analyzed at a different facility using a Beckman Coulter analyzer which revealed a normal serum HCO3- level of 21 mmol/L. Further work up was pursued with SPEP and SIFE revealing an M-spike and presence of IgM and IgA kappa monoclonal proteins respectively, which led to a diagnosis of monoclonal gammopathy.


Paraproteins have been reported to cause interference with multiple laboratory test results. Paraproteins in our case may have resulted in artifactual error of serum HCO3- by direct interaction with assay reagents, binding of paraproteins to an assay reagent, or turbidity caused by precipitation of the monoclonal proteins. Our case highlights the importance of being aware of this phenomenon of pseudohypobicarbonatemia that can occur with certain chemical analyzers.