ASN's Mission

To create a world without kidney diseases, the ASN Alliance for Kidney Health elevates care by educating and informing, driving breakthroughs and innovation, and advocating for policies that create transformative changes in kidney medicine throughout the world.

learn more

Contact ASN

1401 H St, NW, Ste 900, Washington, DC 20005


The Latest on X

Kidney Week

Please note that you are viewing an archived section from 2022 and some content may be unavailable. To unlock all content for 2022, please visit the archives.

Abstract: SA-PO496

Case of Increased Anion Gap Metabolic Acidosis From Acquired Glutathione Deficiency Secondary to Acetaminophen

Session Information

Category: Fluid‚ Electrolyte‚ and Acid-Base Disorders

  • 1002 Fluid‚ Electrolyte‚ and Acid-Base Disorders: Clinical


  • Karimi, Hussain Abde Ali, UPMC, Pittsburgh, Pennsylvania, United States
  • Kaldas, Hoda, UPMC, Pittsburgh, Pennsylvania, United States
  • Asghar, Mariya, Liaquat National Hospital and Medical College, Karachi, Sindh, Pakistan

We describe a case of a 31-year-old female with prolonged hospitalization who had high anion gap metabolic acidosis (HAGMA) secondary to Acetaminophen-induced pyroglutamate excretion.

Case Description

31 y/o F with a past medical history significant for traumatic brain injury secondary to a motor vehicle accident, seizure disorder, bowel perforation status post ileostomy who presented with Pneumonia and UTI (Urinary tract infection) from MDR (multidrug-resistant) organisms, also found to have HAGMA for which Nephrology was consulted.

The patient had a very prolonged hospitalization which was met with multiple complications. She was noted to have HAGMA of 26 and a serum bicarbonate level of 12. Her VBG showed a pH of 7.17, PCO2 of 36, and HCO3 of 13, her delta gap was 1.16 indicating pure HAGMA. Appropriate workup was done which showed negative ACTH stimulation test, creatine phosphokinase levels <10, Lactic acid at 2.0 mmol/L, beta-hydroxybutyrate levels were 0.27 mmol/L, free valproic acid at 4.7 (4.8-17.3 ug/ml), topiramate levels at 6.8 (5-20 ug/ml), Acetaminophen and aspirin levels were undetectable. Ethanol levels were not checked but she had no exposure to it due to the prolonged hospitalization, all medications were reviewed, and propylene glycol was not used as a solvent in any of the meds. Her renal function showed serum creatinine of 0.3 mg/dl, but it was unreliable as she was severely malnourished, urine anion gap was positive. She was started on sodium bicarbonate tablets 650 mg q 8 hours and then transitioned to a bicarbonate drip with 150 meq/L in 1 L of sterile water. Upon further review, it was noted that she had been getting oral acetaminophen 650 mg every 6 hours as needed intermittently for pain, this prompted us to send serum and urine organic acid panel using gas chromatography/mass spectrometry which revealed massive excretion of pyroglutamate in the urine. Her Acetaminophen was stopped and a week later her serum bicarbonate levels improved to 24 without needing any further NaHCO3 tablets.


High anion gap metabolic acidosis due to acquired deficiency of glutathione in malnourished patients who are exposed chronically to Acetaminophen is underinvestigated and underreported. This should be considered as a differential, especially in women with prolonged hospitalization and sepsis when evaluating HAGMA.