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Abstract: SA-PO1017

A Case of Perioperative Euglycemic Ketoacidosis and Concomitant Non-Anion Gap Metabolic Acidosis and AKI Associated with Canagliflozin

Session Information

Category: Nephrology Education

  • 1302 Fellows and Residents Case Reports


  • Gonzalez, Manuel E, Ochsner Clinic Foundation, New Orleans, Louisiana, United States
  • Velez, Juan Carlos Q., Ochsner Clinic Foundation, New Orleans, Louisiana, United States

Oral inhibitors of the renal sodium-glucose cotransporter SGLT2 (“-gliflozins”) are now available for the management of type 2 diabetes mellitus. Reports of euglycemic ketoacidosis caused by these drugs have emerged. However, concomitant acute kidney injury (AKI) and non-anion gap (NAG) metabolic acidosis are not usually present in those cases. We report a case suggestive of euglycemic ketoacidosis due to the SGLT2 inhibitor canagliflozin that was confounded by concomitant AKI and NAG metabolic acidosis.


A 65 year-old Caucasian woman with type 2 diabetes mellitus, hypertension and obesity was evaluated for profound weakness and vomiting on post-operative day 1 after a laparoscopic sleeve gastrectomy indicated for weight loss. Her home medications included dulaglutide, metformin, and canaglifozin. Dulaglutide was stopped 1 week prior to the procedure, and metformin and canaglifozin were stopped 1 day prior her surgery. Upon evaluation, her blood pressure was 131/64 mmHg, her pulse was 94/min and her body mass index was 36 kg/m2. Examination was remarkable for obesity and a mildly tender abdomen with a dressed abdominal incision. Serum studies revealed: sodium 135 mEq/L, chloride 113 mEq/L, total CO2 < 5 mEq/L, potassium 4.8 mEq/L, glucose 128 mg/dL, urea nitrogen 12 mg/dL and a creatinine 1.0 mg/dL (up from a baseline of 0.6 mg/dL). The serum anion gap (AG) was 17 mEq/L. An arterial blood gas revealed a pH 7.1 and a pCO2 20.8 mmHg. She had a normal lactate of 0.9 mmol/L but a positive beta-hydroxybutyrate of 5.1 mmol/L. Urinalysis showed 2+ ketones. The delta AG / delta bicarbonate was 0.3, suggesting co-existence of AG and NAG metabolic acidosis, caused by ketoacidosis and AKI, respectively. She was treated with intravenous isotonic sodium bicarbonate solution, followed by normal saline, insulin infusion with dextrose drip until the AG normalized and her kidney function returned to baseline.


This case illustrates that SGLT2-induced euglycemic ketoacidosis with concomitant AKI can occur as a serious disorder in diabetics. The combination of fasting, volume depletion and deficiency of insulin appear to trigger this relatively novel syndrome. We call for caution in preoperative care of patients taking “-gliflozins”.