Abstract: TH-PO0438
A Case of Drug-Induced Fanconi Syndrome from SGLT2 Inhibitor Use
Session Information
- Fluid, Electrolyte, and Acid-Base Disorders: Clinical - 1
November 06, 2025 | Location: Exhibit Hall, 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
- Schultz, Ryan C, Endeavor Health, Evanston, Illinois, United States
- Osadchuk, Liliana, Endeavor Health, Evanston, Illinois, United States
- Ho, L. Tammy, Endeavor Health, Evanston, Illinois, United States
Introduction
Drug-induced Fanconi Syndrome is a rare acquired proximal convoluted tubule defect that leads to impaired reabsorption of electrolytes and other solutes in the kidney. This malabsorption results in the common laboratory findings seen in Fanconi Syndrome, including proximal Renal Tubular Acidosis from bicarbonate loss, hypophosphatemia, hypokalemia, glucosuria, proteinuria, and elevated urine uric acid levels. In the literature, there have been case reports of drug-induced Fanconi syndrome associated with Canagliflozin, a medication that belongs to the SGLT2 Inhibitor drug class. While a few cases have been reported, it is important to be aware of this potential association so that prompt evaluation and treatment may be provided.
Case Description
A 73-year-old male with a history of type 2 diabetes on canagliflozin 300 mg outpatient and ESRD status-post deceased donor renal transplant in 2016 presented to our hospital with a 1-week history of fatigue, decreased eating/drinking, and urinary frequency with associated incontinence. Laboratory results showed hyperglycemia, anion-gap metabolic acidosis, hypophosphatemia, ketonuria, glucosuria, and proteinuria. The patient was admitted to the Intensive Care Unit for Diabetic Ketoacidosis (DKA) and concern for pyelonephritis seen on CT scan. However, despite the resolution of the patient’s DKA and anion-gap metabolic acidosis, the patient continued to have persistent hypophosphatemia and hypocarbia resulting in a non-anion-gap metabolic acidosis. The patient was subsequently diagnosed with a drug-induced Fanconi syndrome given his known canagliflozin use. The patient’s electrolyte derangements subsequently resolved 3 days later with frequent phosphorus repletion, initiation of oral bicarbonate, and discontinuation of canagliflozin. The patient was subsequently discharged six days after admission.
Discussion
Given the widespread use of SGLT2-Inhibitors in the treatment of type 2 diabetes, heart failure, and Chronic Kidney Disease, clinicians should be familiar with the different adverse effects associated with this drug class, including drug-induced Fanconi syndrome from Canagliflozin use. This can help clinicians effectively identify and address the underlying cause in patients presenting with electrolyte derangements in the setting of a proximal renal tubular acidosis.