A Case of Drug-Induced Fanconi Syndrome from SGLT2 Inhibitor Use

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.

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Journal
Journal of the American Society of Nephrology
Published
2025-10-01
DOI
https://doi.org/10.1681/asn.2025fs2naf4v
Primary Topic
Diabetes Treatment and Management
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article
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article

A Case of Drug-Induced Fanconi Syndrome from SGLT2 Inhibitor Use

Louisa Ho, Robert Schultz, Liliana Osadchuk
Journal of the American Society of Nephrology
Diabetes Treatment and Management
article

A Case of Drug-Induced Fanconi Syndrome from SGLT2 Inhibitor Use

Louisa Ho, Robert Schultz, Liliana Osadchuk
article en

Abstract

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.

Journal of the American Society of NephrologyVol. 36(10S)
Evanston Hospital (US)
Openalex Percentile: Top 58%
Diabetes Treatment and Management
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