Fanconi syndrome associated with SGLT2 inhibitor ...
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Fanconi syndrome associated with SGLT2 inhibitor ...
Nephrology, Hypertension and Renal Transplantation,. University of Florida ... Urinalysis was significant for glycosuria, which is expected with SGLT2 inhibitor ...
Nephrology 23 (2018) 493–495
Correspondence FANCONI SYNDROME ASSOCIATED WITH SGLT2 INHIBITOR, CANAGLIFLOZIN DON H ESPRIT and ABHILASH KORATALA, Division of Nephrology, Hypertension and Renal Transplantation, University of Florida, Gainesville, Florida, USA
Sodium-glucose cotransporter-2 (SGLT2) inhibitors have gained popularity due to convenient, once-daily oral dosing and their association with weight loss, lower blood pressure, and a low risk of hypoglycemia as well as lower cardiovascular mortality as with empagliflozin.1 However, with the increasing use of these drugs, there have been increased reports of adverse effects as well. Based on new data from two large clinical trials, the U.S. Food and Drug Administration (FDA) has concluded that canagliflozin causes an increased risk of leg and foot amputations.2 In addition, there have been reports of euglycemic diabetic ketoacidosis (EuDKA) with the use of this drug.3 Herein, we present the case of a diabetic patient on canagliflozin who presented with EuDKA and found to have proximal renal tubular acidosis with Fanconi syndrome that was attributable to the drug. A 54-year-old Caucasian woman with a past medical history of type 2 diabetes mellitus, hypertension, coronary artery disease, and hyperlipidemia has originally presented with chest pain and found to have EuDKA. Her blood glucose was 175 mg/dL but had anion gap metabolic acidosis with a serum bicarbonate of 9 mmol/L (22-28) and elevated beta-hydroxybutyrate. Serum lactate was 0.65 mmol/L (0.31.5). Her medications consisted of canagliflozin 300 mg daily, metformin 500 mg twice daily, lisinopril 10 mg daily and atorvastatin 20 mg daily. She was treated with insulin until the anion gap closed and then was switched to oral medications. However, she was noted to have persistent non-anion gap metabolic acidosis and hypophosphatemia. Urinalysis was significant for glycosuria, which is expected with SGLT2 inhibitor use. Interestingly, she was found to have phosphaturia with a fractional excretion of phosphate of 23% (normal