Sodium–glucose cotransporter 2 (SGLT2) inhibitors are now an established treatment for heart failure, irrespective of diabetes status (1,2). The practice-changing development has led to widespread uptake of the agents by a range of specialists and primary care physicians. The risk of diabetic ketoacidosis with their use for type 2 diabetes is established, with methods in place for management (3). In contrast, the development of ketoacidosis in patients without diabetes was not reported in clinical trials for heart failure, and mechanistically it is thought to be unlikely (4). We report a case of ketoacidosis in a patient without diabetes after recent commencement of an SGLT2 inhibitor for cardiac failure.
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