Abstract
Sodium-glucose co-transporter-2 (SGLT-2) inhibitor is the latest class of anti diabetic medication that improves glycemic control in insulin independent fashion by increasing urinary loss of filtered glucose. Since its introduction in 2013, several cases of euglycemic DKA have been reported in patients being treated with SGLT-2 inhibitors. Blood glucose levels in range lower than expected for DKA makes the diagnosis challenging if clinical suspicion for euglycemic DKA is not high. We report a case of a patient being treated with canagliflozin who presented with DKA, AKI and mild hyperglycemia that was complicated by stress-induced cardiomyopathy.
Highlights
In March 2013, first Sodium-glucose co-transporter-2 (SGLT-2) inhibitor, canagliflozin, was approved for the treatment of type 2 diabetes mellitus by the US food and drug agency (FDA) (1)
Major adverse effect of SGLT-2 inhibitors is to increase the propensity towards ketoacidosis with lower than anticipated blood glucose level the incidence of DKA has not found to be greater than the general diabetes population [6]
Her left ventricular (LV) dysfunction was felt to be due to stress induced cardiomyopathy as her LV ejection fraction (EF) improved to 55% on TTE a week later, her troponin pleatued at 0.63 ng/ml and she did not had new electrocardiographic ischemic changes
Summary
In March 2013, first Sodium-glucose co-transporter-2 (SGLT-2) inhibitor, canagliflozin, was approved for the treatment of type 2 diabetes mellitus by the US food and drug agency (FDA) (1). SGLT-2 inhibitors reversibly inhibit the SGLT-2 located in the proximal convoluted tubule of the kidney where 90% of filtered sodium and glucose is reabsorbed. By increasing urinary loss of glucose, SGLT-2 improves glycemic control [3]. Major adverse effect of SGLT-2 inhibitors is to increase the propensity towards ketoacidosis with lower than anticipated blood glucose level the incidence of DKA has not found to be greater than the general diabetes population [6]. It has been proposed that acute illness, starvation, deficiency of insulin or oral secretagouges increases the release of counter regulatory hormones that promotes gluconeogenesis and ketogenesis [2,11]. SGLT-2 inhibition is reversed quickly after cessation of SGLT-2 inhibitors
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