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glucose excretion into the urine, transient natriuresis, and mild but persistent osmotic diuresis.5 SGLT2i primarily act on the proximal tubule to induce osmotic diuresis, but this effect is minimal and the principal mechanism for the improvement of prognosis is focused on the loop diuretic effect attributed to resorption in Henle’s loop.6 Thus, SGLT2i reduce body fluid volume, resulting in an antihypertensive effect equivalent to that of low-dose thiazide diuretics.7 In a subanalysis of the EMPA-REG trial,8 myocardial protective agents such as renin-angiotensinaldosterone inhibitors and β-blockers were shown to contribute to the prognosis of HF, independent of SGLT2i. Furthermore, the diuretic effect of SGLT2i has been S odium-glucose cotransporter 2 inhibitors (SGLT2i), a newly emerging class of oral therapeutic agent for diabetes mellitus (DM), inhibit sugar reabsorption in the proximal renal tubule and reduce blood glucose levels by excreting sugar into the urine.1 In recent years, 2 large clinical trials (EMPA-REG OUTCOME and CANVAS) have revealed that SGLT2i can improve the prognosis of type 2 DM patients with high cardiovascular risk.2,3 In particular, an improvement in the hospitalization rate for heart failure (HF) has been presented from the early phases of these trials, with the spotlight on the diuretic effect of SGLT2i as a hypothesized mechanism for improved prognosis. One hypothesized mechanism underlying the cardiovascular benefit of SGLT2i is a diuretic effect (Figure).4 SGLT2i reduce renal glucose reabsorption, leading to Article p 1959

Are Sodium-Glucose Cotransporter 2 Inhibitors Really Useful and Safe for Advanced Heart Failure?