“…These results indicate that ipragliflozin has great potential as a novel and effective diuretic agent. Ipragliflozin treatment also increased potassium excretion without influencing serum potassium concentration, probably due to the increased delivery of sodium to the distal nephron, which activates sodium reabsorption and potassium secretion in the distal convoluted tubule and in the connecting tubule [9].To prevent rehospitalization, patients with HF generally require chronic oral loop diuretic treatment [10], but it can worsen renal function and activate the RAAS and SNS, all of which play fundamental roles in HF progression [4][5][6]. In the present study, short-term ipragliflozin therapy in patients on chronic oral diuretics decreased plasma natriuretic peptide levels without influencing plasma angiotensin II, aldosterone and noradrenaline levels.…”