The kidneys and heart are closely related and have a specific characteristic known as cardiorenal syndrome, in which a dysfunction of one organ leads to a dysfunction of the other. SGLT2 inhibitors could be a candidate strategy for renal impairment associated with heart failure. Tofogliflozin protects against renal damage induced by renal congestion. Mitochondrial dysfunction provoked by renal congestion was also improved by tofogliflozin treatment. Molecules associated with inflammation were increased in the congested kidney and reversed by tofogliflozin treatment. SGLT2 expression was observed in the congested kidney, but suppressed in the damaged tubular cells. Additionally, this treatment effectively reduced renal injury and fibrosis, particularly in the renal cortex. Kidney weight gain and hydration were improved with tofogliflozin treatment. Kidney weight and water content was increased, and renal injury and fibrosis were observed in the left congested kidney. On the third postoperative day, both the right control kidney and the left congested kidney were harvested and analyzed. The SGLT2 inhibitor tofogliflozin or vehicle was orally administered daily from the day before IVC ligation until two days after surgery. Renal congestion was induced in the left kidney of male Sprague-Dawley rats by ligation of the inferior vena cava between the renal veins. Thus, we aimed to clarify the effect of SGLT inhibition in a renal congestion model. However, the effect on renal congestion and its mechanism is not fully understood. Recent clinical and basic studies suggest a renoprotective potential of sodium–glucose cotransporter (SGLT) 2 inhibitors. Renal congestion is an issue of cardiorenal syndrome in patients with heart failure.
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