Sodium-Glucose Cotransporter 2 Inhibitors in Acute Kidney Injury
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Abstract
Acute kidney injury (AKI) is a common complication in hospitalized patients and is associated with an increase in morbidity and mortality. Moreover, patients with a history of AKI have an increased risk for congestive heart failure, rehospitalization, recurrence of AKI, progression to chronic kidney disease, and end-stage kidney disease. Currently, there is no specific treatment for post-AKI survivors. Sodium-Glucose Cotransporter 2 (SGLT2) inhibitors, a new and promising drug class, have now been widely used to control blood sugar, delay chronic kidney disease progression, and improve cardiovascular outcomes. By blocking the SGLT2 cotransporter at the proximal tubules, SGLT2 inhibitors result in glucosuria and natriuresis. In addition to lowering blood glucose levels, the drugs enhance the diuretic effect, minimize intravascular and interstitial volume overload, and reduce sympathetic activity. In the heart, SGLT2 inhibitors reduce oxidative stress and inflammation, which are protective against cardiac injury. The inhibition of Na+/H+ exchanger in cardiomyocytes can also reduce congestive heart failure. In the kidneys, SGLT2 inhibitors can reduce oxygen consumption in the renal cortex. There is currently no direct evidence regarding the protective effect of SGLT2 inhibitors in AKI. However, these promising mechanisms and other indirect evidence suggest that SGLT2 inhibitors may help improve long-term outcomes in patients with AKI.
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