Diabetic nephropathy (DN) is the most common cause of end-stage renal disease worldwide. Sodium-glucose-linked transporter 2 (SGLT2) inhibitors are a new and promising class of antidiabetic agents that target renal tubular glucose reabsorption. Their action is based on the blockage of SGLT2 sodiumglucose cotransporters that are located at the luminal membrane of tubular cells of the proximal convoluted tubule (PCT), inducing glucosuria. It has been proven that they significantly reduce glycated hemoglobin (HbA1c), along with fasting and postprandial plasma glucose in patients with type II diabetes mellitus (T2DM). Glomerular hyperfiltration is a potential risk factor for DN. The SGLT2 inhibitors reduce sodium reabsorption in the proximal tubule, causing, through tubuloglomerular feedback (TGF), afferent arteriole vasoconstriction and reduction in hyperfiltration. The SGLT2 inhibitors reduced glomerular hyperfiltration in patients with T1DM, and in patients with T2DM, they caused transient acute reductions in glomerular filtration rate (GFR), followed by a progressive recovery and stabilization of renal function. Interestingly, recent studies consistently demonstrated a reduction in albuminuria. Recently, it was demonstrated that empagliflozin presents a significant cardioprotective effect. Although the SGLT2 inhibitors' efficacy is affected by renal function, new data have been presented that some SGLT2 inhibitors, even in mild and moderate renal impairments, induce significant HbA1c reduction. Although these data are promising, only dedicated renal outcome trials will clarify whether SGLT2 inhibitors, in addition to their glycemic and blood pressure (BP) benefits, may provide nephroprotective effects.
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