SGLT2 inhibitors reduce the risk of kidney failure in patients with and without type 2 diabetes by mechanisms including reductions in intraglomerular pressure, blood pressure reduction, decreased tubular workload, and increased autophagy. These mechanisms may also explain the beneficial effects of SGLT2 inhibitors on kidney function in patients without type 2 diabetes.
Sodium glucose co-transporter (SGLT) 2 inhibitors reduce the risk of kidney failure in patients with and without type 2 diabetes (T2D). Although the precise underlying mechanisms for these nephroprotective effects are incompletely understood, various hypotheses have been proposed including reductions in intraglomerular pressure through restoration of tubuloglomerular feedback, blood pressure reduction and favorable effects on vascular function, reduction in tubular workload and hypoxia, and metabolic effects resulting in increased autophagy. Here, we review these mechanisms, which may also explain the beneficial effects of SGLT2 inhibitors on kidney function in patients without T2D.
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