Abstract
Sodium-glucose cotransporter 2 (SGLT-2) inhibition and kidney protection: Does improvement in kidney hypoxia play a role?
Highlights
The concept of suppressing renal glucose reabsorption in the proximal tubule to reduce plasma glucose levels and treat patients with diabetes has been elaborated more than 30 years ago when phlorizin, a relatively unselective inhibitor of sodium-glucose cotransporter 2 (SGLT2) was investigated [1]
The renal protective effects of SGLT2 inhibitors go well beyond their ability to control glycaemia and several mechanisms are proposed to explain their ability to reduce kidney outcomes including decreases in blood pressure, serum uric acid and glomerular hyperfiltration [3]. Another interesting hypothesis, linked to the reduction in glomerular hyperfiltration, is that SGLT2 inhibitors correct the intrarenal mismatch between oxygen delivery and oxygen demand characteristic of diabetes and thereby improve kidney oxygenation [4]
In an article published in EClinicalMedicine, Jens Christian Laursen and colleagues present the results of a randomized, double-blind, placebo-controlled crossover study assessing the acute effects of a high dose of dapagliflozin on kidney tissue oxygenation and perfusion in patients with diabetes [5]
Summary
The concept of suppressing renal glucose reabsorption in the proximal tubule to reduce plasma glucose levels and treat patients with diabetes has been elaborated more than 30 years ago when phlorizin, a relatively unselective inhibitor of sodium-glucose cotransporter 2 (SGLT2) was investigated [1]. The renal protective effects of SGLT2 inhibitors go well beyond their ability to control glycaemia and several mechanisms are proposed to explain their ability to reduce kidney outcomes including decreases in blood pressure, serum uric acid and glomerular hyperfiltration [3].
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