To the Editor: Sodium–glucose cotransporter-2 (SGLT-2) inhibitors are a highly promising class of glucose-lowering therapies and have been found to reduce cardiovascular and kidney disease risk in patients with type 2 diabetes [1–3]. The mechanisms underlying these cardio-and renoprotective effects of SGLT-2 inhibition are, however, incompletely understood and it is not known if these beneficial effects are also evident in people with type 1 diabetes.

Hyperglycaemia triggers renal haemodynamic abnormalities in diabetes, which increases glomerular pressure and can lead to hyperfiltration and subsequent renal injury [4]. We have previously shown that empagliflozin increases distal tubular sodium delivery in people with type 1 diabetes, which enhances an autoregulatory mechanism in the kidneys (tubuloglomerular feedback [TGF]) that lowers glomerular pressure and attenuates hyperfiltration [5]. Although these renal haemodynamic effects in response to SGLT-2 inhibition resemble those of therapeutic renin–angiotensin system (RAS) blockade, TGF facilitates a distinct afferent vasoconstrictive mechanism instead of efferent vasodilatation as occurs with RAS blockade. It has therefore been hypothesised that SGLT-2 inhibition may promote global RAS activation resulting from composite renovascular effects such as volume depletion and osmotic diuresis [6].