To the Editor: Renal hyperfiltration in experimental models of early diabetes is associated with increased intraglomerular pressure, and this condition may promote the development of diabetic nephropathy [1]. Despite the functional characterisation of renal hyperfiltration in animal models of diabetes indicating causal involvement of the afferent arteriole, confirmative data in humans are scarce. This is explained by the fact that direct measurements of human glomerular haemodynamic variables, such as afferent (RA) and efferent (RE) arteriolar resistances and glomerular hydrostatic pressure (PGLO), are technically not feasible. To elucidate mechanisms of renal disease in humans, Gomez et al published formulae derived from animal physiological studies in 1951 to estimate glomerular haemodynamic function by using measured mean arterial blood pressure (MAP), GFR, renal plasma flow, haematocrit and total protein concentrations [2]. More recently, selective sodium–glucose co-transporter 2 (SGLT2) inhibitors have been evaluated in studies involving patients with type 2 and type 1 diabetes. In this context, we recently demonstrated, in a stratified, open-label, single-arm 8 week trial, that SGLT2 inhibition with empagliflozin attenuates renal hyperfiltration in patients with type 1 diabetes, an effect likely due to modulation of tubuloglomerular feedback