Supranormal glomerular filtration rates (GFRs) have been recognized in early type 1 diabetes mellitus (T1DM) since at least the early 1950s.1 Mogensen and Andersen2 and Parving et al3 explored this phenomenon in humans in the 1970s and showed its relation to kidney size and glycemic control. In the early 1980s, the hemodynamic basis of the hyperfiltration was defined using micropuncture techniques in a rat model of T1DM.4 Around this time, the increase in single-nephron GFR in a model of reduced renal mass was shown to have a similar pattern of hemodynamic perturbations, namely increased plasma flow and glomerular pressure.