STZ induced hyperglycaemia induces increased SGLT2 dependent proximal tubular sodium reabsorption correlating with glomerular hyperfiltration. These changes do not result in induction of molecular markers associated with development of nephropathy in rodent models. However, compared to the natural history of clinical nephropathy, these experiments are short term. Do such experiments adequately address the role of this mechanism in development of diabetic nephropathy?