Diabetes mellitus is a leading cause of end-stage renal disease. The pathogenesis of diabetic nephropathy is still poorly understood, but renal injury has been ascribed at least in part to glomerular hyperfiltration which occurs early in the course of diabetes mellitus. Common sense may suggest that glomerular hyperfiltration implies some defect in microvascular function or an imbalance of hormones impinging directly on the glomerulus. In contrast, we propose a `tubulo-centric` model in which glomerular hyperfiltration results mainly from primary changes in the proximal tubule. Early diabetes mellitus elicits a primary increase in proximal tubular reabsorption. This is due to tubular growth and enhanced glomerular filtration of glucose and activation of sodium-glucose cotransport (SGLT2/SGLT1). As a consequence less of the glomerular filtrate reaches the macula densa at the end of Henle's loop. The tubuloglomerular feedback (TGF) system senses the decline in salt delivery and elicits an increase in nephron filtration rate and thus hyperfiltration to stabilize electrolyte delivery to the further distal nephron. Another manifestation of the strong tubular control in the early diabetic kidney is its strange response to dietary NaCl. In normal subjects, GFR is either insensitive to dietary NaCl or changes in the same direction as NaCl intake. In contrast, there is negative impact of dietary NaCl on GFR in early diabetes as observed in animal models and human subjects. This strange and counterintuitive "salt paradox" is explained by hypersensitivity of proximal reabsorption to dietary NaCl and involvement of the TGF system. The molecular signature of early tubular growth in diabetes is unique, including aspects of senescence, and we propose that these diabetes-induced tubular signaling cascades not only contribute to the described effects on transport and GFR but can set the stage for progression of diabetic renal disease.