Background Glomerular hyperfiltration plays a role in the pathophysiology of diabetic nephropathy. An increase in glomerular filtration rate (GFR) could result from primary actions at the glomerular/vascular level or could be the consequence of a primary increase in proximal tubular sodium reabsorption resulting in systemic volume expansion. Recently it was hypothesized that an increase in sodium reabsorption may lead to glomerular hyperfiltration through the tubuloglomerular feedback mechanism (tubular-hypothesis) without volume expansion. Methods We have studied 54 normoalbuminuric patients with type 1 diabetes. GFR was measured by inulin clearance. Proximal and distal sodium reabsorption were calculated according to standard formulas using free water clearance technique. Plasma volume, measured by I-albumin method, atrial natriuretic peptide (ANP) and the second messenger cyclic guanosine-3,5-monophosphate (c-GMP) were used as markers of extracellular volume expansion. Results Glomerular hyperfiltration (GFR≥ 130 mL·min−1·1.73m−2) was present in 14 out of 55 diabetes patients (25%). There were no differences in plasma volume between normo(NF) and hyper-filtrating (HF) patients (2933±423 in NF vs 3026±562 mL in HF, NS). Also plasma ANP and c-GMP levels were not significantly different between the groups. The fractional proximal reabsorption of sodium was significantly increased in HF (fPRNa(%) 90.1±2.0 vs 91.5±1.6, p=0.02). There were no differences in distal sodium reabsorption or distal sodium load (≈ macula densa concentration of NaCl) in both groups. Conclusions Our data suggest that the primary event in diabetic glomerular hyperfiltration is an increase in proximal tubular sodium reabsorption. They do not give support to the hypothesis that systemic volume expansion or ANP mediate glomerular hyperfiltration in normoalbuminuric type 1 diabetes patients. As such, changes in tubular sodium handling most probably influence tubulo-glomerular feedback.