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   <subfield code="a">Contrasting renal functional reserve in very long-term Type I diabetic patients with and without nephropathy</subfield>
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   <subfield code="c">[H. Sackmann, T. Tran-Van, I. Tack, H. Hanaire-Broutin, J.-P. Tauber, J.-L. Ader]</subfield>
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   <subfield code="a">Aims. This study was to determine whether renal functional reserve (RFR) is present in patients who have suffered long-lasting Type I (insulin-dependent) diabetes mellitus.¶Methods. Renal functional reserve was elicited by a 3-h amino acid infusion (4.5 mg · kg-1· min-1) in 10 patients with nephropathy (DN +) and 10 patients without nephropathy (DN-) who had lived with diabetes for 24 ± 3 and 27 ± 3 years, respectively and in 15 healthy control subjects. Renal functional reserve was calculated as the difference between amino acid-stimulated and baseline glomerular filtration rates (GFR).¶Results. Baseline glomerular filtration rate in DN- patients (106 ± 8) and control subjects (112 ± 3 ml · min-1· (1.73m2)-1) was significantly higher (p &lt; 0.01) than in DN + patients (79 ± 7 ml · min-1· (1.73m2)-1). Renal functional reserve was absent in DN + patients, whereas it represented 26 ± 4 % of the baseline in DN- patients and 23 ± 2 % in control subjects. Renal vascular resistance decreased statistically significantly during amino acid infusion in DN- patients and control subjects but not in DN + patients.¶Conclusions/hypothesis. These results indicate that very long-term Type I diabetic patients without diabetic nephropathy still have a normal renal functional reserve. In contrast, this reserve is suppressed in similarly long-term macroalbuminuric and hypertensive patients with overt nephropathy in spite of their remarkably maintained glomerular filtration rate. This opposite impairment supports the interpretation that glomerular hyperfiltration is a determining mechanism in human diabetic nephropathy. [Diabetologia (2000) 43: 227-230]</subfield>
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   <subfield code="a">Keywords Type I diabetes, diabetic nephropathy, renal functional reserve, amino acid infusion, glomerular hyperfiltration</subfield>
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