Effect of insulin therapy on renal hemodynamic response to amino acids and renal hypertrophy in non-insulin-dependent diabetes

Effect of insulin therapy on renal hemodynamic response to amino acids and renal hypertrophy in non-insulin-dependent diabetes mellitus (NIDDM). Since renal hemodynamic disturbances are important in renal injury and are exacerbated by elevated plasma amino acid concentrations in insulin-dependent diabetes, we measured glomerular filtration rate (GFR) and renal plasma flow (RPF) after an overnight fast and during amino acid infusion in 12 patients with NIDDM and nine normal subjects. In the diabetic patients (plasma glucose 12.4 ± 0.6mmol/liter), the fasting GFR (113 ± 6 vs. 98 ± 7ml/min · 1.73m2 in normal subjects, P = 0.056) and RPF (635 ± 37 vs. 540 ± 20ml/min · 1.73m2 in normal subjects, P < 0.05) were increased. After amino acid infusion, the increase in GFR (159 ± 7 vs. 121 ± 6ml/min · 1.73m2 in normal subjects, P < 0.05) and RPF (970 ± 51 vs. 700 ± 18ml/min · 1.73m2 in normal subjects, P < 0.05) were augmented. Insulin infusion for 36 hours did not change these responses. After three weeks of insulin therapy (plasma glucose 5.9 ± 0.2mmol/ liter), the amino acid-stimulated GFR (143 ± 5ml/min · 1.73m2) and RPF (836 ± 30ml/min · 1.73m2) declined (P < 0.05), while the fasting values remained unchanged. The right kidney volume was measured by ultrasonography and found to decrease after three weeks of insulin therapy from 188 ± 12 to 165 ± 9ml/1.73m2 (P < 0.05). However, both values were greater than that in the normal subjects, 124 ± 13ml/1.73m2 (P < 0.01). Glomerular hyperfiltration and hyperperfusion became augmented during hyperaminoacidemia in our NIDDM patients. Both the augmented hemodynamic response to amino acids and renal hypertrophy regressed after three weeks of strict glycemic control.