Renal Functional Response to Protein Loading in Type 1 (Insulin-Dependent) Diabetic Patients on Normal or High Salt Intake

Insulin-dependent diabetes mellitus (IDDM) patients may have an increased intrarenal angiotensin II activity. In diabetic patients, captopril increases the renal hemodynamic response to an amino acid infusion. We investigated the effects of two salt diets on arterial pressure and renal response to a protein load in 10 normotensive (blood pressure 2. The mean 24-hour urinary sodium excretion levels were 99 ± 27 and 293 ± 80 mmol (mEq) with normal and high salt intake, respectively. No significant changes were seen in plasma sodium and glucose control with the normal and high salt diets, respectively: plasma sodium 135 ± 3 vs. 137 ± 1 mmol/l (mEq/l), (p = 0.08) and glycated hemoglobin 9.1 ± 1.9 vs. 9.4 ± 2.1% (p = 0.36). The body weight (70.9 ± 12 vs. 71.8 ± 13 kg; p = 0.015) was significantly higher with a high salt diet. The mean arterial pressure was similar with both diets (normal vs. high salt diet 91 ± 9 vs. 89 ± 6 mm Hg, p = 0.25). The plasma renin concentration [28 ± 15 vs. 16 ± 6μU/ml(168 ± 90 vs. 96 ± 36 pmol/l), p = 0.013] and angiotensin II [8.8 ± 4.4 vs. 6.4 ± 3.5 pg/ml (0.052 ± 0.025 vs. 0.038 ± 0.021 nmol/l), p = 0.016] were significantly lower with the high salt diet. Following protein loading, the glomerular filtration rate increased with both diets: normal salt diet 114 ± 26 vs. 128 ± 30ml/min/1.73 m2(1.9 ± 0.43 vs. 2.13 ± 0.50ml/s/1.73 m2), p = 0.04; high salt diet 118 ± 23 vs. 127 ± 29 ml/min/1.73 m2 (1.97 ± 0.38 vs. 2.12 ± 0.48 ml/s/1.73 m2), p = 0.13. The change in renal plasma flow was similar to that of the glomerular filtration rate with normal and high salt intake, respectively: 566 ± 94 vs. 617 ± 142 ml/min/1.73m2 (9.44 ± 1.57 vs. 10.29 ± 2.37 ml/s/173m2), p = 0.0017; 572 ± 125 vs. 600 ± llθml/min/l.73 m2 (9.54 ± 2.08 vs. 10.00 ± 1.83 ml/s/1.73 m2), p = 0.057. In this subset of normotensive normoalbuminuric IDDM patients, a high salt intake did not promote an exaggerated renal response to the protein load despite inhibition of the renin-angiotensin system.