The suggested harmful effect of dietary protein on renal function in diabetic nephropathy was tested in three groups of insulin-dependent diabetic patients: 1) 10 patients without signs of nephropathy in spite of at least 30 years of diabetes; 2) 11 patients with nephropathy and reduced but stable glomerular filtration rate (GFR) (decline less than 4 ml/min per year [mean 1.8] during the last 2 years); 3) 10 patients with progressive nephropathy with GFR declining by an average of 11 ml/min per year. Dietary protein intake was estimated from a dietary history interview, as well as from urinary excretion of nitrogen (mean = 4.7 samples). Both methods showed a wide range of protein intake in all three groups of patients (0.6-2.3 g/kg body weight [BW]). The mean values did not differ between the groups, 1.30, 1.34, and 1.24 g/kg BW by interview, and 1.20, 1.10, and 1.13 g based on urinary nitrogen levels. There was no correlation between rate of decline of GFR and protein intake, even in those patients with no or minimal decline. These results do not support the hypothesis that dietary protein is a factor of importance in the development or progression of human diabetic nephropathy.

Adult↗

PubMedDate not supplied

Sodium excretion and blood pressure.

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Blood Pressure↗

PubMedDate not supplied

Effects of subpressor doses of angiotensin II on renal hemodynamics in relation to blood pressure.

The renal hemodynamic response to subpressor doses of angiotensin II (AII; 0.1 and 0.5 ng/min/kg) was investigated in untreated 49-year-old men (n = 50) representing a wide blood pressure range. Renal blood flow, renal vascular resistance (RVR), glomerular filtration rate (GFR), filtration fraction (FF), plasma renin activity (PRA), plasma AII, plasma aldosterone, and the urinary excretion of sodium and norepinephrine were studied. The higher the initial blood pressure the greater was the increase in RVR in response to AII infusion (p less than 0.002), indicating an increased renal vascular reactivity with increase in initial blood pressure. The AII infusion gave a significant rise in RVR in both the borderline and hypertensive group, but gave no increase in RVR in the normotensive group, implying an enhanced sensitivity of the renal vasculature in the borderline and hypertensive group. The increase in RVR was greater in the hypertensive than in the borderline group, i.e., the hypertensives had a steeper dose-response curve than the borderline group, which points to the presence of structural vascular changes in the renal vessels in the hypertensives. The increase in RVR in response to AII was positively correlated to sodium intake and plasma aldosterone concentration, indicating that these two factors might modulate the renal vascular reactivity. These factors could, however, only partly explain that RVR increased more the higher the initial blood pressure. Thus, the results indicate that there is an increased reactivity of the renal vascular bed to AII in essential hypertension. The increased reactivity seems to be mediated through an increased sensitivity of the renal vasculature to AII in mild essential hypertension and also through the presence of structural vascular changes in established hypertension. These factors may lead to a reduced excretion of sodium and water and may therefore be of importance in the development and progression of essential hypertension.

Aldosterone↗

PubMedDate not supplied

Effect of captopril on renal hemodynamics in the treatment of resistant renal hypertension.

The effects of 6 weeks of treatment with captopril on the renal hemodynamics of 16 patients with treatment-resistant renal hypertension (six had diabetic nephropathy, seven had other renal parenchymatous disease, and three had renovascular disease) were studied. Significant changes in glomerular filtration rate, filtration fraction, plasma renin activity, urinary aldosterone, and mean blood pressure were noted in the patients with renal parenchymatous disease, but not in those with diabetic nephropathy. Renal blood flow remained unchanged in all patients. Captopril was well tolerated.

Blood Flow Velocity↗

PubMedDate not supplied

Pharmacokinetic and pharmacodynamic properties of metoprolol in patients with impaired renal function.

The pharmacokinetics of metoprolol have been studied in a group of patients with varying degrees of renal impairment and in healthy subjects after administration of 20 mg of metoprolol tartrate intravenously and 50 mg orally in a single dose and during steady-state conditions. There were no significant differences in the extent of bioavailability or rate of elimination of the drug between the 2 groups. The fraction of the oral dose systemically available during steady-state was 59 +/- 9% in the renal patients and 55 +/- 7% in the control group. Total body clearance in the patients with renal failure was 1.0 +/- 0.1 L/min and in the healthy subjects it was 0.8 +/- 0.1 L/min. The corresponding values for the elimination half-life were 4.6 +/- 1.2h and 4.1 +/- 1.0h, respectively. The beta-adrenoceptor blocking effect of metoprolol (determined as percent reduction of exercise heart rate) did not differ significantly between the 2 groups during steady-state conditions. The effect on exercise heart rate was linearly related to the log of the plasma concentration of metoprolol. The relationship was identical for the single dose and during steady-state conditions, indicating that accumulation of metabolites in patients with renal failure does not influence the beta-blocking properties of metoprolol.

Adrenergic beta-Antagonists↗

PubMedDate not supplied

The effect of impaired renal function on the plasma concentration and urinary excretion of metoprolol metabolites.

Plasma concentration and urinary excretion of total and 2 active metabolites of metoprolol have been studied in patients with varying degrees of renal impairment and in healthy subjects after intravenous and oral administration of 20 and 50 mg of 3H-metoprolol tartrate respectively. Renal clearance of total metabolites correlated directly with 51Cr-EDTA clearance (r = 0.95, p less than 0.001). A reduction of glomerular filtration rate (GFR) by 70 to 80% increased the elimination half-life of total metabolites and of the active metabolite alpha-hydroxymetoprolol about 3-fold. Significant accumulation was, however, only observed in the patients with a GFR of about 5 ml/min. Even in these patients, the contribution of alpha-hydroxymetoprolol to the beta-adrenoceptor blocking effect of metoprolol will be negligible. The second active metabolite studied is eliminated via biotransformation, and the urinary excretion as well as the plasma concentration of this metabolite were extremely low in comparison with those of the parent drug.

Adult↗