No abstract

Summary. Glomerular filtration rate (GFR, single bolus 51Cr-EDTA technique), serum creatinine, proteinuria and arterial blood pressure have been measured prospectively in 14 young onset insulin-dependent diabetics selected by of persistent proteinuria (> 0.5g/day) secondary to diabetic nephropathy. Twelve of the 14 patients had normal serum creatinine levels. None of the patients received antihypertensive treatment. During the mean observation period of 26 months (range 23 to 33 months) GFR decreased from 107 to 87 ml/min/1.73 m 2 (p < 0.001), serum creatinine remained unchanged: 107 and 112/~tmol/1 (NS), proteinuria increased from 1.8 to 3.3 g/day (p < 0.001) and arterial blood pressure rose from 132/88 to 153/101 mmHg (p < 0.001). Glomerular filtration rate decreased linearly with time (slope = -0.75, r = 0.99, p < 0.001) by a mean of 0.75 ml/min/month (range 0.1 to 1.5 ml/ min/month). The decrease in GFR did not correlate with sex, age at onset, duration of diabetes, arterial blood pressure, proteinuria, insulin requirement, postprandial blood glucose or the initial GFR, but numbers were small. The decline in GFR in each individual was constant, but varied considerably between patients. Increase in arterial blood pressure to a hypertensive level is an early feature of diabetic nephropathy in young insulin-dependent diabetics.

No abstract

The purpose of our prospective study was to evaluate the long-term effect of aggressive antihypertensive treatment on glomerular filtration rate and albuminuria in young female and male patients with insulin-dependent diabetes mellitus with diabetic nephropathy and blood pressure greater than 90 mm Hg. Eight patients received treatment with metoprolol (200-400 mg/day), hydraiazine (100-200 mg/day), and furosemide (80-500 mg/day). The untreated control group consisted of eight patients matched for age (mean 32 years), diabetes duration (mean 17 years), and sex (two female and six male patients). All patients except one had diabetic retinopathy. Glomerular filtration rate was measured after a single intravenous injection of 5l Cr-labeled ethylenediaminetetraacetic acid. Urinary albumin concentration was determined with a radial immunodiffusion method. The investigations were performed two to four times per year in each patient. The mean observation period was 59 and 27 months in the treated and untreated groups respectively. Due to a considerable rise in arterial blood pressure, it was considered unethical to prolong the observation in the untreated group. Arterial blood pressure rose from 140/96 ± 4/1 to 150/100 ± 3/2 mm Hg; albuminuria increased from 1517 ± 502 to 1911 ± 120 /xg/min; and glomerular filtration rate decreased by a mean of 0.84 ± 0.17 ml/min/mo in the untreated group. Antihypertensive treatment induced blood pressure reduction 151/100 ± 3/2 to 131/87 ± 2/1 mm Hg; diminished albuminuria 1467 ± 515 to 729 ± 65 Mg/min; and caused a slow rate of decline in GFR, mean 0.37 ± 0.08 ml/min/mo. Our prospective study suggests that prolonged reduction in arterial blood pressure to near normal levels reduces the rate of decline in glomerular filtration rate, and albuminuria in young patients with insulin-dependent diabetes mellitus and diabetic nephropathy. (Hypertension 7 [Suppl II]: 11-114-11-117, 1985) KEY WORDS • glomerular filtration arterial blood pressure albuminuria * insulin-dependent diabetes mellitus

The effect of acute arterial blood pressure lowering upon albumin extravasation was studied in 10 patients with nephropathy and retinopathy due to long-standing Type 1 (insulin-dependent) diabetes. The following variables were measured: transcapillary escape rate of albumin (initial disappearance of intravenously injected 125I-labelled human serum albumin), and urinary albumin excretion rate (radial immunodiffusion). The study was performed twice within 2 weeks, with the patients receiving an intravenous injection of either clonidine (225 micrograms) or saline (0.154 mmol/l). The clonidine injection induced the following changes: arterial blood pressure decreased from 134/87 to 107/73 mmHg (p less than 0.01), transcapillary escape rate of albumin declined from 8.1 to 6.7% of the intravascular mass of albumin/h (p less than 0.01), albuminuria diminished from 1434 to 815 micrograms/min (p less than 0.01), and plasma volume raised slightly from 2916 to 2995 ml (p less than 0.05). Our findings demonstrate that the enhanced albumin passage through the wall of the microvasculature characteristically found in long-term Type 1 diabetic patients with clinical microangiopathy is pressure-dependent to a large extent. This may be due to elevated hydrostatic pressure in the microcirculation.