microalbuminuria and macroalbuminuria was significantly higher in patients whose diabetes had developed before rather than after the age of 20. The prevalence of arterial hypertension increased with increased albuminuria, being 19%, 30%, and 65% in patients with normoalbuminuria, microalbuminuria, and macroalbuminuria respectively. The prevalence of proliferative retinopathy and blindness rose with increasing albuminuria, being 12% and 1-4%, respectively, in patients with normoalbuminuria, 28% and 5*6% in those with microalbuminuria and 58% and 10-6% in those with macroalbuminuria. An abnormal vibratory perception threshold was more common in patients with microalbuminuria (31%) and macroalbuminuria (50%) than in those with normoalbuminuria (21%). This study found a high prevalence (22%) ofmicroalbuminuria, which is predictive of the later development of diabetic nephropathy. Microalbuminuria is also characterised by an increased prevalence of arterial hypertension, proliferative retinopathy, blindness, and peripheral neuropathy. Thus, urinary excretion of albumin should be monitored routinely in patients with insulin dependent diabetes.

To evaluate the influence of angiotensin II on kidney function in diabetic nephropathy we investigated the effect of angiotensin converting enzyme inhibition with captopril on glomerular filtration rate and albuminuria in hypertensive diabetics dependent on insulin and with persistent albuminuria.

The relationship between arterial blood pressure and diabetic nephropathy was examined in 61 Type 1 (insulin-dependent) diabetic patients (22 females and 39 males). All patients fulfilled the following criteria: persistent proteinuria (greater than 0.5 g/day), onset of diabetes before 31 years of age, age less than 42 years, serum creatinine less than 130 mumol/l, and no antihypertensive treatment. Thirty Type 1 diabetic patients without persistent proteinuria but matched for sex, age, ideal body weight and duration of diabetes, and 30 healthy subjects matched for sex, age and ideal body weight were also studied as controls. The diabetic patients with persistent proteinuria had elevated blood pressures (146/96 +/- 17/10 mmHg, mean +/- SD) compared with 123/75 +/- 11/8 mmHg in diabetic patients without persistent proteinuria, and normal subjects (120/77 +/- 6/6 mmHg; p less than 0.001 for each). Diastolic blood pressure greater than or equal to 95 mmHg was found in 51% of the group with persistent proteinuria. Elevated arterial blood pressure is frequently present in young Type 1 diabetic patients with diabetic nephropathy and normal serum creatinine.

We evaluated the epidemiology of diabetic ketoacidosis in the period 1960-1979. In Frederiksborg County, Denmark, the incidence of ketoacidosis at the county hospital increased from 60 per 100,000 in the period 1943-1963 to 120 per 100,000 in the period 1960-1979. In the investigation period we found an increasing incidence confined to urban areas. Precipitating factors were not somatic in 53% of the cases. Patients in the lowest social class (V) were in a higher risk group, experiencing ketoacidosis more often and having a higher frequency of severe acidosis. Forty-nine percent of the patients have had a diabetes duration of more than 5 yr. The lethality rate decreased from the period 1943-1963 and was 4.7% in the investigation period 1960-1979.

The effect of an acute reduction in arterial blood pressure upon kidney function was studied in 12 patients with Type 1 (insulin-dependent) diabetes and incipient nephropathy (persistent microalbuminuria). Renal function was assessed by measurement of the glomerular filtration rate (single bolus 51Cr-EDTA technique) and by the urinary albumin excretion rate (radioimmunoassay). The study was performed twice within 2 weeks, with the patients receiving a slow intravenous injection of either clonidine (225 micrograms) or saline (154 mmol/l) in random order. Clonidine reduced arterial blood pressure from 125/79 +/- 13/8 to 104/68 +/- 9/7 mmHg (p less than 0.01), urinary albumin excretion rate from 68 (31-369) to 46 (6-200) micrograms/min (median and range) (p less than 0.01), and fractional clearance of albumin in all patients (median 29%) (p less than 0.01). Glomerular filtration rate was 110 +/- 11 before and 106 +/- 13 ml/min/1.73 m2 after clonidine injection. The blood glucose concentration was 15 +/- 4 mmol/l before and 14 +/- 5 mmol/l after clonidine injection. In agreement with findings in animal studies, our results suggest that microalbuminuria is to a large extent pressure-dependent, probably because of glomerular hypertension, and that autoregulation of glomerular filtration rate is normal in most patients with incipient diabetic nephropathy.