Objective-To determine whether inhibition of angiotensin converting enzyme can reduce the rate of decline in kidney function more than reducing blood pressure with other antihypertensive treatment.Design-Prospective, open randomised study lasting a mean of 2*2 years in patients with diabetic nephropathy.Setting-Three outpatient nephrology clinics.Patients-40 patients with insulin dependent diabetes and diabetic nephropathy with reduced renal function.Intervention-Antihypertensive treatment with enalapril or metoprolol, usually combined with frusemide.Main outcome measure-Rate of decline in glomerular filtration rate measured as chromium-51 edetic acid clearance.Results-Glomerular filtration rate declined a mean of 2-0 (SD 3.2) ml/min/year in the group given enalapril and 5-6 (5.9) ml/min/year in the control group. The mean arterial blood pressure during the study was 102 (5) mm Hg in the patients given enalapril and 103 (5) mm Hg in the patients given metoprolol. Urinary albumin excretion during treatment with enalapril was 60% lower than during treatment with metoprolol.

These results indicate that the lipoprotein abnormalities of renal insufficiency contribute to the progression of renal failure in human chronic renal disease.

The effects of angiotensin converting enzyme inhibition with captopril were investigated in patients with diabetic nephropathy and hypertension. After nine days' treatment with captopril glomerular filtration rate was unchanged in 13 patients, whereas renal plasma flow had increased from 265 to 302 ml/min/173 ml body surface area (p

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Objective-To assess whether angiotensin converting enzyme inhibition reduces proteinuria in diabetic nephropathy more than blood pressure reduction with other antihypertensive treatment.Design-Prospective, open randomised study lasting eight weeks in patients with diabetic nephropathy.Setting-Outpatient nephrology clinics.Patients-40 Patients with type I diabetes and diabetic nephropathy with reduced renal function.Intervention-Antihypertensive treatment with enalapril or metoprolol, usually combined with frusemide.Main outcome measures-Arterial blood pressure and urinary excretion of albumin and protein.Results-Arterial blood pressure after eight weeks was 135/82 (SD 13/7) mm Hg in the group given enalapril and 136/86 (16/12) mm Hg in the group given metoprolol. Proteinuria and albuminuria were similar in both groups before randomisation. After eight weeks' treatment, the geometric mean albumin excretion was 0-7 (95% confidence interval 0 5 to 1-2) g/24 h in the patients given enalapril and 1-6 (1-1 to 2 5) g/24 h in the patients given metoprolol (p<002). The proteinuria was 1-1 (0.7 to 1.7) and 2-4 (1-6 to 3.6) g/24 h respectively (p<002).Conclusions-Antihypertensive treatment with enalapril reduced proteinuria in patients with diabetic nephropathy more than an equally effective antihypertensive treatment with metoprolol. This points to a specific antiproteinuric effect of the angiotensin converting enzyme inhibitor independent ofthe effect on systemic blood pressure.

When constructing arteriovenous fistulas for haemodialysis in chronic renal failure patients, one of the main problems is still their clotting tendency. Ticlopidine is an effective inhibitor of platelet aggregation. In this randomized double-blind study placebo or ticlopidine 250 mg twice daily was given to chronic uremic patients up to 4 weeks after construction of an arteriovenous fistula. 42 patients were recruited and 36 completed the trial. The fistula clotted in 8 patients on placebo and in 2 patients on ticlopidine. The difference is significant. This effect was achieved without an increased frequency of side effects compared with placebo. It is concluded that ticlopidine has a function as a thromboprophylactic drug in chronic uremic patients.

In this retrospective observational study, effective blood-pressure control was associated with a low rate of decline in renal function and a low urinary albumin excretion. The correlation between glycaemic control and decline in renal function indicates that poor glycaemic control can accelerate the loss of renal function in diabetic nephropathy.