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Prevention of diabetic nephropathy with enalapril in normotensive diabetics with microalbuminuria.

Michel Marre, +5 more
- 29 Oct 1988 - 
- Vol. 297, Iss: 6656, pp 1092-1095
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TLDR
Inhibition of angiotensin converting enzyme prevents development of nephropathy in normotensive diabetics with persistent microalbuminuria and may be due to reduction in intraglomerular pressure and to prevention of increased systemic blood pressure.
Abstract
STUDY OBJECTIVE--To assess the effectiveness of inhibition of angiotensin converting enzyme in preventing diabetic nephropathy. DESIGN--Randomised follow up study of normotensive diabetics with persistent microalbuminuria (30-300 mg/24 hours) treated with enalapril or its matched placebo for one year. Double blind for first six months, single blind for last six months. SETTING--Diabetic clinic in tertiary referral centre. PATIENTS--Treatment group and placebo group each comprised 10 normotensive diabetics with persistent microalbuminuria. INTERVENTIONS--Treatment group was given enalapril 20 mg daily and controls matched placebo. Patients were given antihypertensive treatment after one year. END POINT--Albumin excretion, arterial pressure, and renal function. MAIN RESULTS--In last three months of trial three of 10 patients taking placebo had diabetic nephropathy (albumin excretion greater than 300 mg/24 hours). No patients taking enalapril developed nephropathy and five showed normal albumin excretion (less than 30 mg/24 hours) (p = 0.005, Mann-Whitney test). Mean arterial pressure was reduced by enalapril throughout study (p less than 0.005) but increased linearly with placebo (p less than 0.05). Albumin excretion decreased linearly with enalapril but not placebo. An increase in albumin excretion with placebo was positively related to the increase in mean arterial pressure (r = 0.709, p less than 0.05, Spearman's rank test). With enalapril total renal resistances and fractional albumin clearances improved progressively (time effect, p = 0.0001). CONCLUSION--Inhibition of angiotensin converting enzyme prevents development of nephropathy in normotensive diabetics with persistent microalbuminuria. This may be due to reduction in intraglomerular pressure and to prevention of increased systemic blood pressure. Future studies should compare long term effects of inhibitors of converting enzyme with other antihypertensive drugs.

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Citations
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Journal ArticleDOI

The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy. The collaborative study group

TL;DR: Captopril protects against deterioration in renal function in insulin-dependent diabetic nephropathy and is significantly more effective than blood-pressure control alone.
Journal ArticleDOI

The effect of angiotensin-converting-enzyme inhibition on diabetic nephropathy.

TL;DR: Whether captopril has kidney-protecting properties independent of its effect on blood pressure in diabetic nephropathy is determined.
Journal Article

Efficacy of atenolol and captopril in reducing risk of macrovascular and microvascular complications in type 2 diabetes: UKPDS 39

M R Stearne, +262 more
- 12 Sep 1998 - 
TL;DR: This study provided no evidence that either drug has any specific beneficial or deleterious effect, suggesting that blood pressure reduction in itself may be more important than the treatment used.
Journal ArticleDOI

Long-term complications of diabetes mellitus

TL;DR: Retinopathy is so characteristic of diabetes that its presence has been incorporated into the nosologic definition of NIDDM, while lower levels of hyperglycemia that are of sufficient magnitude to be associated with retinopathy are classified as NID DM.
References
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Journal ArticleDOI

Microalbuminuria Predicts Clinical Proteinuria and Early Mortality in Maturity-Onset Diabetes

TL;DR: It is concluded that microalbuminuria in patients with Type II diabetes is predictive of clinical proteinuria and increased mortality.
Journal ArticleDOI

Predicting Diabetic Nephropathy in Insulin-Dependent Patients

TL;DR: It is concluded that microalbuminuria predicts the development of diabetic nephropathy and that elevated glomerular filtration rates and increased blood pressure may also contribute to this progression.
Journal ArticleDOI

Structural-functional relationships in diabetic nephropathy.

TL;DR: All light and electron microscopic measures of mesangial expansion were strongly related to the clinical manifestations of diabetic nephropathy, although in the absence of these clinical findings, it was not possible to predict the severity of any of the diabetic glomerular lesions.
Journal ArticleDOI

Prevention of diabetic glomerulopathy by pharmacological amelioration of glomerular capillary hypertension.

TL;DR: Prevention of glomerular capillary hypertension in rats with diabetes mellitus effectively protects against the subsequent development ofglomerular structural injury and proteinuria, further supporting the view that hemodynamic rather than metabolic factors predominate in the pathogenesis of diabetic glomerulopathy.
Journal ArticleDOI

Therapeutic advantage of converting enzyme inhibitors in arresting progressive renal disease associated with systemic hypertension in the rat.

TL;DR: Control of systemic blood pressure is insufficient to prevent progressive renal injury in rats with reduced renal mass, and failure of triple drug therapy to control glomerular hypertension was associated with progressive proteinuria and glomersular lesions comparable to those seen in untreated group 4 rats.
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