Diabetic nephropathy is a clinical syndrome characterized by persistent albuminuria (>300 mg/24h), a relentless decline in glomerular filtration rate (GFR), and raised arterial blood pressure. The prevalence of abnormal elevated albumin excretion rate (>30 mg/24h) is approximately 40% in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM) patients. Diabetes has become the leading cause of end-stage renal failure in the United States of America and Japan and it remains the second leading cause in Europe. Patients suffering from diabetic nephropathy have an enormous increase in morbidity and mortality from cardiovascular disease in addition to renal death. Elevated blood pressure is an early and frequent phenomenon and furthermore accelerates the course of diabetic nephropathy. Studies in humans suggest that angiotensin-converting enzyme (ACE) inhibitors postpone and may even prevent progression to clinical overt diabetic nephropathy in normotensive IDDM and NIDDM patients with persistent microalbuminuria. Conventional antihypertensive therapy and ACE inhibition usually combined with a diuretic reduces albuminuria and postpones renal insufficiency in hypertensive IDDM patients with overt nephropathy. A more beneficial effect on the rate of decline in glomerular filtration rate has been demonstrated by ACE inhibitors compared to conventional antihypertensive treatment in IDDM patients with diabetic nephropathy and reduced kidney function (serum creatinine >133 mmol/L). These findings suggest that ACE inhibition causes renal protection (i.e. a beneficial effect on kidney function [structure] above and beyond what would be expected from blood pressure lowering effect alone). Finally, it should be stressed that ACE inhibition and conventional antihypertensive treatment postpone end-stage renal failure and improve survival in diabetic nephropathy.
|Udgave nummer||SUPPL. 1|
|Status||Udgivet - 1 jan. 1996|