Diabetic nephropathy is a clinical syndrome characterized by persisten
t albuminuria (>300 mg/24 h), a relentless decline in glomerular filtr
ation rate (GFR), and raised arterial blood pressure. The prevalence o
f abnormal elevated albumin excretion rate (>30 mg/24 h) is approximat
ely 40% in insulin-dependent (IDDM) and non-insulin-dependent (NIDDM)
patients. Diabetes has become the leading cause of end-stage renal fai
lure in the United States of America and Japan and it remains the seco
nd leading cause in Europe. Patients suffering from diabetic nephropat
hy have an enormous increase in morbidity and mortality from cardiovas
cular disease in addition to renal death. Elevated blood pressure is a
n early and frequent phenomenon and furthermore accelerates the course
of diabetic nephropathy. Studies in humans suggest that angiotensin-c
onverting enzyme (ACE) inhibitors postpone and may even prevent progre
ssion to clinical overt diabetic nephropathy in normotensive IDDM and
NIDDM patients with persistent microalbuminuria. Conventional antihype
rtensive therapy and ACE inhibition usually combined with a diuretic r
educes albuminuria and postpones renal insufficiency in hypertensive I
DDM patients with overt nephropathy. A more beneficial effect on the r
ate 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 (s
erum creatinine >133 mmol/L). These findings suggest that ACE inhibiti
on causes renal protection (i.e. a beneficial effect on kidney functio
n [structure] above and beyond what would be expected from blood press
ure lowering effect alone). Finally, it should be stressed that ACE in
hibition and conventional antihypertensive treatment postpone end-stag
e renal failure and improve survival in diabetic nephropathy.