Angiotensin-converting enzyme inhibitors and progression of nondiabetic chronic renal disease

Long-Term Enalapril Therapy in Patients with Chronic Renal Failure on a Low-Protein Diet

“…Many previous studies have suggested that ACEIs supress the progression of renal failure or reduce proteinuria [2, 3, 4, 8, 9, 10]. However, most of them were based on a short-term follow-up of less than 12 months, and only 3 randomized controlled studies have been conducted for 1 year or longer to evaluate the renoprotective effect of ACEIs in comparison with other antihypertensive agents [8, 9, 10].…”

“…Angiotensin-converting enzyme inhibitors (ACEIs) were reported by some authors to have a specific suppressive effect on the progression of renal failure which cannot be explained by their antihypertensive effect [2, 3, 4]. However, the few long-term prospective randomized studies that assessed the renoprotective effect of ACEIs actually provided no substantial evidence supporting the specific renoprotective effect [2].…”

“…However, no previous studies [2, 3, 4] on the renal effect of ACEIs were performed in patients on a restricted protein intake.…”

Acute and long-term effects of ACE inhibition on renal haemodynamics in glomerular and interstitial nephropathies

“…Concerning the first result, it is known that, in normal subjects and essential hypertensives, ACE inhibition causes an increase in ERPF, with no substantial changes in GFR and FF. In chronic renal failure patients, there have been surprisingly few studies on the effects of acute ACE inhibition; however, from the review of the effects of ACE-I on renal function in non-diabetic chronic renal diseases by ter Wee & Epstein, 3 it can be argued that both GFR and ERPF tend to decrease more in short-term studies (range <1-26 weeks) than in long-term ones (52-156 weeks) with a calculated FET of 0.006 and 0.03 for GFR and ERPF, respectively. Although the comparison of effects seen after hours with those seen after days to weeks of treatment is debatable, our results support the view that the acute and short-term modifications of renal haemodynamics produced by ACE-I are different from the long-term ones, presumably because of the increased intrarenal levels of angiotensin II (Ang II) in circumstances of decreased renal perfusion.This view is supported by the lack of decrease in GFR that we observed after long-term ACE inhibition.…”

“…The treatment of patients with diabetic and nondiabetic renal diseases with angiotensin-converting enzyme inhibitors (ACE-I) reduces urinary protein excretion and may slow the progression of renal failure more than any other antihypertensive treatment. [1][2][3][4] However, not every trial has shown a favourable effect of ACE-I. These contrasting results could depend on different pathophysiological mechanisms of renal failure progression in different nephropathies: for example, in autosomal polycistic kidney disease the protective effect of ACE-I seems to be absent.…”