Angiotensin-Converting Enzyme Inhibition and Renal Protection

Abstract

The role of hypertension in the pathogenesis of renal damage is a subject of both historical interest and current investigation. Because of the difficulty associated with studying the pathophysiologic role of glomerular injury in systemic hypertension, experimental models have provided much of the data in this field. The mechanisms leading to glomerular injury are complex and not fully elucidated. Mesangial and endothelial cell injury are thought to be important pathophysiologic mechanisms in the renal injury associated with hypertension. One hypothesis suggests that glomerular hypertension (ie, a hemodynamic event) is the primary pathogenetic mechanism, but another supports the notion that glomerular hypertrophy (ie, abnormal growth-related events) contributes to injury. The intrarenal renin-angiotensin system may play an important pathogenetic role in end-stage renal disease. Angiotensin-converting enzyme (ACE) inhibition has been shown to arrest the progression of renal injury in animal models. Although the clinical database is incomplete, the findings of anecdotal reports and short-term studies suggest that ACE inhibition may preserve renal function in patients with scleroderma renal crisis, reduce proteinuria in patients with diabetic nephropathy, and normalize renal hemodynamics in patients with a variety of renal diseases. The beneficial effects of ACE inhibition may be due to both hemodynamic (eg, reduction in glomerular capillary and intraglomerular pressures) and nonhemodynamic (eg, potassium-sparing and reduction in mesangial proliferation) mechanisms. The precise role of ACE inhibitors in the prevention of renal damage awaits the results of ongoing long-term, double-blind clinical studies. Nevertheless, ACE inhibition may be an appropriate therapeutic alternative in the hypertensive patient whose renal injury is progressing despite aggressive antihypertensive therapy.

ACE-inhibitor use and the long-term risk of renal failure in diabetes

“…Several other trials showed that ACE inhibitors clearly reduce albuminuria in both type I and type II diabetes mellitus, irrespective of blood pressure level, with consistent antiproteinuric effects. 12,[18][19][20][21][22][23][24][25][26][27][28][29] Although evidence from these studies has been interpreted as clearly demonstrating the beneficial renal effects of ACE inhibitors, there have been dissenting opinions [30][31][32][33][34][35][36][37] and calls for definitive long-term clinical trials to provide proof for the postulated effects. 38 One of the central issues in interpreting these and other studies on this issue revolves around the choice of outcome.…”

Angiotensin-Converting Enzyme Inhibitors; Their Efficacy, Adverse Effects, and the Genetic Influence on Cough They May Cause

“…Hyperkalemia could be extremely harmful in patients who have renal insufficiency, are diabetic, and in those using nonsteroidal anti-inflammatory drugs and salt substitutes (Ben Salem et al 2014). Renal impairment is another possible side effect of ACE-Is, induced by reduced renal perfusion due to inhibition of angiotensin II (Hollenberg 1985). Other common side effects include headache, dizziness, rash, and fever.…”