Angiotensin II Receptor Blockade and Renal Protection

Abstract

It is now well-established that inhibition of the angiotensin-converting enzyme (ACE) can retard the progression of chronic renal failure in a variety of experimental and clinical settings. The recent introduction of highly specific angiotensin receptor type 1 (AT₁) antagonists has raised the issue whether these compounds produce comparable beneficial effects on the natural progression of chronic renal injury. Currently, a large body of experimental and clinical evidence indicates that both ACE inhibition and AT₁ blockade lead to similar changes in renal hemodynamics and proteinuria. Animal studies have also shown that AT₁ blockade effectively attenuates the development and progression of renal injury caused by a variety of mechanisms ranging from unilateral ureteric obstruction to renal ablation or immune-mediated acute glomerular injury. These findings make it likely that AT₁ blockade may ultimately prove to be a promising new therapy for slowing the progression of renal injury in patients with kidney disease.