Physiologic evidence of renoprotection by antihypertensive therapy

Hypertension is vastly prevalent worldwide and constitutes the second leading cause of end-stage renal disease. Therefore, treating hypertension and protecting the kidney from deterioration are exceedingly important. Although previous studies have explored the renal effects of various antihypertensive drugs in animal models and humans, recent clinical trials are all the more convincing. This review summarizes the latest data demonstrating the physiologic evidence of renoprotection by antihypertensive therapy.

Experimental studies in various models of hypertension with renal injury have demonstrated clearly that angiotensin-converting enzyme inhibitors, angiotensin II type 1 receptor blockers, or aldosterone antagonists promote beneficial renal actions, through hemodynamic and nonhemodynamic mechanisms. Of particular significance, recent clinical trials have demonstrated renoprotection by angiotensin II inhibition in patients with hypertension and chronic kidney disease. Angiotensin-converting enzyme inhibition and angiotensin II type 1 receptor blockade have provided equivalent renal benefits, and their dual action seems to confer greater renoprotection. The available data on the renal outcomes of other antihypertensive drugs such as calcium antagonists have been inconsistent.

The results of the numerous experimental and clinical studies have established the renoprotective properties of renin-angiotensin-aldosterone inhibitors, which confer greater benefit by virtue of their effects over and beyond blood pressure reduction. These findings provide the convincing basis for the recommendation of angiotensin-converting enzyme inhibitors, angiotensin II type 1 receptor blockers, or both as first-line therapy in hypertension with chronic kidney disease.