Renoprotective effects of antihypertensive drugs

Abstract

Regardless of the specific antihypertensive agent used, the most important aspect of the management of the patient with coexistent hypertension and renal disease is adequate control of the blood pressure. The current JNC VI recommendation is for a reduction to a target blood pressure of 130/85 mm Hg, or to a lower value of 125/75 in patients with greater than 1 g proteinuria per day. Impaired renal sodium excretion leading to extracellular fluid volume (ECFV) expansion is the most clinically important mechanism leading to renal parenchymal hypertension. Sodium restriction and loop diuretics constitute the cornerstone of effective antihypertensive therapy. Control of blood pressure in patients with chronic renal disease may be difficult without measures that address ECFV. JNC VI recommends the use of angiotensin converting enzyme (ACE) inhibitors in patients with hypertension and chronic renal disease to control hypertension and to slow progressive renal failure. ACE inhibitors have been found by clinical trials to be useful agents in the settings of established insulin-dependent diabetes mellitus (IDDM) nephropathy, non-insulin-dependent diabetes mellitus (NIDDM) nephropathy, IDDM patients with normal blood pressures and microalbuminuria, NIDDM patients with microalbuminuria and normal renal function, and a variety of nondiabetic renal diseases, especially in the setting of significant proteinuria. Calcium antagonists are effective for treating hypertensive patients with chronic renal impairment but have not been studied as intensively as ACE inhibitors with regard to their ability to slow the progression of renal insufficiency independently of their blood-pressure-lowering effects. The initial results for calcium antagonists and for combination calcium antagonist-ACE inhibitor therapy have been promising. The angiotensin II antagonists have theoretical advantages for use in renal impairment, and seem to have similar renal hemodynamic and antiproteinuric effects to ACE inhibitors, but further clinical study is needed.