Lance D Dworkin Douglas G Shemin

Hypertension is a cause and consequence of chronic renal disease. Data from the United States Renal Data System (USRDS) identifies systemic hypertension as the second most common cause of end-stage renal disease, with diabetes mellitus being the first. Renal failure in patients with hypertension has many causes, including functional impairment secondary to vascular disease and hypertensive nephrosclerosis. Even in those in whom hypertension is not the primary process damaging the kidney, elevations in systemic blood pressure may accelerate the rate at which kidney function is lost. This accelerated loss of kidney function occurs particularly in patients with glomerular diseases and clinically evident proteinuria.

Hypertension may damage the kidney by several mechanisms. Because autoregulation of glomerular pressure is impaired in chronic renal disease, elevations in systemic blood pressure also are associated with increased glomerular capillary pressure. Glomerular hypertension results in increased protein filtration and endothelial damage, causing increased release of cytokines and other soluble mediators that promote replacement of normal kidney tissue by fibrosis. An important factor contributing to progressive renal disease is activation of the renin-angiotensin system, which not only tends to increase blood pressure but also promotes cell proliferation, inflammation, and matrix accumulation.

Numerous studies in experimental animals suggest that antihyper-tensive drugs can slow the progression of chronic renal disease. Drugs that inhibit the renin-angiotensin system may be more effective than are other agents in retarding renal disease progression.

For many reasons, the effects of angiotensin II receptor antagonists and angiotensin-converting enzyme (ACE) inhibitors may not be identical. Calcium channel blockers also are beneficial in some settings; however, this effect is critically dependent on the degree of blood pressure reduction.

The relationship between hypertension and progression of chronic renal disease has been examined in a number of clinical trials. Individuals with systemic hypertension are at increased risk for developing end-stage renal disease. The rate at which kidney function is lost increases in patients with poorly controlled systemic hypertension. Antihypertensive therapy can slow the rate of loss of kidney function in patients with diabetic and nondiabetic renal disease. Studies suggest that ACE inhibitors are particularly useful in patients with hypertension and proteinuria of over 1g/24 h. Calcium channel blockers also may slow the progression of renal disease; however, whether all classes of calcium channel blockers have equivalent renal protective effects is uncertain.

Patients with hypertension and chronic renal disease should be treated aggressively. A 24-hour urine collection determines the extent of proteinuria. The patient who excretes more than 1 g/24 h of protein or who has diabetes mellitus should receive an ACE inhibitor. The target in this group of patients is to reduce the blood pressure to lower than 120/80 mm Hg. Most often, reaching this goal requires the use of combinations of antihypertensive agents, diuretics, or calcium channel blockers. Patients who excrete less than 1 g/24 h of protein may be treated according to standard recommendations with diuretics, beta blockers, ACE inhibitors, or other agents. The target blood pressure for this group of patients is lower than 130/85 mm Hg.

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