Effect of Calcium Channel or beta-Blockade on the Progression of Diabetic Nephropathy in African Americans

beta-Blockers are known to slow the progression of diabetic nephropathy by lowering arterial pressure. Moreover, in individuals with diabetic nephropathy, antihypertensive agents that provide sustained reductions in proteinuria slow the rate of decline in renal function compared with agents without...

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Veröffentlicht in:Hypertension (Dallas, Tex. 1979) Tex. 1979), 1997-03, Vol.29 (3), p.744-750
Hauptverfasser: Bakris, George L, Mangrum, Amy, Copley, J. Brian, Vicknair, Nancy, Sadler, Rebecca
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container_end_page 750
container_issue 3
container_start_page 744
container_title Hypertension (Dallas, Tex. 1979)
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creator Bakris, George L
Mangrum, Amy
Copley, J. Brian
Vicknair, Nancy
Sadler, Rebecca
description beta-Blockers are known to slow the progression of diabetic nephropathy by lowering arterial pressure. Moreover, in individuals with diabetic nephropathy, antihypertensive agents that provide sustained reductions in proteinuria slow the rate of decline in renal function compared with agents without this antiproteinuric effect. To examine whether differential effects on proteinuria affect the progression of diabetic nephropathy, we conducted a randomized study that compared the effects of a heart rate-lowering calcium channel blocker, sustained-release verapamil, with those of a beta-blocker, atenolol, on the progression of diabetic renal disease. The primary end point of the study was a change in creatinine clearance slope. Thirty-four African Americans with the following inclusion criteria were randomized to one of the two groupsserum creatinine greater than 1.4 mg/dL, proteinuria greater than 1500 mg/d, longer than a 5-year history of both non-insulin-dependent diabetes mellitus and hypertension, and exclusion of other renal diseases. Goal blood pressure was less than 140/90 mm Hg. All subjects received loop diuretics as second line agents to help achieve the blood pressure goal. Twenty-four-hour urinary protein and sodium excretions as well as creatinine clearance were measured at 6-month intervals. Blood pressure was measured every 3 months. After a mean follow-up of 54 +/- 6 months, the calcium channel blocker group demonstrated both a slower rate of decline in creatinine clearance (-1.7 +/- 0.9 versus -3.7 +/- 1.4 mL/min per year per 1.73 m, P < .01) and a greater reduction in proteinuria compared with the atenolol group. Additionally, a greater proportion of the atenolol group had a 50% or more increase in serum creatinine compared with the verapamil group (32 +/- 9% versus 16 +/- 7%, P < .05). These between-group differences could not be explained by differences in blood pressure control. These data support the concept that antihypertensive agents that persistently maintain reductions in both arterial pressure and proteinuria slow the progression of diabetic renal disease in African Americans to a greater extent than those agents without these effects. (Hypertension. 1997;29:744-750.)
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Brian</creatorcontrib><creatorcontrib>Vicknair, Nancy</creatorcontrib><creatorcontrib>Sadler, Rebecca</creatorcontrib><title>Effect of Calcium Channel or beta-Blockade on the Progression of Diabetic Nephropathy in African Americans</title><title>Hypertension (Dallas, Tex. 1979)</title><addtitle>Hypertension</addtitle><description>beta-Blockers are known to slow the progression of diabetic nephropathy by lowering arterial pressure. Moreover, in individuals with diabetic nephropathy, antihypertensive agents that provide sustained reductions in proteinuria slow the rate of decline in renal function compared with agents without this antiproteinuric effect. To examine whether differential effects on proteinuria affect the progression of diabetic nephropathy, we conducted a randomized study that compared the effects of a heart rate-lowering calcium channel blocker, sustained-release verapamil, with those of a beta-blocker, atenolol, on the progression of diabetic renal disease. The primary end point of the study was a change in creatinine clearance slope. Thirty-four African Americans with the following inclusion criteria were randomized to one of the two groupsserum creatinine greater than 1.4 mg/dL, proteinuria greater than 1500 mg/d, longer than a 5-year history of both non-insulin-dependent diabetes mellitus and hypertension, and exclusion of other renal diseases. Goal blood pressure was less than 140/90 mm Hg. All subjects received loop diuretics as second line agents to help achieve the blood pressure goal. Twenty-four-hour urinary protein and sodium excretions as well as creatinine clearance were measured at 6-month intervals. Blood pressure was measured every 3 months. After a mean follow-up of 54 +/- 6 months, the calcium channel blocker group demonstrated both a slower rate of decline in creatinine clearance (-1.7 +/- 0.9 versus -3.7 +/- 1.4 mL/min per year per 1.73 m, P &lt; .01) and a greater reduction in proteinuria compared with the atenolol group. Additionally, a greater proportion of the atenolol group had a 50% or more increase in serum creatinine compared with the verapamil group (32 +/- 9% versus 16 +/- 7%, P &lt; .05). These between-group differences could not be explained by differences in blood pressure control. These data support the concept that antihypertensive agents that persistently maintain reductions in both arterial pressure and proteinuria slow the progression of diabetic renal disease in African Americans to a greater extent than those agents without these effects. 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Blood pressure was measured every 3 months. After a mean follow-up of 54 +/- 6 months, the calcium channel blocker group demonstrated both a slower rate of decline in creatinine clearance (-1.7 +/- 0.9 versus -3.7 +/- 1.4 mL/min per year per 1.73 m, P &lt; .01) and a greater reduction in proteinuria compared with the atenolol group. Additionally, a greater proportion of the atenolol group had a 50% or more increase in serum creatinine compared with the verapamil group (32 +/- 9% versus 16 +/- 7%, P &lt; .05). These between-group differences could not be explained by differences in blood pressure control. These data support the concept that antihypertensive agents that persistently maintain reductions in both arterial pressure and proteinuria slow the progression of diabetic renal disease in African Americans to a greater extent than those agents without these effects. (Hypertension. 1997;29:744-750.)</abstract><cop>Philadelphia, PA</cop><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>9052890</pmid><doi>10.1161/01.HYP.29.3.744</doi><tpages>7</tpages></addata></record>
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source MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals
subjects Adrenergic beta-Antagonists - therapeutic use
Aged
Antihypertensive agents
Atenolol - therapeutic use
Biological and medical sciences
Black or African American
Black People
Blood Pressure - drug effects
Calcium Channel Blockers - therapeutic use
Cardiovascular system
Creatinine - blood
Delayed-Action Preparations
Diabetes Mellitus, Type 2 - complications
Diabetic Nephropathies - ethnology
Diabetic Nephropathies - prevention & control
Female
Humans
Hypertension - complications
Hypertension - drug therapy
Hypertension - ethnology
Male
Medical sciences
Middle Aged
Pharmacology. Drug treatments
Random Allocation
Verapamil - therapeutic use
title Effect of Calcium Channel or beta-Blockade on the Progression of Diabetic Nephropathy in African Americans
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