TY - JOUR
T1 - Intensive blood-pressure control in hypertensive chronic kidney disease
AU - Appel, Lawrence J.
AU - Wright, Jackson T.
AU - Greene, Tom
AU - Agodoa, Lawrence Y.
AU - Astor, Brad C.
AU - Bakris, George L.
AU - Cleveland, William H.
AU - Charleston, Jeanne
AU - Contreras, Gabriel
AU - Faulkner, Marquetta L.
AU - Gabbai, Francis B.
AU - Gassman, Jennifer J.
AU - Hebert, Lee A.
AU - Jamerson, Kenneth A.
AU - Kopple, Joel D.
AU - Kusek, John W.
AU - Lash, James P.
AU - Lea, Janice P.
AU - Lewis, Julia B.
AU - Lipkowitz, Michael S.
AU - Massry, Shaul G.
AU - Miller, Edgar R.
AU - Norris, Keith
AU - Phillips, Robert A.
AU - Pogue, Velvie A.
AU - Randall, Otelio S.
AU - Rostand, Stephen G.
AU - Smogorzewski, Miroslaw J.
AU - Toto, Robert D.
AU - Wang, Xuelei
N1 - Copyright:
Copyright 2017 Elsevier B.V., All rights reserved.
PY - 2010/9/2
Y1 - 2010/9/2
N2 - Background: In observational studies, the relationship between blood pressure and end-stage renal disease (ESRD) is direct and progressive. The burden of hypertension-related chronic kidney disease and ESRD is especially high among black patients. Yet few trials have tested whether intensive blood-pressure control retards the progression of chronic kidney disease among black patients. Methods: We randomly assigned 1094 black patients with hypertensive chronic kidney disease to receive either intensive or standard blood-pressure control. After completing the trial phase, patients were invited to enroll in a cohort phase in which the blood-pressure target was less than 130/80 mm Hg. The primary clinical outcome in the cohort phase was the progression of chronic kidney disease, which was defined as a doubling of the serum creatinine level, a diagnosis of ESRD, or death. Follow-up ranged from 8.8 to 12.2 years. Results: During the trial phase, the mean blood pressure was 130/78 mm Hg in the intensive-control group and 141/86 mm Hg in the standard-control group. During the cohort phase, corresponding mean blood pressures were 131/78 mm Hg and 134/78 mm Hg. In both phases, there was no significant between-group difference in the risk of the primary outcome (hazard ratio in the intensive-control group, 0.91; P = 0.27). However, the effects differed according to the baseline level of proteinuria (P = 0.02 for interaction), with a potential benefit in patients with a protein-to-creatinine ratio of more than 0.22 (hazard ratio, 0.73; P = 0.01). Conclusions: In overall analyses, intensive blood-pressure control had no effect on kidney disease progression. However, there may be differential effects of intensive blood-pressure control in patients with and those without baseline proteinuria. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Center on Minority Health and Health Disparities, and others.)
AB - Background: In observational studies, the relationship between blood pressure and end-stage renal disease (ESRD) is direct and progressive. The burden of hypertension-related chronic kidney disease and ESRD is especially high among black patients. Yet few trials have tested whether intensive blood-pressure control retards the progression of chronic kidney disease among black patients. Methods: We randomly assigned 1094 black patients with hypertensive chronic kidney disease to receive either intensive or standard blood-pressure control. After completing the trial phase, patients were invited to enroll in a cohort phase in which the blood-pressure target was less than 130/80 mm Hg. The primary clinical outcome in the cohort phase was the progression of chronic kidney disease, which was defined as a doubling of the serum creatinine level, a diagnosis of ESRD, or death. Follow-up ranged from 8.8 to 12.2 years. Results: During the trial phase, the mean blood pressure was 130/78 mm Hg in the intensive-control group and 141/86 mm Hg in the standard-control group. During the cohort phase, corresponding mean blood pressures were 131/78 mm Hg and 134/78 mm Hg. In both phases, there was no significant between-group difference in the risk of the primary outcome (hazard ratio in the intensive-control group, 0.91; P = 0.27). However, the effects differed according to the baseline level of proteinuria (P = 0.02 for interaction), with a potential benefit in patients with a protein-to-creatinine ratio of more than 0.22 (hazard ratio, 0.73; P = 0.01). Conclusions: In overall analyses, intensive blood-pressure control had no effect on kidney disease progression. However, there may be differential effects of intensive blood-pressure control in patients with and those without baseline proteinuria. (Funded by the National Institute of Diabetes and Digestive and Kidney Diseases, the National Center on Minority Health and Health Disparities, and others.)
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U2 - 10.1056/NEJMoa0910975
DO - 10.1056/NEJMoa0910975
M3 - Article
C2 - 20818902
AN - SCOPUS:77956274457
SN - 0028-4793
VL - 363
SP - 918
EP - 929
JO - New England Journal of Medicine
JF - New England Journal of Medicine
IS - 10
ER -