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Intensive Blood-Pressure Control in Hypertensive Chronic Kidney Disease

Open access
Appel, Lawrence J., Wright, Jackson T., Greene, Tom, Agodoa, Lawrence Y., Astor, Brad C., Bakris, George L., Cleveland, William H., Charleston, Jeanne, Contreras, Gabriel, Faulkner, Marquetta L., Gabbai, Francis B., Gassman, Jennifer J., Hebert, Lee A., Jamerson, Kenneth A., Kopple, Joel D., Kusek, John W., Lash, James P., Lea, Janice P., Lewis, Julia B., Lipkowitz, Michael S., Massry, Shaul G., Miller, Edgar R., Norris, Keith, Phillips, Robert A., Pogue, Velvie A., Randall, Otelio S., Rostand, Stephen G., Smogorzewski, Miroslaw J., Toto, Robert D., Wang, Xuelei·2010·New England Journal of Medicine

Abstract

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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Metadata

Authors
Appel, L. J., Wright, J. T., Greene, T., Agodoa, L. Y., Astor, B. C., Bakris, G. L., Cleveland, W. H., Charleston, J., Contreras, G., Faulkner, M. L., Gabbai, F. B., Gassman, J. J., Hebert, L. A., Jamerson, K. A., Kopple, J. D., Kusek, J. W., Lash, J. P., Lea, J. P., Lewis, J. B., Lipkowitz, M. S., Massry, S. G., Miller, E. R., Norris, K., Phillips, R. A., Pogue, V. A., Randall, O. S., Rostand, S. G., Smogorzewski, M. J., Toto, R. D., & Wang, X.
Venue
New England Journal of Medicine
Published
2010-09-02
Volume
363
Issue
10
Pages
918-929
ISSN
  • 0028-4793 (ISSN-L)
  • 1533-4406
OpenAlex
W2123196786
Cited by
719
References
4
FWCI
48.03
Type
journal article
Language
en
Open access
bronze

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CoChat. (2026). Citation check: Intensive Blood-Pressure Control in Hypertensive Chronic Kidney Disease. https://app.cochat.ai/papers/10.1056/nejmoa0910975
The paper
Appel, L. J., Wright, J. T., Greene, T., Agodoa, L. Y., Astor, B. C., Bakris, G. L., Cleveland, W. H., Charleston, J., Contreras, G., Faulkner, M. L., Gabbai, F. B., Gassman, J. J., Hebert, L. A., Jamerson, K. A., Kopple, J. D., Kusek, J. W., Lash, J. P., Lea, J. P., Lewis, J. B., . . . Wang, X. (2010). Intensive Blood-Pressure Control in Hypertensive Chronic Kidney Disease. New England Journal of Medicine. https://doi.org/10.1056/nejmoa0910975

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Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.