Intensive blood-pressure control in hypertensive chronic kidney disease

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

Research output: Contribution to journalArticle

378 Citations (Scopus)

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.)

Original languageEnglish (US)
Pages (from-to)918-929
Number of pages12
JournalNew England Journal of Medicine
Volume363
Issue number10
DOIs
StatePublished - Sep 2 2010

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Chronic Renal Insufficiency
Blood Pressure
Chronic Kidney Failure
Proteinuria
Control Groups
Creatinine
National Institute of Diabetes and Digestive and Kidney Diseases (U.S.)
Minority Health
Kidney Diseases
Observational Studies
Disease Progression
Hypertension
Health
Serum
Proteins

ASJC Scopus subject areas

  • Medicine(all)

Cite this

Appel, L. J., Wright, J. T., Greene, T., Agodoa, L. Y., Astor, B. C., Bakris, G. L., ... Wang, X. (2010). Intensive blood-pressure control in hypertensive chronic kidney disease. New England Journal of Medicine, 363(10), 918-929. https://doi.org/10.1056/NEJMoa0910975

Intensive blood-pressure control in hypertensive chronic kidney disease. / 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.

In: New England Journal of Medicine, Vol. 363, No. 10, 02.09.2010, p. 918-929.

Research output: Contribution to journalArticle

Appel, LJ, Wright, JT, Greene, T, Agodoa, LY, Astor, BC, Bakris, GL, Cleveland, WH, Charleston, J, Contreras, G, Faulkner, ML, Gabbai, FB, Gassman, JJ, Hebert, LA, Jamerson, KA, Kopple, JD, Kusek, JW, Lash, JP, Lea, JP, Lewis, JB, Lipkowitz, MS, Massry, SG, Miller, ER, Norris, K, Phillips, RA, Pogue, VA, Randall, OS, Rostand, SG, Smogorzewski, MJ, Toto, RD & Wang, X 2010, 'Intensive blood-pressure control in hypertensive chronic kidney disease', New England Journal of Medicine, vol. 363, no. 10, pp. 918-929. https://doi.org/10.1056/NEJMoa0910975
Appel LJ, Wright JT, Greene T, Agodoa LY, Astor BC, Bakris GL et al. Intensive blood-pressure control in hypertensive chronic kidney disease. New England Journal of Medicine. 2010 Sep 2;363(10):918-929. https://doi.org/10.1056/NEJMoa0910975
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. / Intensive blood-pressure control in hypertensive chronic kidney disease. In: New England Journal of Medicine. 2010 ; Vol. 363, No. 10. pp. 918-929.
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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.)",
author = "Appel, {Lawrence J.} and Wright, {Jackson T.} and Tom Greene and Agodoa, {Lawrence Y.} and Astor, {Brad C.} and Bakris, {George L.} and Cleveland, {William H.} and Jeanne Charleston and Gabriel Contreras and Faulkner, {Marquetta L.} and Gabbai, {Francis B.} and Gassman, {Jennifer J.} and Hebert, {Lee A.} and Jamerson, {Kenneth A.} and Kopple, {Joel D.} and Kusek, {John W.} and Lash, {James P.} and Lea, {Janice P.} and Lewis, {Julia B.} and Lipkowitz, {Michael S.} and Massry, {Shaul G.} and Miller, {Edgar R.} and Keith Norris and Phillips, {Robert A.} and Pogue, {Velvie A.} and Randall, {Otelio S.} and Rostand, {Stephen G.} and Smogorzewski, {Miroslaw J.} and Toto, {Robert D.} and Xuelei Wang",
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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

PY - 2010/9/2

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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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