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1 March 2005 | Volume 142 Issue 5 | Pages 342-351
Background: Hypertension is a risk factor for progression of chronic kidney disease. The optimal blood pressure to slow progression is unknown.
Objective: To evaluate the effects of a low target blood pressure on kidney failure and all-cause mortality.
Design: Long-term follow-up of the Modification of Diet in Renal Disease Study, a randomized, controlled trial conducted from 1989 to 1993.
Setting: 15 outpatient nephrology practices.
Participants: 840 persons with predominantly nondiabetic kidney disease and a glomerular filtration rate of 13 to 55 mL/min per 1.73 m2.
Intervention: A low target blood pressure (mean arterial pressure < 92 mm Hg) or a usual target blood pressure (mean arterial pressure < 107 mm Hg).
Measurements: After the randomized trial was completed, kidney failure (defined as initiation of dialysis or kidney transplantation) and a composite outcome of kidney failure or all-cause mortality were ascertained through 31 December 2000.
Results: Kidney failure occurred in 554 participants (66%), and the composite outcome occurred in 624 participants (74%). After Cox proportional hazards modeling and intention-to-treat analysis, the adjusted hazard ratios were 0.68 (95% CI, 0.57 to 0.82; P < 0.001) for kidney failure and 0.77 (CI, 0.65 to 0.91; P = 0.0024) for the composite outcome in the low target blood pressure group compared with the usual target blood pressure group. Evidence was insufficient to conclude that the benefit of a low target blood pressure differed according to the cause of kidney disease, baseline glomerular filtration rate, or degree of proteinuria.
Limitations: The exact mechanism underlying the benefit of a low target blood pressure is unknown.
Conclusions: Assignment to a low target blood pressure slowed the progression of nondiabetic kidney disease in patients with a moderately to severely decreased glomerular filtration rate.
Editors' Notes
Context
Contribution
Implications
–The Editors
Author and Article Information
From Tufts-New England Medical Center, Boston, Massachusetts; Cleveland Clinic Foundation, Cleveland, Ohio; National Institute of Health, Bethesda, Maryland; and U.S. Renal Data System, Minneapolis, Minnesota.
Presented in part at the 2003 Annual Meeting of the American Society of Nephrology, San Diego, California, 14 to 17 November 2003.
Grant Support: By grants K23 DK 02904 and UO1 DK 35073 from the National Institutes of Diabetes and Digestive and Kidney Diseases.
Potential Financial Conflicts of Interest: None disclosed.
Requests for Single Reprints: Mark J. Sarnak, MD, Box 391, Division of Nephrology, Tufts-New England Medical Center, 750 Washington Street, Boston, MA 02111; e-mail, msarnak{at}tufts-nemc.org.
Current Author Addresses: Drs. Sarnak and Levey: Division of Nephrology, Tufts-New England Medical Center, 750 Washington Street, Boston, MA 02111.
Drs. Greene, Wang, and Beck: Cleveland Clinic Foundation, 9500 Euclid Avenue, Cleveland, OH 44195.
Dr. Kusek: National Institutes of Health, Room 617, 6707 Democracy Boulevard, Bethesda, MD 20817.
Dr. Collins: U.S. Renal Data System, 914 South 8th Street, D-206, Minneapolis, MN 55404.
Author Contributions: Conception and design: M.J. Sarnak, T. Greene, G. Beck, J.W. Kusek, A.J. Collins, A.S. Levey.
Analysis and interpretation of the data: M.J. Sarnak, T. Greene, X. Wang, G. Beck, J.W. Kusek, A.S. Levey.
Drafting of the article: M.J. Sarnak, T. Greene, A.S. Levey.
Critical revision of the article for important intellectual content: M.J. Sarnak, T. Greene, G. Beck, J.W. Kusek, A.S. Levey.
Final approval of the article: M.J. Sarnak, T. Greene, X. Wang, G. Beck, J.W. Kusek, A.J. Collins, A.S. Levey.
Provision of study materials or patients: A.J. Collins, A.S. Levey.
Statistical expertise: T. Greene, X. Wang, G. Beck.
Obtaining of funding: M.J. Sarnak, G. Beck, J.W. Kusek, A.S. Levey.
Administrative, technical, or logistic support: M.J. Sarnak, G. Beck, A.S. Levey.
Collection and assembly of data: M.J. Sarnak, T. Greene, G. Beck, J.W. Kusek, A.J. Collins. ARTICLE
The Effect of a Lower Target Blood Pressure on the Progression of Kidney Disease: Long-Term Follow-up of the Modification of Diet in Renal Disease Study
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