Mark J. Sarnak, MD; Tom Greene, PhD; Xuelei Wang, MS; Gerald Beck, PhD; John W. Kusek, PhD; Allan J. Collins, MD; Andrew S. Levey, MD
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, firstname.lastname@example.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.
Hypertension is a risk factor for progression of chronic kidney disease. The optimal blood pressure to slow progression is unknown.
To evaluate the effects of a low target blood pressure on kidney failure and all-cause mortality.
Long-term follow-up of the Modification of Diet in Renal Disease Study, a randomized, controlled trial conducted from 1989 to 1993.
15 outpatient nephrology practices.
840 persons with predominantly nondiabetic kidney disease and a glomerular filtration rate of 13 to 55 mL/min per 1.73 m2.
A low target blood pressure (mean arterial pressure < 92 mm Hg) or a usual target blood pressure (mean arterial pressure < 107 mm Hg).
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.
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.
The exact mechanism underlying the benefit of a low target blood pressure is unknown.
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.
Sarnak MJ, Greene T, Wang X, Beck G, Kusek JW, Collins AJ, et al. 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. Ann Intern Med. ;142:342–351. doi: 10.7326/0003-4819-142-5-200503010-00009
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Published: Ann Intern Med. 2005;142(5):342-351.
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