Bryan Kestenbaum, MD, MS; Kyle D. Rudser, PhD; Ian H. de Boer, MD, MS; Carmen A. Peralta, MD; Linda F. Fried, MD, MPH; Michael G. Shlipak, MD, MPH; Walter Palmas, MD, MS; Catherine Stehman-Breen, MD, MS; David S. Siscovick, MD, MPH
Acknowledgment: The authors thank the other investigators, the staff, and the participants of MESA for their valuable contributions. A full list of participating MESA investigators and institutions can be found at http://www.mesa-nhlbi.org.
Grant Support: By contracts N01-HC-95159 through N01-HC-95165 and N01-HC-95169 from the National Heart, Lung, and Blood Institute and by a National Institutes of Health Career Development Award (K23 DK63274-01).
Potential Financial Conflicts of Interest:Employment: C. Stehman-Breen (Amgen). Grants pending: L.F. Fried (Merck).
Reproducible Research Statement:Study protocol: The complete MESA protocol is available online at http://www.mesa-nhlbi.org/moreinfo.aspx. Statistical code: Statistical code for these analyses is available from Dr. Kestenbaum (e-mail, firstname.lastname@example.org). Data set: The MESA data are available for researchers with a MESA sponsor and approved manuscript proposal. A list of participating institutions and principal investigators can be found at http://www.mesa-nhlbi.org/institutions.aspx.
Requests for Single Reprints: Bryan Kestenbaum, MD, MS, University of Washington, Division of Nephrology, Harborview Medical Center, Room 10EH11, 325 Ninth Avenue, Seattle, WA 98104-2499; e-mail, email@example.com.
Current Author Addresses: Dr. Kestenbaum: University of Washington, Division of Nephrology, Harborview Medical Center, Room 10EH11, 325 Ninth Avenue, Seattle, WA 98104.
Dr. Rudser: University of Washington, 1705 Northeast Pacific Street, Box 357232, Seattle WA 98195.
Dr. de Boer: University of Washington, 1959 Northeast Pacific Street, Box 356521, Seattle, WA 98195.
Dr. Peralta: University of California San Francisco, 505 Parnassus Avenue, San Francisco, CA 94143.
Dr. Fried: Veterans Affairs Pittsburgh Healthcare System, University Drive, Pittsburgh, PA 15240.
Dr. Shlipak: San Francisco Veterans Affairs Medical Center, 4150 Clement Street, 111A-1, San Francisco, CA 94131.
Dr. Palmas: Columbia University, 622 West 168th Street, New York, NY 10032.
Dr. Stehman-Breen: Amgen, 1 Amgen Center Drive, Thousand Oaks, CA 91320.
Dr. Siscovick: Cardiovascular Health Research Unit, Metropolitan Park, East Tower, 1730 Minor Avenue, Suite 1360, Seattle, WA 98101.
Author Contributions: Conception and design: B. Kestenbaum, K.D. Rudser, I.H. de Boer, C. Stehman-Breen.
Analysis and interpretation of the data: B. Kestenbaum, K.D. Rudser, I.H. de Boer, C.A. Peralta, L.F. Fried, M.G. Shlipak, C. Stehman-Breen, D.S. Siscovick.
Drafting of the article: B. Kestenbaum, K.D. Rudser, W. Palmas, C. Stehman-Breen.
Critical revision of the article for important intellectual content: B. Kestenbaum, K.D. Rudser, I.H. de Boer, C.A. Peralta, L.F. Fried, M.G. Shlipak, W. Palmas, C. Stehman-Breen, D.S. Siscovick.
Final approval of the article: B. Kestenbaum, K.D. Rudser, I.H. de Boer, C.A. Peralta, L.F. Fried, M.G. Shlipak, W. Palmas, C. Stehman-Breen, D.S. Siscovick.
Provision of study materials or patients: M.G. Shlipak, D.S. Siscovick.
Statistical expertise: B. Kestenbaum, K.D. Rudser.
Collection and assembly of data: W. Palmas.
Kestenbaum B, Rudser KD, de Boer IH, Peralta CA, Fried LF, Shlipak MG, et al. Differences in Kidney Function and Incident Hypertension: The Multi-Ethnic Study of Atherosclerosis. Ann Intern Med. 2008;148:501-508. doi: 10.7326/0003-4819-148-7-200804010-00006
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Published: Ann Intern Med. 2008;148(7):501-508.
The kidneys play a central role in the regulation of blood pressure (1, 2). Although most individuals with established kidney disease have hypertension, the direction of the association between kidney dysfunction and elevated blood pressure remains controversial (3–7).
Evidence suggests that early disturbances in kidney function may contribute to the development of hypertension. Transplantation of kidneys from Dahl and other hypertensive rat species transfers hypertension to recipient animals (8). Renal ischemia in early stages of kidney disease stimulates the renin–angiotensin–aldosterone and sympathetic nervous systems, which promotes sodium retention and increase peripheral resistance (9, 10). Evidence links low birthweight, a surrogate marker for reduced nephron number, with a greater risk for hypertension later in life (11). Accident victims with essential hypertension have a documented decrease in nephron number compared with matched control participants (12).
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Cardiology, Nephrology, Hypertension, Coronary Risk Factors.
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