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Central Pulse Pressure in Chronic Kidney Disease A Chronic Renal Insufficiency Cohort Ancillary Study

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posted on 2011-05-27, 00:00 authored by Raymond R. Townsend, Julio A. Chirinos, Afshin Parsa, Matthew A. Weir, Stephen M. Sozio, James P. Lash, Jing Chen, Susan P. Steigerwalt, Alan S. Go, Chi-yuan Hsu, Mohammed Rafey, Jackson T. Jr. Wright, Mark J. Duckworth, Crystal A. Gadegbeku, Marshall P. Joffe
Central pulse pressure (PP) can be noninvasively derived using the radial artery tonometric methods. Knowledge of central pressure profiles has predicted cardiovascular morbidity and mortality in several populations of patients, particularly those with known coronary artery disease and those receiving dialysis. Few data exist characterizing central pressure profiles in patients with mild-moderate chronic kidney disease who are not on dialysis. We measured central PP cross-sectionally in 2531 participants in the Chronic Renal Insufficiency Cohort Study to determine correlates of the magnitude of central PP in the setting of chronic kidney disease. Tertiles of central PP were <36 mm Hg, 36 to 51 mm Hg, and >51 mm Hg with an overall mean (+/-SD) of 46 +/- 19 mm Hg. Multivariable regression identified the following independent correlates of central PP: age, sex, diabetes mellitus, heart rate (negatively correlated), glycosylated hemoglobin, hemoglobin, glucose, and parathyroid hormone parathyroid hormone concentrations. Additional adjustment for brachial mean arterial pressure and brachial PP showed associations for age, sex, diabetes mellitus, weight, and heart rate. Discrete intervals of brachial PP stratification showed substantial overlap within the associated central PP values. The large size of this unique chronic kidney disease cohort provides an ideal situation to study the role of brachial and central pressure measurements in kidney disease progression and cardiovascular disease incidence. (Hypertension. 2010; 56: 518-524.)

Funding

R.R.T. received funding from the National Institutes of Health/National National Institute of Diabetes and Digestive and Kidney Diseases. These studies were supported by National Institutes of Health/National National Institute of Diabetes and Digestive and Kidney Diseases grants including R01-DK-067390 and U01-DK-060984 and National Institutes of Health/National Center for Research Resources grants UL1-RR024134, UL1 RR-025005, M01 RR-16500, UL1 RR-024989, M01 RR-000042, UL1 RR-024986, UL1RR029879, M01 RR-05096, and UL1 RR-024131.

History

Publisher Statement

The original source for this publication is at the American Heart Association; DOI: 10.1161/HYPERTENSIONAHA.110.153924

Publisher

American Heart Association

Language

  • en_US

issn

0194-911X

Issue date

2010-09-01

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