Background Whether ambulatory BP monitoring is of value in evaluating risk for outcomes in patients with CKD is not clear. Methods We followed 1502 participants of the Chronic Renal Insufficiency Cohort (CRIC) Study for a mean of 6.72 years. We evaluated, as exposures, ambulatory BP monitoring profiles (masked uncontrolled hypertension, white-coat effect, sustained hypertension, and controlled BP), mean ambulatory BP monitoring and clinic BPs, and diurnal variation in BP-reverse dipper (higher at nighttime), nondipper, and dipper (lower at nighttime). Outcomes included cardiovascular disease (a composite of myocardial infarction, cerebrovascular accident, heart failure, and peripheral arterial disease), kidney disease (a composite of ESKD or halving of the eGFR), and mortality. Results Compared with having controlled BP, the presence of masked uncontrolled hypertension independently associated with higher risk of the cardiovascular outcome and the kidney outcome, but not with all-cause mortality. Higher mean 24-hour systolic BP associated with higher risk of cardiovascular outcome, kidney outcome, and mortality, independent of clinic BP. Participants with the reverse-dipper profile of diurnal BP variation were at higher risk of the kidney outcome. Conclusions In this cohort of participants with CKD, BP metrics derived from ambulatory BP monitoring are associated with cardiovascular outcomes, kidney outcomes, and mortality, independent of clinic BP. Masked uncontrolled hypertension and mean 24-hour BP associated with high risk of cardiovascular disease and progression of kidney disease. Alterations of diurnal variation in BP are associated with high risk of progression of kidney disease, stroke, and peripheral arterial disease. These data support the wider use of ambulatory BP monitoring in the evaluation of hypertension in patients with CKD.
Bibliographical noteFunding Information:
Funding for the CRIC Study was obtained under a cooperative agreement from National Institute of Diabetes and Digestive and Kidney Diseases, grants U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, and U01DK060902. In addition, this work was supported in part byPerelman School of Medicine at the University of Pennsylvania Clinical and Translational Science Award, National Institutes of Health (NIH)/National Center for Advancing Translational Sciences (NCATS) grant UL1TR000003, Johns Hopkins University grant UL1 TR-000424, the Clinical and Translational Science Collaborative of Cleveland, from NCATS component of NIH and NIH Roadmap for Medical Research grant UL1TR000439, the Michigan Institute for Clinical and Health Research grant UL1TR000433, the University of Illinois at Chicago Clinical and Translational Science Award grant UL1RR029879, the Tulane COBRE for Clinical and Translational Research in Cardiometabolic Diseases grant P20 GM109036-COBRA; University of Maryland grant GCRC M01 RR-16500; National Center for Research Resources grant UCSF-CTSI UL1 412 RR-02413; and the Leonard C. Rosenberg Foundation. J. Lash reports receiving grants from NIH (U01DK060980), during the conduct of the study. M. Rahman reports receiving grants from NIH (U01DK061021), during the conduct of the study. R. Townsend reports receiving grants from NIH (U01DK060984), during the conduct of the study.
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