4.7 Article

Inflammation and Apparent Treatment-Resistant Hypertension in Patients With Chronic Kidney Disease The Results From the CRIC Study

Journal

HYPERTENSION
Volume 73, Issue 4, Pages 785-793

Publisher

LIPPINCOTT WILLIAMS & WILKINS
DOI: 10.1161/HYPERTENSIONAHA.118.12358

Keywords

cardiovascular diseases; hypertension; inflammation; patients; renal insufficiency; chronic

Funding

  1. National Institute of Diabetes and Digestive and Kidney Diseases [U01DK060990, U01DK060984, U01DK061022, U01DK061021, U01DK061028, U01DK060980, U01DK060963, U01DK060902]
  2. Perelman 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) [UL1TR000003]
  3. Johns Hopkins University [UL1 TR-000424]
  4. University of Maryland General Clinical Research Center [M01 RR-16500]
  5. Clinical and Translational Science Collaborative of Cleveland from the NCATS component of the NIH [UL1TR000439]
  6. NIH roadmap for Medical Research, Michigan Institute for Clinical and Health Research [UL1TR000433]
  7. University of Illinois at Chicago Clinical and Translational Science Awards [UL1RR029879]
  8. Tulane Centers of Biomedical Research Excellence for Clinical and Translational Research in Cardiometabolic Diseases [P20 GM109036]
  9. Kaiser Permanente NIH/National Center for Research Resources, University of California San Francisco-Clinical & Translational Science Institute [UL1 RR-024131]

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Apparent treatment-resistant hypertension (ATRH) is highly prevalent and associated with cardiovascular disease risk in patients with chronic kidney disease. We analyzed the association of inflammatory biomarkers with ATRH and its complications in patients with chronic kidney disease. ATRH was defined as blood pressure >= 140/90 mm Hg while taking >= 3 antihypertensive medications or blood pressure <140/90 mm Hg while taking >= 4 medications. Analyses included 1359 CRIC study (Chronic Renal Insufficiency Cohort) participants with ATRH and 2008 hypertensive participants without. Logistic regression was used to examine cross-sectional associations of inflammatory biomarkers and ATRH adjusting for demographic, lifestyle, and clinical risk factors and treatments. Cox proportional hazards models were used to assess the impact of inflammatory biomarkers on associations of ATRH with composite cardiovascular disease and mortality beyond conventional risk factors. Multivariable-adjusted odds ratio (95% CI) of ATRH for the highest tertile versus the lowest tertile of inflammatory biomarker levels was 1.29 (95% CI, 1.05-1.59) for IL (interleukin)-6, 1.49 (95% CI, 1.20-1.85) for TNF-alpha (tumor necrosis factor-alpha), and 0.77 (95% CI, 0.63-0.95) for TGF-beta (transforming growth factor-beta). High-sensitivity CRP (C-reactive protein), fibrinogen, IL-1 beta, and IL-1 receptor antagonist were not significantly associated with ATRH. Adding inflammatory biomarkers to Cox models did not attenuate the significant association of ATRH with cardiovascular disease and mortality. Our findings show higher levels of IL-6 and TNF-alpha and lower levels of TGF-beta were independently associated with odds of ATRH. Targeting specific inflammatory pathways may improve blood pressure control in patients with chronic kidney disease.

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