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Hypertension. 2019 Apr;73(4):785-793. doi: 10.1161/HYPERTENSIONAHA.118.12358.

Inflammation and Apparent Treatment-Resistant Hypertension in Patients With Chronic Kidney Disease.

Author information

1
From the Department of Medicine (J.C., L.L.H., J.H.), Tulane University School of Medicine, New Orleans, LA.
2
Department of Epidemiology (J.C., J.D.B., L.L.H., J.H.), Tulane University School of Medicine, New Orleans, LA.
3
Tulane University Translational Science Institute, New Orleans, LA (J.C., L.L.H., J.H.).
4
Department of Preventive Medicine, Northwestern University Feinberg School of Medicine, Chicago, IL (J.D.B.).
5
Department of Medicine, University of California San Francisco School of Medicine, CA (C.-y.H.).
6
Department of Medicine, University of Illinois College of Medicine, Chicago (J.L.).
7
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD (E.R.M.).
8
Department of Nephrology and Hypertension, Cleveland Clinic, OH (G.T.).
9
Department of Medicine (D.L.C.), University of Pennsylvania Perelman School of Medicine, Philadelphia.
10
Department of Medicine, University of Maryland School of Medicine, Baltimore (M.R.W.).
11
Department of Medicine, Georgetown University School of Medicine, Washington, DC (D.S.R.).
12
Department of Biostatistics, Epidemiology, and Informatics (H.-y.C., D.X.), University of Pennsylvania Perelman School of Medicine, Philadelphia.
13
Department of Medicine, University of Michigan School of Medicine, Ann Arbor (P.R.).
14
Department of Medicine, Case Western Reserve University School of Medicine, Cleveland, OH (J.T.W., M.R.).

Abstract

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-α (tumor necrosis factor-α), and 0.77 (95% CI, 0.63-0.95) for TGF-β (transforming growth factor-β). High-sensitivity CRP (C-reactive protein), fibrinogen, IL-1β, 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-α and lower levels of TGF-β were independently associated with odds of ATRH. Targeting specific inflammatory pathways may improve blood pressure control in patients with chronic kidney disease.

KEYWORDS:

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

PMID:
30776971
PMCID:
PMC6416070
[Available on 2020-04-01]
DOI:
10.1161/HYPERTENSIONAHA.118.12358

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