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Resistant hypertension and obstructive sleep apnea in the setting of kidney disease

Abdel-Kader, Khaleda,*; Dohar, Sheenab,*; Shah, Nirava; Jhamb, Manishaa; Reis, Steven E.c; Strollo, Patrickd; Buysse, Daniele; Unruh, Mark L.a

doi: 10.1097/HJH.0b013e328351d08a
ORIGINAL PAPERS: Resistant and malignant hypertension

Objectives: To explore the relationship between obstructive sleep apnea (OSA) and resistant hypertension in chronic kidney disease (CKD) and end-stage renal disease (ESRD).

Methods: We examined sleep parameters and blood pressure (BP) in 224 community-based, non-CKD participants from the Sleep-SCORE study: 88 nondialysis-dependent CKD and 95 ESRD participants. Unattended home polysomnography with standardized scoring protocols and automated BP monitors were used. Resistant hypertension was defined as a BP of at least 140/90 mmHg despite at least three antihypertensive drugs.

Results: Mean SBP of the CKD and ESRD groups were significantly higher than that of the non-CKD group [148.2 (23.8), 144.5 (26.7) vs. 132.2 mmHg (26.7), respectively; P < 0.0001] despite the use of more antihypertensive medications. The CKD and ESRD groups had higher rates of resistant hypertension than the non-CKD group (41.4, 22.6 vs. 6.7%, respectively; P < 0.0001). The severity of sleep apnea was associated with a higher risk of resistant hypertension. Although resistant hypertension was associated with severe sleep apnea in participants with ESRD [odds ratio (OR) 7.1, 95% confidence interval (CI) 2.2–23.2), there was no significant association in the non-CKD (OR 3.5, 95% CI 0.8–15.4) or CKD groups (OR 1.2, 95% CI 0.4–3.7) after accounting for case-mix.

Conclusion: The association between resistant hypertension and sleep apnea appeared robust in ESRD. OSA may contribute to resistant hypertension or both may be linked to a common underlying process such as volume excess. Future studies in patients with kidney disease should further characterize the resistant hypertension–OSA relationship and determine whether treatment of underlying mechanisms may improve outcomes.

aRenal-Electrolyte Division, University of Pittsburgh, Pittsburgh, Pennsylvania

bWest Virginia University School of Medicine, Morgantown, West Virginia

cDivision of Cardiology

dDepartment of Psychiatry

eDivision of Pulmonary, Allergy and Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania, USA

*Khaled Abdel-Kader and Sheena Dohar contributed equally to the writing of this article.

Correspondence to Khaled Abdel-Kader, Renal-Electrolyte Division, University of Pittsburgh, 3550 Terrace Street, A909 Scaife Hall, Pittsburgh, PA 15261, USA. Tel: +1 412 802 6854; fax: +1 412 647 6222; e-mail:

Abbreviations: AHI, apnea–hypopnea index; BP, blood pressure; CI, confidence interval; CKD, chronic kidney disease; CPAP, continuous positive airway pressure; eGFR, estimated glomerular filtration rate; ESRD, end-stage renal disease; ESS, Epworth Sleepiness Scale; HTN, hypertension; OR, odds ratio; OSA, obstructive sleep apnea; PSG, polysomnography; PSQI, Pittsburgh Sleep Quality Index; REM, rapid eye movement; TST, total sleep time

Received 22 August, 2011

Revised 7 December, 2011

Accepted 25 January, 2012

An abstract based on the content of this manuscript was presented as a poster at the October 2009 American Society of Nephrology annual meeting in San Diego, California, USA.

© 2012 Lippincott Williams & Wilkins, Inc.