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

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

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Abstract

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.

© 2012 Lippincott Williams & Wilkins, Inc.

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