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Volume 10, Issue 1, Pages 47-54 (January 2009)


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Decreased chemosensitivity and improvement of sleep apnea by nocturnal hemodialysis

Jaime M. Beecrofta, James Duffinb, Andreas Pierratosc, Christopher T. Chand, Philip McFarlaned, Patrick J. HanlyaCorresponding Author Informationemail address

Received 22 August 2007; received in revised form 15 November 2007; accepted 16 November 2007.

Abstract 

Background:

Sleep apnea occurs in up to 50% of patients with end-stage renal disease and is improved by nocturnal hemodialysis. We hypothesized that its pathogenesis is related to changes in chemoreflex responsiveness.

Methods:

Twenty-four patients receiving conventional hemodialysis (4h/day, 3 times/week) had overnight polysomnography and measurement of the ventilatory response to carbon dioxide during isoxic hypoxia and hyperoxia using a modified rebreathing technique. Measurements were repeated following conversion from conventional to nocturnal hemodialysis (8h/night, 3–6 nights/week). Patients were divided into apneic and non-apneic groups based on apnea–hypopnea index ⩾15/h at baseline (17 apneics and 7 non-apneics), and the apneic group was further divided into “responders” and “non-responders” based on a significant reduction in AHI at follow-up.

Results:

Conversion from conventional to nocturnal hemodialysis was associated with a decrease in the ventilatory sensitivity to hypercapnia during hyperoxia in responders (3.2±1.0 vs. 2.3±1.3L/min/mmHg) but not in non-responders (2.8±1.3 vs. 2.9±1.6L/min/mmHg). The change in ventilatory sensitivity was correlated with the change in apnea–hypopnea index in all apneic patients (r=.528, p=0.029).

Conclusions:

Improvement of sleep apnea following conversion from conventional to nocturnal hemodialysis is associated with a decrease in chemoreflex responsiveness. This finding suggests that increased chemoreflex responsiveness contributes to the pathogenesis of sleep apnea in some patients with end-stage renal disease.

a Department of Medicine, University of Calgary, 1421 HSC, 3330 Hospital Drive NW, Calgary, Alta., Canada T2N 4N1

b Department of Physiology, University of Toronto, Ont., Canada

c Department of Medicine, Humber River Regional Hospital, Toronto, Ont., Canada

d Department of Medicine, University of Toronto, Ont., Canada

Corresponding Author InformationCorresponding author. Tel.: +1 403 220 2865; fax: +1 403 283 6151.

PII: S1389-9457(07)00429-7

doi:10.1016/j.sleep.2007.11.017


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