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NDT Advance Access originally published online on September 22, 2007
Nephrology Dialysis Transplantation 2008 23(2):673-679; doi:10.1093/ndt/gfm598
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© The Author [2007]. Published by Oxford University Press on behalf of ERA-EDTA. All rights reserved. For Permissions, please email: journals.permissions@oxfordjournals.org


Nocturnal haemodialysis increases pharyngeal size in patients with sleep apnoea and end-stage renal disease

Jaime M. Beecroft1, Victor Hoffstein2, Andreas Pierratos3, Christopher T. Chan2, Philip McFarlane2 and Patrick J. Hanly1

1Department of Medicine, University of Calgary, Alberta, 2Department of Medicine, University of Toronto and 3Department of Medicine, Humber River Regional Hospital, Toronto, Ontario, Canada

Correspondence to: Patrick J. Hanly, MD, 1421 HSC, 3330 Hospital Drive NW, Calgary, Alberta, Canada T2N 4N1. Email: phanly{at}ucalgary.ca



   Abstract
Top
 Abstract
Introduction
 Subjects and methods
 Results
 Discussion
 References
 
Background. Sleep apnoea is common in patients with end-stage renal disease (ESRD) and is improved by nocturnal haemodialysis (NHD). Recent findings from our laboratory indicate the development of ESRD is associated with pharyngeal narrowing. We hypothesized that NHD increases pharyngeal cross-sectional area and that this is associated with an improvement in sleep apnoea.

Methods. Twenty-four patients (aged 32–68 years), receiving conventional haemodialysis (CHD) (4 h/day, 3 days/week), were recruited for overnight polysomnography and estimation of pharyngeal cross-sectional area at functional residual capacity (FRC) and residual volume (RV). Patients were divided into apnoeic and non-apnoeic groups based on an apnoea–hypopnoea index (AHI) ≥15/h. Following conversion from CHD to NHD (8 h/night, 3–6 nights/week) all measurements were repeated and apnoeic patients were classified as ‘responders’ if AHI fell to <15 events/h.

Results. Conversion from CHD to NHD was associated with an increase in pharyngeal cross-sectional area (FRC: 3.29 ± 0.67 vs 3.39 ± 0.75 cm2; RV: 1.91 ± 0.51 vs 2.13 ± 0.48 cm2, P < 0.05), which was not significantly different between groups. Sleep apnoea improved in three patients.

Conclusions. Conversion from CHD to NHD is associated with an increase in pharyngeal cross-sectional area. This may play a role in some patients whose sleep apnoea improves on NHD.

Keywords: nocturnal haemodialysis; pharyngometry; sleep apnoea; upper airway



   Introduction
Top
 Abstract
 Introduction
Subjects and methods
 Results
 Discussion
 References
 
Although large, well-controlled, epidemiological studies have not been performed to evaluate the prevalence of sleep apnoea in patients with end-stage renal disease (ESRD), it has been consistently reported to be higher than in the general population [1–8]. Furthermore, the pathogenesis of sleep apnoea in ESRD remains unclear. Previous investigators have observed features of both central and obstructive sleep apnoea (OSA) in patients with ESRD [2–6,9,10], which suggests that its pathogenesis is related both to destabilization of central respiratory control and upper airway occlusion. Recent findings from our laboratory indicate that the development of ESRD is associated with pharyngeal narrowing [11]. Narrowing of the upper airway increases the likelihood of occlusion during sleep, when diminished dilator muscle tone and gravitational forces associated with the supine position combine to narrow the airway further.

Although sleep apnoea is not corrected by conventional haemodialysis (CHD) [2,4], it is improved by nocturnal haemodialysis (NHD) [2], which may alter the size and function of the upper airway in several ways. Firstly, fluid overload associated with ESRD may cause oedema of the pharyngeal wall or para-pharyngeal tissues, both of which could narrow the airway. This may be corrected by improved haemodynamic stability and more effective ultrafiltration [12,13], both of which have been described in NHD. Second, uraemic neuropathy is common in ESRD [14] and may involve the innervation of upper airway muscles. This could compromise pharyngeal function by reducing sensory feedback and/or motor output. Features of both sensory and motor neuropathy have been described in OSA patients with normal renal function [15,16]. Third, uraemic myopathy affecting the pharyngeal dilator muscles may promote upper airway occlusion during sleep by reducing upper airway muscle tone. Improved clearance of uraemic toxins, including middle molecules [17] and proinflammatory cytokines [18] by NHD may correct such neuromuscular dysfunction in the upper airway and thereby improve sleep apnoea.

We hypothesized that NHD increases pharyngeal area in patients with ESRD and that this is associated with improvement in the severity of sleep apnoea. The specific objective of the study was to compare the dimensions of the pharynx before and after conversion from CHD to NHD and to determine whether these changes were associated with the correction of sleep apnoea, reflected by a fall in the apnoea–hypopnoea index (AHI).



   Subjects and methods
Top
 Abstract
 Introduction
 Subjects and methods
Results
 Discussion
 References
 
Patient recruitment and study protocol
Patients enrolled in the home NHD program at Humber River Regional Hospital, the Toronto General Hospital and St Michael's Hospital were invited to participate in our study. All patients who entered the study were receiving treatment with CHD for 4 h, on 3 days/week and were considered candidates for home haemodialysis (HD) training. Eligible patients had central venous access or arteriovenous fistula available for HD, no contraindications to systemic anti-coagulation, demonstrated an ability to learn the technique of NHD and had a supportive home environment. Baseline measurements were performed during treatment with CHD and consisted of overnight polysomnography and acoustic pharyngometry, which were performed within 24 h of the most recent dialysis session. Subsequently, patients underwent 5–6 weeks of home HD training and were restudied once they were using NHD at home without difficulty, which was usually 3–6 months later. Repeat polysomnography and acoustic pharyngometry were performed within 24 h of the most recent dialysis session on a night when the patient was not undergoing NHD. A venous blood sample (3–5 ml) was drawn on the evening of polysomnography at baseline and follow-up to determine blood urea nitrogen (BUN) and serum creatinine. The study protocol was reviewed and approved by the research ethics board at St Michael's Hospital, and all patients gave written informed consent to participate in the study.

Nocturnal haemodialysis
Training for NHD was performed while on CHD, in the dialysis centre, with a nurse to patient ratio of 1:1 and was followed by three overnight treatments in the dialysis centre. While undergoing treatment with NHD, patients performed their own dialysis at home, during sleep for 6–10 h per night, on 3–6 nights per week. High-flux polysulfone dialysers (Fresenius Medical Care, Lexington, MA, USA) were used by all patients. During NHD, typical blood and dialysate flow were 250 and 300 ml/min, respectively with a usual dialysate composition including sodium 140 mEq/l, potassium 2 mEq/l, bicarbonate 28–35 mEq/l and calcium 3–3.5 mEq/l [17]. Effectiveness of HD was determined by estimating the percent reduction in urea per dialysis session (PRU) [19]. The calculation, where pre- and post-BUN represent pre- and post-dialysis BUN is as follows:


Formula

Measurements of PRU were obtained from the dialysis clinics at the time of baseline and follow-up studies.

Polysomnography
Polysomnographic recordings were performed by continuous monitoring of the electroencephalogram (EEG), electrooculogram and sub-mental electromyogram (EMG), electrocardiogram, nasal airflow (Ultima Dual Airflow Pressure Sensor, Braebon Medical Corporation, Kanata, ON, USA), chest and abdominal respiratory movements (Respitrace, Ambulatory Monitoring; Ardsley, NY, USA) and oximetry (Mallinckrodt/Nellcor Puritan Bennett, Hazelwood, MO, USA). The recordings were performed and scored by registered polysomnographic technologists according to published criteria [20]. Apnoea was defined as absence of airflow for >10 s and hypopnoea was defined as a reduction in respiratory effort for 10 s or more associated with an arousal and/or reduction in oxygen saturation >3%. These events were further classified as central if abdominal and ribcage movements were synchronous, as obstructive if the movements were paradoxical, and mixed if a central event had terminal obstructive features.

Pharyngometry
On the evening that polysomnography was performed, an acoustic pharyngometer (Eccovision, Hood Laboratories, Washington, MA, USA) was used to measure pharyngeal cross-sectional area. The acoustic reflection technique is a non-invasive method for measuring pharyngeal area. It is based on the assumption that the respiratory tract can be modelled as a series of branched tubes of varying cross-sectional area. When a sound wave is sent along such a tract, the wave is partially reflected back every time there is a change in the cross-sectional area of the tract. Measuring the arrival time of these reflections and assuming the speed of sound in the airway, it is possible to calculate the distance travelled by the sound. Knowing the amplitude of the reflected waves, one can calculate the cross-sectional area of the tube. Theoretical considerations and limitations of this method have been described previously [21,22].

Measurements were obtained at the end of a normal tidal breath (functional residual capacity—FRC) and at the end of a forced expiration (residual volume—RV). These measurements were performed during oral breathing and nose-clips were worn to prevent nasal breathing. We estimated pharyngeal cross-sectional area between the oropharyngeal junction and the glottis (Figure 1). These anatomic landmarks were identified by instructing patients to breathe through the nose, which causes airway narrowing at the oropharyngeal junction, and by performing a Valsalva maneuver, which causes airway narrowing at the glottis. Expiratory reserve volume (ERV) was measured using spirometry (Vmax Series 2130 Spirometer, SensorMedics, Yorba Linda, CA, USA).


Figure 1
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  		Fig. 1. Example of a typical pharyngogram. The vertical axis is cross-sectional area and the horizontal axis is the distance into the airway, with 0.0 cm corresponding to the position of the incisor teeth. Mean pharyngeal cross-sectional area is calculated between the oro-pharyngeal junction (OPJ) and the glottis.

 
All patients were studied during wakefulness while seated in the upright position with the pharyngometer held in a horizontal position and connected to the patient through a mouthpiece. Subjects were instructed to fix their gaze straight ahead at eye level with their head and shoulders aligned, in order to avoid excessive head movement. Measurements were taken during four trials at each lung volume (FRC and RV) and the average of these four trials was calculated. Known sources of artefact, including head extension or flexion and uncontrolled tongue position were avoided [23].

Analysis
Mean data were analysed using one-way analysis of variance and Tukey post hoc analysis at baseline, repeated measures analysis of variance at follow-up and one-way analysis of the change within each group with Tukey post hoc analysis. Relationships between variables were analysed using Pearson correlation. Nominal data were analysed using chi-squared analysis. All statistical analysis was performed using computer software (SPSS 14.0, SPSS Inc., Chicago, IL, USA). All P-values of <0.05 were considered statistically significant.



   Results
Top
 Abstract
 Introduction
 Subjects and methods
 Results
Discussion
 References
 
Patient demographics
Twenty-four patients (15 males, 9 females), aged 32–68 years, were studied (Table 1). Patients were divided into apnoeic and non-apnoeic groups based on AHI ≥15 events/h during their baseline sleep study. In contrast to previous work [2], conversion from CHD to NHD did not correct sleep apnoea in the majority of our patients. Consequently, we classified apnoeic patients post hoc as ‘responders’ if their AHI was reduced to <15 events/h following conversion from CHD to NHD, and as ‘non-responders’ if this criterion was not met. During treatment with CHD, sleep apnoea was present in 16 patients (67%) and three of these patients (19%) met our criterion for a significant reduction in AHI following conversion to NHD. Responders were significantly younger than non-responders and tended to be lighter, although this did not reach statistical significance. Gender distribution, body mass index (BMI) and the ratio of neck circumference to height were not significantly different between groups. Chronic glomerulonephritis was the most common cause of ESRD, followed by diabetes, hypertension and polycystic kidney disease (PCKD). In two patients, the cause of ESRD was unknown.


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  		Table 1. Patient demographics

 
During treatment with CHD, there were no inter-group differences in PRU or serum creatinine, although BUN was significantly lower in responders than non-responders (Table 2). Conversion from CHD to NHD was associated with a significant increase in PRU and reduction in serum creatinine and the extent of these changes were similar between groups.


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  		Table 2. Indices of dialysis effectiveness

 
Polysomnography
By definition, baseline AHI during treatment with CHD was significantly higher in the apnoeic group (Table 3). Apnoeas and hypopnoeas were predominantly obstructive, with a small proportion classified as central or mixed. Baseline oxygenation during sleep was not significantly different between groups, although it tended to be higher in non-apnoeic patients. Following conversion from CHD to NHD, AHI decreased from 42.5 ± 23.9 to 7.3 ± 4.2 events/h in apnoeic responders and this was associated with a significant increase in oxygenation.


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  		Table 3. Polysomnography

 
Pharyngometry
The estimated pharyngeal cross-sectional area was virtually the same in all three groups during treatment with CHD, both at FRC and RV (Table 4). As expected, pharyngeal area was significantly lower at RV than at FRC. Conversion from CHD to NHD was associated with a significant increase in mean pharyngeal cross-sectional area (FRC: 3.29 ± 0.67 vs 3.39 ± 0.75 cm2; RV: 1.91 ± 0.51 vs 2.13 ± 0.48 cm2, P < 0.05). These changes were not significantly different between groups. There was a significant increase in ERV associated with conversion to NHD, which was greatest among apnoeic responders. There were no significant changes in BMI or neck circumference indexed to patient height.


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  		Table 4. Pharyngometry

 


   Discussion
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
References
 
Sleep apnoea is common in patients with ESRD [2–8], although its pathogenesis remains unclear. Recent findings from our laboratory suggest that the development of ESRD is associated with pharyngeal narrowing [11]. In the present study, we found pharyngeal cross-sectional area at FRC increased by 7% in all apnoeic patients, and by 22% in apnoeic responders based on a post hoc analysis of the change in AHI, following conversion from CHD to NHD. Recent investigators using the same methodology as ours have demonstrated that increasing pharyngeal cross-sectional area by 6%, concurrent with weight loss, was sufficient to reduce the severity of sleep apnoea (reflected by a reduction in the AHI) by 74% [24]. Thus, the changes we observed are likely to have a beneficial effect on the severity of sleep apnoea in patients with ESRD and generate several hypotheses regarding the pathogenesis of sleep apnoea in this patient population.

In our apnoeic patients, conversion from CHD to NHD was associated with an increase in upper airway calibre in both responders and non-responders. However, the change in pharyngeal cross-sectional area was not correlated with the change in AHI (FRC: r = 0.095, P = 0.658; RV: r = 0.048, P = 0.822). These findings suggest the reversal of pharyngeal narrowing alone does not account for the improvement of sleep apnoea by NHD. Previous work from our laboratory suggests the pathogenesis of sleep apnoea may also be related to enhanced chemoreflex responsiveness [25], which is reduced following conversion from CHD to NHD [26]. It is possible that both increased pharyngeal size and additional benefits of NHD, such as alterations in respiratory chemoreflex control, are required to correct sleep apnoea in patients with ESRD. In our non-apnoeic patients, upper airway calibre did not increase following conversion to NHD. These findings may indicate that pharyngeal narrowing was not due to fluid overload in our non-apnoeic patients and therefore would not be expected to improve on NHD. The trend for pharyngeal size to narrow in these patients may reflect non-fluid related weight gain, as evidenced by the small increase in BMI and neck circumference.

Pharyngeal narrowing has been described in OSA patients with normal renal function and its aetiology is multi-factorial. Obesity is associated with increased para-pharyngeal fat deposition leading to upper airway narrowing in patients with OSA [27]. Weight loss is associated with reduced fat around the pharynx [28], improvement in upper airway function and resolution of sleep apnoea [29]. However, weight change does not fully explain our findings since BMI and neck circumference were not significantly different on CHD and NHD.

Upper airway size is significantly altered by changes in lung volume, widening as lung volume increases and narrowing as lung volume falls [30]. Accordingly, it is possible the increase in pharyngeal cross-sectional area we observed is a result of changes in the lung volume at which our measurements were performed. Although we did not measure FRC and RV directly, the increase in ERV in our patients most likely reflects an increase in FRC. Effective fluid removal from the lung by NHD could decrease lung stiffness, reducing lung recoil and thereby increasing FRC [31]. However, we found no significant relationship between the change in ERV and the change in pharyngeal cross-sectional area at FRC (r = –0.284, P = 0.200) or RV (r = –0.281, P = 0.204), indicating that changes in lung volume alone do not explain our findings.

The NHD is associated with more effective ultrafiltration than CHD, leading to an improvement in blood pressure control, regression of left ventricular hypertrophy and a reduction in extracellular fluid volume [12,13]. This raises the potential for upper airway oedema associated with fluid overload and/or impaired ventricular function to cause pharyngeal narrowing and for correction of upper airway oedema by NHD to reverse such changes. This suggestion is supported by the recent demonstration that fluid displaced rostrally from the legs increases pharyngeal cross-sectional area and upper airway resistance in healthy subjects [32,33]. Moreover, preliminary findings suggest that diuretic therapy increases pharyngeal cross-sectional area and reduces AHI in OSA patients with co-existing heart failure [34]. However, the relationship between fluid removal and upper airway structure and function has not been explored in patients with ESRD.

Uraemic neuropathy can involve both sensory and motor neurons [14] that may include the innervation of upper airway dilator muscles. Correction of sensory neuropathy by NHD may increase upper airway size by restoring mechanoreceptor sensitivity to changes in transmural pressure. Mechanoreceptors are thought to play an important role in maintaining upper airway patency; topical anaesthesia of the upper airway induces apnoea in healthy subjects and increases apnoea duration in patients with OSA [35,36]. Correction of motor neuropathy involving upper airway dilator muscles could increase pharyngeal size by enhancing transmural pressure across the upper airway.

NHD may increase pharyngeal size by directly improving the strength and endurance of upper airway dilator muscles. Uraemic myopathy is common in ESRD and is associated with accumulation of uraemic toxins and malnutrition [14], both of which are improved by NHD [17]. Uraemic myopathy can affect respiratory muscles [37] and is characterized by muscle atrophy and rapid fatigability [14]. Conversion from CHD to NHD is associated with increased exercise capacity and duration [38], indicating an improvement in skeletal muscle function. It is therefore possible NHD increases pharyngeal size by correcting upper airway dilator muscle dysfunction caused by uraemic myopathy.

ESRD is a chronic inflammatory state, characterized by elevated levels of proinflammatory cytokines [39]. This may lead to pharyngeal narrowing due to upper airway inflammation, oedema or contractile dysfunction of upper airway dilator muscles through direct effects on muscles fibres and/or muscle innervation. For example, tumour necrosis factor-{alpha} reduces the force generating capacity of muscle fibres and can induce nerve degeneration [40,41]. NHD has been reported to normalize cytokine levels [18], which may contribute to the salutary effect of NHD on upper airway function.

In contrast to previous work [2], conversion from CHD to NHD did not correct sleep apnoea in the majority of our patients. This discrepancy may be related to the scheduling and timing of dialysis. Dialysis schedules for patients reported in this study varied from alternate nights (i.e. 3–4 nights/week) to 5 or 6 nights/week. In contrast, previous evaluation was performed on patients receiving NHD on 6 nights/week [2]. In addition, our patients were studied on a night while they were not undergoing NHD, a period during which sleep apnoea may partially return [2]. Further investigation is necessary to determine the amount of NHD that is required to correct sleep apnoea.

Some of our non-responders may have developed sleep apnoea independently of renal failure and consequently, would not be expected to benefit from a change in the mode of dialysis. The majority of non-responders in this study were male, in contrast to responders, who were all female. Male gender is a risk factor for sleep apnoea in the general population [42], which may partially explain the lack of male responders. However, a larger sample size is required to address whether there is a true gender difference in the response of sleep apnoea to NHD. Obesity may also have contributed to sleep apnoea in some of our non-responders, who tended to have a higher BMI that was not reduced following conversion from CHD to NHD. Selection of patients whose sleep apnoea developed in association with ESRD may have yielded a higher proportion of ‘responders’. This also requires further study.

Our study does have some limitations. Firstly, lack of power due to small sample size may have limited some of our analyses. Inclusion of additional patients would have strengthened our comparison between responders and non-responders. Unfortunately, for logistical reasons, we were unable to increase our sample size further. Second, we did not study patients who remained on CHD. However, previous reports of serial polysomnography on patients with ESRD [2,4] have shown that sleep apnoea persists on CHD, which suggests that pharyngeal size does not change significantly. Third, acoustic reflection measurements in the upper airway vary significantly both between and within individuals. This inherent variability limits our ability to make comparisons between apnoeic responders and non-responders. Finally, upper airway measurements were performed during wakefulness while seated in the upright position. We acknowledge that gravitational forces and sleep onset induce changes in the upper airway that are pivotal to the development of OSA. However, we believe that the relative increase in pharyngeal size we observed during wakefulness is similar in the supine position and during sleep.

In summary, pharyngeal cross-sectional area is increased following conversion from CHD to NHD. Since pharyngeal narrowing predisposes patients to upper airway occlusion during sleep, the reversal of such changes may contribute to the improvement of sleep apnoea in some patients receiving NHD. These findings generate a number of intriguing hypotheses regarding the pathogenesis of pharyngeal narrowing and sleep apnoea in patients with ESRD. Further studies are required to understand how NHD increases upper airway size and to determine the impact of changes in upper airway dimensions on the severity of sleep apnoea in patients with ESRD.

Conflict of interest statement. None declared.



   References
Top
 Abstract
 Introduction
 Subjects and methods
 Results
 Discussion
 References
 

  1. Zoccali C, Mallamaci F, Tripepi G. Sleep apnea in renal patients. J Am Soc Nephrol (2001) 12:2854–2859.[Free Full Text]
  2. Hanly PJ, Pierratos A. Improvement of sleep apnea in patients with chronic renal failure who undergo nocturnal haemodialysis. N Engl J Med (2001) 344:102–107.[Abstract/Free Full Text]
  3. Kimmel PL, Miller G, Mendelson WB. Sleep apnea syndrome in chronic renal disease. Am J Med (1989) 86:308–314.[CrossRef][Web of Science][Medline]
  4. Mendelson WB, Wadhwa NK, Greenberg HE, et al. Effects of hemodialysis on sleep apnea syndrome in end-stage renal disease. Clin Nephrol (1990) 33:247–251.[Web of Science][Medline]
  5. Wadhwa NK, Mendelson WB. A comparison of sleep-disordered respiration in ESRD patients receiving haemodialysis and peritoneal dialysis. Adv Perit Dial (1992) 8:195–198.[Medline]
  6. Stepanski E, Faber M, Zorick F, et al. Sleep disorders in patients on continuous ambulatory peritoneal dialysis. J Am Soc Nephrol (1995) 6:192–197.[Abstract]
  7. Unruh ML, Sanders MH, Redline S, et al. Sleep apnea in patients on conventional thrice-weekly hemodialysis: comparison with matched controls from the Sleep Heart Health Study. J Am Soc Nephrol (2006) 17:3503–3509.[Abstract/Free Full Text]
  8. Kuhlmann U, Becker HF, Birkhahn M, et al. Sleep-apnea in patients with end-stage renal disease and objective results. Clin Nephrol (2000) 53:460–466.[Web of Science][Medline]
  9. Auckley DH, Schmidt-Nowara W, Brown LK. Reversal of sleep apnea hypopnoea syndrome in end-stage renal disease after kidney transplantation. Am J Kidney Dis (1999) 34:739–744.[Web of Science][Medline]
  10. Langevin B, Fouque D, Leger P, et al. Sleep apnea syndrome and end-stage renal disease. Cure after renal transplantation. Chest (1993) 103:1330–1335.[CrossRef][Web of Science][Medline]
  11. Beecroft JM, Hoffstein V, Pierratos A, et al. Pharyngeal narrowing in end-stage renal disease: implications for obstructive sleep apnea. Eur Respir J (2007) doi: 10.1183/09031936.00161906.
  12. Chan CT, Floras JS, Miller JA, et al. Regression of left ventricular hypertrophy after conversion to nocturnal haemodialysis. Kidney Int (2002) 61:2235–2239.[CrossRef][Web of Science][Medline]
  13. Chan CT, Harvey PJ, Picton P, et al. Short-term blood pressure, noradrenergic, and vascular effects of nocturnal home haemodialysis. Hypertension (2003) 42:925–931.[Abstract/Free Full Text]
  14. Brouns R, De Deyn PP. Neurological complications in renal failure: a review. Clin Neurol Neurosurg (2004) 107:1–16.[CrossRef][Web of Science][Medline]
  15. Kimoff RJ, Sforza E, Champagne V, et al. Upper airway sensation in snoring and obstructive sleep apnea. Am J Respir Crit Care Med (2001) 164:250–255.[Abstract/Free Full Text]
  16. Boyd JH, Petrof BJ, Hamid Q, et al. Upper airway muscle inflammation and denervation changes in obstructive sleep apnea. Am J Respir Crit Care Med (2004) 170:541–546.[Abstract/Free Full Text]
  17. Pierratos A. Daily nocturnal home haemodialysis. Kidney Int (2004) 65:1975–1986.[CrossRef][Web of Science][Medline]
  18. Yuen D, Richardson RM, Fenton SS, et al. Quotidian nocturnal hemodialysis improves cytokine profile and enhances erythropoietin responsiveness. ASAIO J (2005) 51:236–241.[CrossRef][Web of Science][Medline]
  19. Jindal KK, Manuel A, Goldstein MB. Percent reduction in blood urea concentration during haemodialysis (PRU). A simple and accurate method to estimate Kt/V urea. ASAIO Trans (1987) 33:286–288.[Medline]
  20. Rechtschaffen A, Kales A. A manual of standardized terminology, techniques and scoring system for sleep stages of human subjects. Brain Information Service/Brain Research Institute, University of California at Los Angeles, CA, 1968 (NIH publication no. 204).
  21. Fredberg JJ, Wohl ME, Glass GM, et al. Airway area by acoustic reflections measured at the mouth. J Appl Physiol (1980) 48:749–758.[Abstract/Free Full Text]
  22. Hoffstein V, Fredberg JJ. The acoustic reflection technique for non-invasive assessment of upper airway area. Eur Respir J (1991) 4:602–611.[Abstract]
  23. Rubinstein I, McClean PA, Boucher R, et al. Effect of mouthpiece, noseclips, and head position on airway area measured by acoustic reflections. J Appl Physiol (1987) 63:1469–1474.[Abstract/Free Full Text]
  24. Busetto L, Enzi G, Inelmen EM, et al. Obstructive sleep apnea syndrome in morbid obesity: effects of intragastric balloon. Chest (2005) 128:618–623.[CrossRef][Web of Science][Medline]
  25. Beecroft J, Duffin J, Pierratos A, et al. Enhanced chemo-responsiveness in patients with sleep apnea and end-stage renal disease. Eur Respir J (2006) 28:151–158.[Abstract/Free Full Text]
  26. Beecroft J, Duffin J, Pierratos A, Chan C, McFarlane P, Hanly P. Chemoreflex responsiveness is decreased in patients whose sleep apnea is improved by nocturnal haemodialysis [abstract]. Proc Am Thorac Soc (2006) 3:A193.[CrossRef]
  27. Shelton KE, Woodson H, Gay S, et al. Pharyngeal fat in obstructive sleep apnea. Am Rev Respir Dis (1993) 148:462–466.[Web of Science][Medline]
  28. Welch KC, Foster GD, Ritter CT, et al. A novel volumetric magnetic resonance imaging paradigm to study upper airway anatomy. Sleep (2002) 25:532–542.[Web of Science][Medline]
  29. Rubinstein I, Colapinto N, Rotstein LE, et al. Improvement in upper airway function after weight loss in patients with obstructive sleep apnea. Am Rev Respir Dis (1988) 138:1192–1195.[Web of Science][Medline]
  30. Hoffstein V, Zamel N, Phillipson EA. Lung volume dependence of pharyngeal cross-sectional area in patients with obstructive sleep apnea. Am Rev Respir Dis (1984) 130:175–178.[Web of Science][Medline]
  31. Snapper JR. Lung mechanics in pulmonary oedema. Clin Chest Med (1985) 6:393–412.[Web of Science][Medline]
  32. Chiu KL, Ryan CM, Shiota S, et al. Fluid shift by lower body positive pressure increases pharyngeal resistance in healthy subjects. Am J Respir Crit Care Med (2006) 174:1378–1383.[Abstract/Free Full Text]
  33. Shiota S, Ryan CM, Chiu KL, et al. Alterations in upper airway cross-sectional area in response to lower body positive pressure in healthy subjects. Thorax (2007) doi: 10.1136/thx.2006.071183.
  34. Bucca CB, Brussino L, Battisti A, et al. Pharyngeal oedema in severe OSA [abstract]. Am J Respir Crit Care Med (2007) 175:A356.
  35. McNicholas WT, Coffey M, McDonnell T, et al. Upper airway obstruction during sleep in normal subjects after selective topical oropharyngeal anesthesia. Am Rev Respir Dis (1987) 135:1316–1319.[Web of Science][Medline]
  36. Cala SJ, Sliwinski P, Cosio MG, et al. Effect of topical upper airway anesthesia on apnea duration through the night in obstructive sleep apnea. J Appl Physiol (1996) 81:2618–2626.[Abstract/Free Full Text]
  37. Tarasuik A, Heimer D, Bark H. Effect of chronic renal failure on skeletal and diaphragmatic muscle contraction. Am Rev Respir Dis (1992) 146:1383–1388.[Web of Science][Medline]
  38. Chan CT, Notarius CF, Merlocco AC, et al. Improvement in exercise duration and capacity after conversion to nocturnal home haemodialysis. Nephrol Dial Transplant (2007) doi:10.1093/ndt/gfm368.
  39. Stenvinkel P, Ketteler M, Johnson RJ, et al. IL-10, IL-6, and TNF-alpha: central factors in the altered cytokine network of uremia–the good, the bad, and the ugly. Kidney Int (2005) 67:1216–1233.[CrossRef][Web of Science][Medline]
  40. Reid MB, Lannergren J, Westerblad H. Respiratory and limb muscle weakness induced by tumor necrosis factor-alpha: involvement of muscle myofilaments. Am J Respir Crit Care Med (2002) 166:479–484.[Abstract/Free Full Text]
  41. Creange A, Barlovatz-Meimon G, Gherardi RK. Cytokines and peripheral nerve disorders. Eur Cytokine Netw (1997) 8:145–151.[Web of Science][Medline]
  42. Guilleminault C, Bassiri A. Clinical features and evaluation of obstructive sleep apnea-hypopnea syndrome and the upper airway resistance syndrome. In: Principles and Practices of Sleep Medicine.—Kryger MH, Roth T, Dement WC, eds. (2005) Philadelphia, PA: Elsevier. 1043–1052.
Received for publication: 17. 5.07
Accepted in revised form: 1. 8.07


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