Download Sleep disordered breathing in patients with chronic kidney disease

Review Article
Indian J Med Res 131, February 2010, pp 277-284
Sleep disordered breathing in patients with chronic kidney disease
Manju Mavanur, Mark Sanders* & Mark Unruh
Renal-Electrolyte Division, University of Pittsburgh School of Medicine, Pittsburgh Pennsylvania &
*
Pittsburgh, Pennsylvania, USA
Received January 20, 2009
The prevalence of sleep-disordered breathing (SDB) in the advanced chronic kidney disease (CKD) patient
population has been estimated to be more than 50 per cent. SDB is associated with episodic upper airway
obstruction or cessation of breathing during sleep leading to repetitive episodes of hypoxaemia, hypercapnia,
and sleep fragmentation, activation of the sympathetic nervous system, endothelial dysfunction, oxidative
stress, and inflammation. Clinical consequences of this disorder may include excessive daytime sleepiness,
depressed mood, cognitive impairment, hypertension, as well as increased risk for cardiovascular disease
and metabolic dysregulation. SDB may also contribute substantially to the daytime sleepiness, poor quality
of life, and high rate of cardiovascular disease in CKD patients. Although the causal links between CKD
and SDB remain speculative, there are multiple factors related to fluid overload and azotaemia that may
contribute to the increased propensity to SDB. Renal transplantation, nocturnal automated peritoneal
dialysis and nocturnal haemodialysis have been found to be associated with a reduction in the severity of
SDB when compared to conventional forms of dialysis. Nocturnal dialysis modalities may facilitate further
understanding of the pathophysiology of SDB as well as provide therapeutic alternatives for patients with
both kidney failure and SDB. SDB is an important but often overlooked public health problem in the CKD
patient population. Early diagnosis and treatment of SDB may provide better quality of life and attenuate
the cardiovascular risk of morbidity and mortality in these patients.
Key words Chronic kidney disease - end-stage renal disease haemodialysis - sleep disordered breathing
Introduction
electrolytes, secrete or excrete hormones, handle the
daily dietary and metabolic acid load, and maintain
fluid balance. In the United States, the incidence
and prevalence of advanced CKD requiring renal
replacement therapy has doubled in the past ten years2.
The true prevalence of CKD is unknown in India due
to lack of a renal registry but some community-based
population studies have reported the prevalence of
kidney failure to be between 0.16 and 0.79 per cent3.
The potential importance of sleep disordered breathing
The prevalence of chronic kidney disease (CKD) is
increasing worldwide, and there is increasing evidence
linking sleep-disordered breathing (SDB) with kidney
disease. CKD describes patients with a chronically
decreased glomerular filtration rate (GFR) or other
evidence of kidney damage. There are different levels
of CKD, which provide the basis of an international
classification system1 (Table). CKD is associated with
the inability to excrete waste products, control serum
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INDIAN J MED RES, FEBRUARY 2010
Table. Stages of chronic kidney disease
Stage Description
GFR (ml/min/1.73m )
2
1
Kidney damage with normal or ↑
GFR
≥90
2
Kidney damage with mildly ↓
GFR
60-89
3
Moderate decrease in GFR
30-59
4
Severe decrease in GFR
5
Kidney failure
GFR, glomerular filtration rate
Source: Ref. 1
15-29
< 15
in the CKD population is highlighted by the worldwide
mortality in end stage renal disease (ESRD) patients as
high as 20 per cent per annum and the leading cause
of mortality and morbidity in this patient population
is cardiovascular disease. One of the risk factors for
cardiovascular disease in the general population is
SDB4,5 and the high rate of SDB in the CKD population
may contribute to the burden of cardiovascular disease
found in this population.
While the prevalence of SDB in the general
population is 5-12 per cent using an apnoea hypopnoea
cut off of greater than 15, several studies in the
advanced CKD patient population have shown a much
higher prevalence; ranging from 18 to 80 per cent6-10.
The most precise estimates in the US ESRD population
demonstrate that SDB is four times more prevalent
in patients with advanced CKD on haemodialysis
than in the general population and several studies
have demonstrated a higher risk in patients with
milder CKD11-13. Most investigators have outlined the
potential for CKD to contribute to SDB, however, it is
also possible that there is bi-directional causality such
that SDB also contributes to the progression of kidney
disease7,14-16. Given the high prevalence and severe
consequences of untreated SDB in the CKD population.
The clinical diagnosis, treatment, and pathophysiology
of SDB in the context of CKD are reviewed. Also, the
disease-targeted treatment of SDB in advanced CKD
will be assessed and the extent to which novel dialysis
therapies and kidney transplantation improve SDB in
this patient population will also be examined.
Definition of SDB
Various definitions of SDB have been employed
across studies in CKD, making a unified description
of the distribution and determinants of SDB difficult in
this high-risk population. SDB refers to an abnormal
respiratory pattern (apnoeas, hypopnoeas, or respiratory
effort related arousals) or an abnormal reduction in
gas exchange (hypoventilation) during sleep. Some
studies in CKD have relied on questionnaires and/or
pulse oximetry to investigate SDB17. However, these
techniques are neither sufficiently sensitive nor specific.
At best, they may provide only a rough estimate of the
prevalence of SDB. Moreover, they do not determine
the type of SDB. SDB can be obstructive, central, or
mixed. An obstructive apnoea is characterized by a
period of absent or nearly absent air flow for at least
10 sec despite persistent inspiratory efforts. Central
apnoea reflects absent airflow for at least 10 sec in
conjunction with absent inspiratory efforts18. Primary
central Sleep Apnoea is defined as five or more central
apnoeas per hour of sleep in association with patient
report of either excessive daytime sleepiness or frequent
arousals and awakenings during sleep or awakening
short of breath19. Mixed apnoea reflects an initial
interval during which there is no inspiratory effort (i.e.,
central apnoea pattern) and a subsequent interval during
which there are obstructed breathing efforts. In general,
hypopnoea reflects a reduction in airflow that does not
reach the criterion for an apnoea and lasting at least
10 sec. Additional criteria that have been used include
oxyhaemoglobin saturation and arousal. It is not feasible
to distinguish obstructive from central hypopnoeas
without quantitative measure of inspiratory effort such
as esophageal pressure, diaphragm EMG or calibrated
inductance plethysmography18,20. Although an updated
definition of hypopnoea has been recently modified by
the American Academy of Sleep Medicine18, the existing
literature is inconsistent21,22. The apnoea-hypopnoea
index (AHI) is the total number of apnoeas and
hypopnoeas during sleep divided by the total number of
sleep hours. SDB is mild if the AHI is 5-15, moderate if
15-30, and severe if >30. Most studies in CKD have used
an AHI cut-off of 10-15/h21-23 to diagnose SDB in their
patients, while others have used a higher AHI measure of
>30/h24. In addition to PSG (polysomnography)
performed for studies, epidemiologic reports have
demonstrated a higher risk of SDB in CKD using billing
codes for sleep apnoea and positive airway pressure
devices12. These inconsistent definitions and methods
have influenced the interpretation of study findings and
may lead to disparate conclusions on the prevalence
and predictors of SDB in CKD.
Clinical features, diagnosis and treatment of SDB
in CKD
SDB in CKD may not be recognized by clinicians
either due to the shared symptom complex between
MAVANUR et al: SLEEP DISORDERED BREATHING IN CHRONIC KIDNEY DISEASE
uraemia and SDB or the lack of association between
the normal risk factors for SDB in the setting of CKD.
The presentation of SDB in patients with CKD differs
in that bed-partners report apnoeas during sleep less
frequently, snoring is less intense and patients are often
not overweight25. Unlike the general population, obesity
and hypertension are not consistently associated with
SDB in dialysis patients7,26-28. This is probably related
to the unique role of uraemic toxins, volume overload,
and autonomic dysfunction in promoting SDB among
the advanced CKD patient population. The association
between SDB and daytime sleepiness is weaker in the
CKD population27.
While questionnaires and oximetry have been
used in the general population for screening, there
has not been strong evidence supporting their use
for clinical care in the CKD population. In order to
facilitate prioritization of patients for diagnostic
studies, investigators have attempted to identify the
clinical features that are most useful in estimating
the probability that a patient had SDB by comparing
scores on self-reported disease-specific questionnaires
with objective PSG data. The Berlin questionnaire,
for example, has been validated against PSG in the
general population. Scoring high risk patients using
the Berlin questionnaire had a sensitivity of 0.86 and
specificity of 0.7717. Flemons et al29 investigated the
likelihood ratios for a SDB clinical prediction rule.
Predictors of SDB included neck circumference,
hypertension, habitual snoring, and bed partner
reports of nocturnal gasping/choking respirations.
A SDB clinical score of less than 5 had a likelihood
ratio of 0.25 and a corresponding post-test probability
of 17 per cent, while a score of greater than 15 had a
likelihood ratio of 5.17 and post-test probability of 81
per cent. The use of pulse oximetry may provide the
opportunity to screen the high risk CKD population
with limited costs30,31. However, other studies have
challenged the use of overnight oximetry alone in
the diagnosis of SDB as it was found to be either a
sensitive or a specific test for SDB, but not both32,33.
In sum, there is currently no evidence-based strategy
for screening CKD patients for SDB.
The gold standard for the diagnosis of SDB is still
an overnight in-laboratory PSG including monitoring
of the electrooculogram, electroencephalogram (EEG),
submental electromyogram, oral airflow by thermistors
and nasal airflow by recording pressure fluctuations
at the nares, Chest wall (rib cage and abdominal)
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movement, usually by inductance plethysmography
to reflect ventilatory effort, oxygen saturation,
electrocardiogram (ECG), body position and video.
Disadvantages of PSG include the need for specialized
equipment and personnel which engenders high cost
and limited availability. Portable monitoring refers to
the diagnostic evaluation of SDB outside a conventional
sleep laboratory. It has evolved as an alternative to
PSG because it is convenient, relatively accurate, and
less costly. Fewer physiologic variables are measured
using portable monitors compared to PSG, but the use
of portable monitors can be performed in the patient’s
home or in a hospital room without a technician to attend
the study. The American Academy of Sleep Medicine
has recommended that portable monitors should only
be used for the diagnostic evaluation of suspected
SDB when patients have a high pre-test probability of
having moderate to severe SDB and have no co-morbid
medical or sleep disorders34. This recommendation
limits the use of portable monitors in dialysis patients,
for whom it is otherwise an attractive option given the
convenience of scheduling studies around their dialysis
treatments.
Many sleep specialists advocate initiation of
treatment for SDB when the AHI is greater than
15 events per hour, or the AHI is between 5 and 14
events per hour with associated clinical sequelae35-37.
Clinical sequelae may include excessive sleepiness,
impaired neurocognitive function, mood disorders,
insomnia, and/or cardiovascular disease (e.g.,
hypertension, ischaemic heart disease, and stroke).
Although lifestyle management such as weight loss,
cessation of smoking and avoiding caffeinated drinks
and alcohol is recommended, evidence of their
effectiveness is lacking in patients with CKD38. The
mainstay of medical treatment is continuous positive
airways pressure (CPAP) which introduces positive
pressure to the upper air passages via a nasal interface,
face mask or specialized oral appliance. About 20 to
40 per cent of patients will not use CPAP, and others
do not use it throughout the entire night39,40. In the
general population, treatment of SDB with CPAP
has been shown to improve vigilance, cognition,
sexual performance, quality of life and also to restore
nocturnal blood pressure dipping41. Pressman et al42
studied the effect of CPAP on eight ESRD patients with
SDB and demonstrated an improvement in nocturnal
oxygenation as well as daytime alertness. Larger
studies are required to evaluate the efficacy of CPAP
treatment for CKD population.
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Pathophysiology of SDB in the CKD patients
The aetiology of SDB among patients with the
advanced CKD patients is likely multifactorial and
may be due to ventilatory instability, volume overload,
upper airway narrowing, older age, and other comorbidities such as diabetes. Obstructive SDB is the
predominant type in the general population, as well as
in the CKD patients21,22,43,44. Earlier studies in the CKD
patients undergoing haemodialysis demonstrated a
distribution of both central and obstructive SDB. Here,
it is important to recognize the possible role of acetate,
once a commonly used buffer for haemodialysis. It
favours development of intradialytic hypoxaemia
through hypoventilation and ventilation-perfusion
changes. Jean et al28 assessed the influence of buffer,
acetate or bicarbonate, on sleep and ventilation.
Central apnoea occurred more frequently during
the night following acetate dialysis and obstructive
apnoeas were not different. The respiratory drive
operates mainly under chemoreflex control. Effective
ventilatory rhythmogenesis in the absence of stimuli
associated with wakefulness is critically dependent on
chemoreceptor stimulation secondary to PCO2 during
non rapid eye movement (NREM) sleep45. However,
increased chemoresponsiveness associated with ESRD
can increase loop-gain promoting destabilization of
central respiratory control and contributing to SDB46,47.
Patients with CKD may also develop SDB through
mechanisms that promote upper airway occlusion during
sleep. CKD patients are vulnerable to fluid overload which
could contribute to pharyngeal narrowing by causing
increased fluid volume in the neck and peripharyngeal
structures. In a study by Chiu et al48 a significant increase in
neck circumference and pharyngeal resistance was found
with only 0.5 l of fluid shift in healthy patients during
recumbency. Most of the CKD patients on conventional
haemodialysis require an average of 2 to 3 l of ultrafiltration
per thrice-weekly dialysis session. Beecroft et al49 showed
that the pharynx is narrower in patients with CKD on
haemodialysis when compared to those with normal
renal function, which may contribute to the upper airway
occlusion and thereby to SDB in dialysis patients. Another
potential cause of pharyngeal narrowing is upper airway
dilator muscle dysfunction secondary to neuropathy or
myopathy associated with either chronic uraemia50 or the
underlying cause of CKD, such as diabetes mellitus.
Clinical impact of SDB on CKD patients
Similar to findings in the general population,
SDB is associated with impaired quality of life in
CKD patients on dialysis6,7,51,52. SDB causes excessive
daytime sleepiness which has been linked to hazardous
driving and may contribute to poorer vocational and
rehabilitation potential in CKD patients. SDB has
been linked with markers of cardiovascular disease in
CKD16,53. SDB in those with CKD disrupts the normal
NREM sleep, attenuates the vagal modulation of heart
rate, with a predominance of the sympathetic nervous
system. Increased cardiac and peripheral adrenergic
drive may help explain why nocturnal hypoxaemia
has been associated with left ventricular hypertrophy,
hypertension and increased cardiovascular events
in the haemodialysis population4,5,54,55. Jung et al56
demonstrated both an association between the
severity of SDB and coronary calcification scores and
an association of nocturnal hypoxia with decreased
total antioxidant status in patients on haemodialysis.
A significant positive correlation between obstructive
AHI and coronary atherosclerotic plaque volume,
even in the absence of significant oxygen desaturation
was shown by Turmel et al57 in non- CKD patients
suggesting a role of sleep fragmentation itself in
atherosclerosis.
Impact of the mode of dialysis therapy on SDB in
CKD
While conventional forms of dialysis have not been
shown to reduce SDB, the conversion from daytime
to nocturnal dialysis has been associated with reduced
SDB among both haemodialysis and peritoneal dialysis
patients. Nocturnal haemodialysis patients undergo
overnight home dialysis (6-7 times per week) and it
has been associated with improvements in several
cardiovascular risk factors including hypertension,
left ventricular hypertrophy58, as well as impaired left
ventricular systolic function59. Chan et al60 showed that
higher heart rates and impaired vagal and augmented
sympathetic heart rate modulations during sleep in
ESRD patients are normalized by nocturnal haemo
dialysis (NHD). Hanly et al22 demonstrated that
conversion from CHD to NHD was associated with
reduction in AHI in patients with sleep apnoea (Fig. 1).
Of the 14 patients were studied, seven had AHI>15. In
these seven patients, the AHI significantly (P< 0.006)
decreased from 46 ± 19 to 9 ± 9 per hour.
Thus improvement in SDB from nocturnal
haemodialysis is likely related to both better toxin
clearance and ultrafiltration. Beecroft et al61 found that
the conversion from thrice-weekly haemodialysis to
NHD was associated with an increase in the pharyngeal
MAVANUR et al: SLEEP DISORDERED BREATHING IN CHRONIC KIDNEY DISEASE
281
Renal transplantation and sleep disordered breathing
Apnoea-hypopnoea index in seven patients with a base-line
apnoea-hypopnoea index higher than 15.
Fig. 1. Decreased severity of sleep apnoea associated with nocturnal
haemodialysis.
Source: Ref. 22 (Reproduced with permission)
cross-sectional area in all patients with sleep apnoea.
No significant relationship was found between change
in lung volumes or BMI and the pharyngeal size.
Previous work from the same group62 has shown that
chemoreflex responsiveness is decreased in patients
following conversion from thrice-weekly haemodialysis
to NHD. Increased chemoresponsiveness is associated
with propensity for increased loop-gain and ventilatory
instability; therefore, if NHD reduces chemosensitivity,
it should dampen loop-gain, improve ventilatory
stability and thereby NHD should contribute to
reducing SDB.
While nocturnal haemodialysis was associated
with improvement in SDB, nocturnal peritoneal
dialysis (NPD) was also associated with attenuation
in the severity of SDB. Tang et al23 compared the
effect of the timing and delivery of peritoneal dialysis
on SDB. They recruited 23 NPD (nocturnal cycler
assisted PD) and 23 CAPD patients. The prevalence
of SDB with AHI>15 was 52 per cent for NPD and
91 per cent for CAPD patients. They also studied 24
incident peritoneal dialysis patients who underwent
PSG study during mandatory NPD while awaiting their
turn for CAPD training. A second PSG was done after
they were established on CAPD. Prevalence of SDB
was significantly lower with NPD (4.2%) than CAPD
(33.3%). AHI markedly increased from 3.4 + 1.34
during NPD to 14.0 + 3.46 during CAPD (P<0.001).
One contributor to the improvement in SDB may be
that NPD reduced total body water based on their
bioelectrical impedance analysis.
Similar to nocturnal haemodialysis, improved
clearance of uraemic toxins after successful renal
transplant would be expected to alleviate SDB. However,
with the exception of two case reports describing
reversal of SDB after transplantation63,64, other studies
have failed to show significant benefit. Beecroft et al21
reported that kidney transplantation was associated
with a significant reduction in blood urea nitrogen
and serum creatinine without significant changes in
AHI. Only 3 of the 11 patients with SDB improved.
Whilst the authors found no significant correlation of
responders with BMI and co-morbid conditions, the
role of steroids/ immunosuppressive protocol was not
investigated. SDB may contribute to the high prevalence
of sleep-related complaints in this patient population65-67.
Since cardiovascular disease remains the leading cause
of mortality in renal transplant patients68 and sleep
complaints are prevalent in transplant patients, further
research is required to determine the extent to which
kidney transplantation may improve SDB.
Conclusion
SDB is highly prevalent in patients with CKD
where it may contribute to the cardiovascular disease,
adding a significant burden to the substantial morbidity
and mortality found in this population. As outlined
in Fig. 2, the optimal approach to managing SDB in
patients with CKD remains under study. The screening
for the disorder and appropriate referral for sleep
studies in high risk individuals is vital, but the best
approach remains to be demonstrated and depends on
Long-term implications
of SDB treatment in ESRD
Fig. 2. Implications of sleep-disordered breathing (SDB) treatment
in CKD. PSG, polysomnography; CPAP, continuous positive
airways pressure; LVH, left ventricular hypertrophy.
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INDIAN J MED RES, FEBRUARY 2010
local resources. A careful history and exam should be
performed and then the next diagnostic steps should
be considered. Oximetry alone is not an acceptable
screening tool and a negative portable monitor study
does not exclude the diagnosis of SDB. In addition to
the usual therapy of SDB such as CPAP in CKD patients
with dialysis-dependent kidney failure, clinicians may
consider both nocturnal forms of dialysis as well as
aggressive management of volume status. Larger
studies are needed to further elucidate the aetiology of
SDB in CKD and its impact on mortality and morbidity
in this patient population. It may be that patients with
CKD would benefit from disease-specific treatments of
SDB.
Conflict of interest: Mark Sanders is a scientific
consultant to Philips-Respironics which manufactures
devices used to monitor sleep, diagnose and treat
Sleep-Disordered Breathing and non-invasive
ventilation. Consistent with this, he is a co-inventor
of BiPAP®, manufactured by Philips-Respironics
and has a financial interest in this brand and related
technologies by Philips-Respironics. In the past, he
received research support from Respironics and was on
their Speakers Bureau. In the past he was on advisory
panels for Sanofi and Cephalon.
Mark Unruh has research support from Baxter
Healthcare, Dialysis Clinics Inc., and a Norman S.
Coplon Award from Satellite Healthcare.
Acknowledgment
This work was supported by Paul Teschan Research Grant,
NIH DK66006 and DK77785 (Unruh). References
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Reprint requests: Dr Mark Unruh, Assistant Professor of Medicine, Renal-Electrolyte Division, University of Pittsburgh School of Medicine
200 Lothrop Street, PUH C-1111, Pittsburgh, PA 15213, USA
e-mail: [email protected]