Nephrol Dial Transplant (2010) 25: 2011–2015doi: 10.1093/ndt/gfp752Advance Access publication 14 January 2010

Sleep-disordered breathing changes after kidney transplantation:a polysomnographic study

Cassio J. O. Rodrigues1, Odair Marson1, Sonia M. G. P. Togeiro2, Sergio Tufik2, Artur B. Ribeiro1

and Agostinho Tavares1

1Nephrology Division, Federal University of São Paulo, Brazil and 2Sleep Division, Federal University of São Paulo, Brazil

Correspondence and offprint requests to: C.J.O. Rodrigues; E-mail: cjorodrigues@uol.com.br

AbstractBackground: Sleep disorders are common in patients withend-stage renal disease (ESRD) and are not improved byeither conventional haemodialysis or peritoneal dialysis.Sleep-disordered breathing (SDB) is associated with car-diovascular disease and contributes to high mortality foundin patients with ESRD. Cure of SDB after transplantationhas been anecdotally reported.Methods: Thirty-four non-diabetic patients with ESRDwere studied, and clinical, laboratory test and polysomno-graphic features were determined and compared prior toand after transplantation and between groups with or with-out SDB, defined as having an apnoea–hypopnoea index(AHI) ≥5.Results: An AHI ≥5 was present in nine patients (26.5%)prior to and seven (21%) after transplantation, and nosignificant reduction of mean AHI was found betweenstudy phases (5.3 ± 7.3 vs 3.1 ± 4.5; P > 0.05). Trans-plantation was associated with a significant improvementin sleep architecture.Conclusions: Kidney transplantation is associated with animprovement in sleep architecture, but does not cure SDBin all patients.

Keywords: kidney transplantation; sleep-disordered breathing

Introduction

Cardiovascular disease is the leading cause of mortalityand morbidity, both in patients with end-stage renal disease(ESRD) and in those after kidney transplantation [1].

Poor sleep is common in dialysis patients and is associ-ated with lower quality of life [2], and this is an indepen-dent predictor of mortality [3]. Sleep-disordered breathing(SDB) is characterized by intermittent episodes of breath-ing cessation during sleep. The severity of SDB is mea-sured by the apnoea–hypopnoea index (AHI), obtainedby counting the total number of apnoeas and hypopnoeasduring sleep and dividing that by the hours of sleep. AnAHI >5 is considered pathological [4]. Although the prev-alence of SDB in the general population is 2% to 4% [5],

this percentage goes as high as 30% to 80% in patientswith ESRD [6]. SDB has been associated with left ventric-ular hypertrophy [7], hypertension [8] and increased car-diovascular events [9] in patients with ESRD. The highprevalence of coronary disease, stroke and congestiveheart failure in ESRD patients could be partially relatedto the high prevalence of SDB [10].

Although dialysis does not reduce the prevalence ofsleep disorders in ESRD patients [11], previous case re-ports have described instances of SDB reversal after kid-ney transplantation [12,13]. Two longitudinal case serieshave shown discrepant results [14,15], and a single studysuggested that the prevalence of SDB in transplant patientsdoes not differ from that in the general population [16].We conducted this study to further clarify the effects ofkidney transplantation on SDB by analysing physicaland biochemical parameters and objective measures ofsleep disorders.

Subjects and methods

Patients on chronic haemodialysis thrice a week for at least 6 months andawaiting kidney transplantation were enrolled in the study. They were in-cluded regardless of sleep complaints. In order to exclude sleep distur-bances not directly associated with renal dysfunction, patients withdiabetes, pulmonary disease, evidenced by clinical, radiological and func-tional alterations and symptomatic heart failure were excluded. The EthicsCommittee of the Federal University of São Paulo approved the protocol,and written informed consent was obtained from each participant. Thestudy was conducted in accordance with the Declaration of Helsinkiand with Brazilian National Ministry of Health Resolution CNS 196/96.

The patients underwent a polysomnographic evaluation at night after ahaemodialysis session. All of them had to have their dry weight assessedto be included in the protocol. Prior to polysomnography, clinical exam-ination was made, and weight, height and blood pressure (BP) were re-corded, according to recommendations of the VII Report of the JointNational Committee on Prevention, Detection, Evaluation and Treatmentof High Blood Pressure [17]. Body mass index (BMI = weight / square ofheight) was calculated according to World Health Organization classifica-tion [18]. Just after polysomnography, blood samples were taken for glu-cose, creatinine, urea, alkaline phosphatase, haematocrit, haemoglobin,intact parathormone (PTH), pH and bicarbonate. Kt/V index was calcu-lated by the formula -log (R − 0.03) + [(4 − 3.5 × R) × (UF:W)], whereUF is ultrafiltration volume (litre), W is weight (kilogram) after dialysisand R is the pre- and post-dialysis urea ratio. The glomerular filtrationrate (GFR) was estimated using the equations described in the Modifica-tion of Diet in Renal Disease study [19]. All patients underwent a living

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donor kidney transplantation. The same protocol was repeated in all pa-tients 3 to 6 months after transplantation.

The polysomnography recording started at the patient's usual bedtimeand was carried out using a Polysmith Neurotronics Inc. System, with 14channels distributed as follows: three for electroencephalography, two foroculogram, one for chin electromyography, one for tibial electromyogra-phy, one for electrocardiography, one for airflow, two for thoracic–abdom-inal movements, one for pulse oximetry, one for tracheal sound (snoring)and one for detection of body position. The system automatically analysessleep stages using Rechtschaffen and Kales criteria [20] and arousals ac-cording to American Sleep Disorders Association criteria [21].

A physician, blinded to the protocol and well trained in polysomnogra-phy, reanalysed the computer-generated staging according to these criteria.

The normal values used for analysis of sleep variables were those pro-posed by Carskadon and Dement [22]. The respiratory events (apnoeasand hypopnoeas) were classified according to the American Academyof Sleep Medicine Task Force criteria [23].

The variables analysed during polysomnography were: sleep efficiency(ratio of total sleep time to total time spent in bed), sleep stages: 1, 2, 3, 4,rapid eye movement (REM) sleep and slow-wave sleep (stages 3 and 4)(percentage of total sleep time), REM sleep + slow-wave sleep, number ofarousals per hour of sleep and apnoea/hypopnoea index (AHI).

We studied the prevalence of SDB (defined as AHI ≥5) and comparedclinical, laboratory test and polysomnographic features prior to and afterkidney transplantation. Differences in clinical and laboratory test featuresbetween groups with AHI ≥5 and AHI <5 were assessed in each studyphase. In a separate analysis, we examined the effect of kidney transplan-tation on AHI in patients with and without SDB prior to transplantation.

Statistical analysis was performed using SPSS 15.0. Comparisons ofgroups with and without SDB were made with Student's t-test. Paired t-tests were done to examine AHI changes in both groups with and with-out SDB prior to transplantation. Relationships between variables wereanalysed with Pearson's correlation when both variables were numericaland normal or Spearman's rank correlation when numerical variableswere not normally distributed. Significance was accepted as a P-value<0.05.

Results

Of the original sample of 46 patients, nine with diabetes,one with pulmonary disease and one with symptomaticheart failure were excluded. One patient refused to partic-ipate after kidney transplantation and was also excludedfrom the analysis. The remaining 34 patients (aged 35 ±10.4 years, 58% male) completed the study and are pre-

sented here. Chronic glomerulonephritis was the maincause of chronic renal failure (44%), and median time ondialysis was 16 months.

Prior to kidney transplantation, 85% had BP >140/90mmHg, although the great majority (71%) were takingantihypertensive medications. Similarly, anaemia was ausual finding; only 53% had a haematocrit >33%, as rec-ognized for ESRD patients [24]. Metabolic acidosis wasalso frequent (78% had pH <7.35), and mean Kt/V was1.32 ± 0.4.

Following kidney transplantation, all subjects were tak-ing corticosteroids and a combination of two other immuno-suppressive drugs and were free of acute rejection andinfectious or acute cardiovascular events. Three patients de-veloped diabetes, and seven were treated for episodes ofacute rejection. Four participants had BMI ≥30 kg/m2.The prevalence of hypertension remained high, and 56%were taking antihypertensive drugs. Metabolic acidosiswas observed in half of the population. Mean weight,BMI, haemoglobin, haematocrit and pH were significantlyincreased, and significant reductions in DBP, creatinine,urea and PTH were observed after transplantation. Clinicaland laboratory findings prior to and after transplantation areshown in Table 1.

Table 2 shows polysomnographic findings prior to andafter transplantation. The prevalence of SDB was 26.5%[95% confidence interval (12.9%; 44.4%)] prior to and21% [95% confidence interval (8.7%; 37.9%)] aftertransplantation. Mild cases predominated in both phasesof the study, where only three patients before and twoafter transplantation had an AHI ≥15. Kidney transplan-

Table 1. Clinical and laboratory test findings pre- and post-kidneytransplantation

Pre Post P-value

SBP (mmHg) 153.4 ± 20.8 144.9 ± 16.4 0.088DBP (mmHg) 100.8 ± 16.2 93.1 ± 11.2 0.030Weight (Kg) 61.2 ± 11.5 66.9 ± 12.0 <0.001BMI (Kg/m2) 22.3 ± 4.1 24.4 ± 4.2 <0.001Haemoglobin (g/dL) 10.7 ± 2.1 12.4 ± 2.1 0.002Haematocrit (%) 32.3 ± 6.0 37.1 ± 6.3 0.002Creatinine (mg/dL) 10.9 ± 2.6 1.7 ± 0.5 <0.001Ureaa (mg/dL) 153.6 ± 31.1 57.7 ± 20.6 <0.001PTHb (pg/mL) 298.0 ± 316.1 179.5 ± 134.6 0.016Alkaline phosphataseb (UI) 106.0 ± 95.8 92.1 ± 50.4 0.406pHb 7.29 ± 0.07 7.34 ± 0.05 0.002Bicarbonateb (mEq/L) 22.2 ± 4.7 23.5 ± 2.5 0.191

Data are shown as mean ± standard deviation; Student's t-test.aTwo patients without data.bSeven patients without data.SBP= systolic blood pressure; DBP= diastolic blood pressure; BMI = bodymass index; PTH = parathormone.

Table 2. Polysomnographic findings pre- and post-kidney transplantation(n = 34)

Pre Post P-value

AHI 5.3 ± 7.3 3.1 ± 4.5 0.132Central apnoea (%) 7.6 ± 13.5 4.9 ± 10.8 0.301Apnoeas in REM (%) 16.6 ± 21.3 24.8 ± 28.3 0.122Sleep efficiency (%) 80.2 ± 19.4 89.0 ± 22.5 0.072Wake stage (%) 19.3 ± 19.4 14.7 ± 12.9 0.205Stage 1 (%) 20.5 ± 21.2 9.0 ± 6.1 0.002Stage 2 (%) 41.0 ± 14.8 46.6 ± 13.8 0.067Stage 3 (%) 7.5 ± 4.7 10.5 ± 3.7 0.008Stage 4 (%) 12.0 ± 8.4 14.9 ± 8.4 0.109REM sleep (%) 18.8 ± 11.0 18.9 ± 8.3 0.952Slow-wave sleep (%) 20.9 ± 13.7 25.4 ± 8.5 0.082Slow-wave sleep + REM (%) 38.3 ± 14.9 44.0 ± 12.6 0.041O2 desaturation episodes per hour 2.5 ± 5.5 2.1 ± 6.9 0.751Arousals per hour 26.6 ± 19.5 19.3 ± 11.3 0.072

Data are shown as mean ± standard deviation; Student's t-test.AHI = apnoea–hypopnoea index; REM = rapid eye movement.

Table 3. AHI pre- and post-kidney transplantation (n = 34)

AHI Pre Post

<5 25 (73.5%) 27 (79.4%)≥5 9 (26.5%) 7 (20.6%)

AHI = apnoea–hypopnoea index; McNemar test: P = 0.754.

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tation was associated with significantly higher percen-tages of deep stages of sleep in contrast to a reductionin sleep stage 1. Sleep efficiency tended to increase,and a reduction in the number of arousals was also ob-served. Although a reduction in the number of patientswith SDB was demonstrated, there was no statistical sig-nificance in this improvement (Table 3). There was nocorrelation between AHI or variation in AHI with theclinical and laboratory variables. There were also no cor-relations between changes in AHI with modifications inthe sleep stages.

Figures 1 and 2 show the development of patients withAHI ≥5 in the two phases of the study. Of the nine indi-viduals with AHI ≥5 before kidney transplantation, eightdemonstrated some reduction in AHI, while one individualshowed a worse picture. On the other hand, of the sevenindividuals with AHI ≥5 after kidney transplantation, fiveshowed lower levels in the dialysis phase. In the group as awhole, 22 patients showed a reduction in AHI, and 12 hadan increase in AHI. When we analysed only the group withAHI ≥5 prior to transplantation, there was a significant re-duction in AHI (15.4 ± 7.8 vs 4.4 ± 4.4, pre- and post-transplantation, respectively; P = 0.008). Considering onlypatients with AHI <5 prior to transplantation, the differ-ence was not significant (1.6 ± 1.3 vs 2.7 ± 4.5, pre- andpost-transplantation, respectively; P = 0.21).

Discussion

Sleep disturbances show a high prevalence in dialysis pa-tients. Subjective sleep complaints are reported in up to80% of those surveyed. SDB, restless syndrome and period-ic limb movement disorder are much more prevalent than inthe general population [6]. Thirty-four ESRD patients onchronic haemodialysis who received a living donor kidneytransplant and underwent polysomnographic studies prior toand after that are described. They served as their own con-trols, prior to and after transplantation. We found a highprevalence of SDB in the population while undergoing dial-ysis (26.5% of the patients with AHI≥5), regardless of sleepcomplaints, confirming other studies [25–28].

Sleep deprivation has been implicated as a cause of im-paired immune function [29,30] and cardiovascular dis-ease [31]. Our findings about sleep quality are similar tothose of previous studies that have demonstrated a shortand fragmented sleep in patients on chronic dialysis[11,32–34], with increased amounts of stage 1 and de-creased sleep efficiency and slow-wave sleep. In our study,kidney transplantation was associated with an increase inslow-wave sleep and a decrease in stage 1 sleep, with atrend for higher sleep efficiency. Various factors havebeen proposed as being associated with the improvementof sleep architecture after transplantation, such as the re-duction in periodic limb movements during sleep (PLMS)and restless legs syndrome (RLS), correction of anaemiaand disturbances in calcium and phosphorus metabolism,and the recovery of renal function [35,36]. In our study,there were no correlations between improvement in sleeppattern and the modifications of clinical parameters orAHI, such that we could not determine which factors wereresponsible for the better quality of sleep after transplan-tation. The improvement in sleep architecture could pos-sibly explain part of the better quality of life after kidneytransplantation.

Previous case reports have demonstrated an improve-ment in SDB after kidney transplantation in three patients[12,13]. More recently, a study of 841 patients submittedto kidney transplantation demonstrated, through the use ofself-administered questionnaires, that such individualsshow a high risk for sleep apnoea syndrome [37]. How-ever, no polysomnographic examinations were performedthat could prove these alterations. Two longitudinal studieswere able to analyse the presence of sleep apnoea in renaltransplantation utilizing polysomnographic examinations,but with discrepant results. While one study demonstrateda reduction in AHI in eight of nine of the individuals stud-ied [14], another, evaluating 18 patients before and afterliving donor renal transplantation [15], yielded findingssimilar to ours, in that, transplantation does not lead tothe cure of alterations, since of the eleven patients withAHI >10 in the first phase of the study, only three showedimprovement after transplantation. In both studies, thegroups consisted of individuals with some type of clinicalsuspicion, which in a way tend to demonstrate an elevatedprevalence of alteration. The authors of the aforemen-tioned studies did not mention possible new cases of al-terations arising after transplantation. Later, a report of

Fig. 2. AHI in patients with AHI ≥5 post-transplantation.

Fig. 1. AHI in patients with AHI ≥5 pre-transplantation.

Sleep-disordered breathing changes after kidney transplantation: a polysomnographic study 2013

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47 patients also demonstrated a high prevalence of SDB ina transplantation group, but without demonstrating databefore transplantation [38].

In the general population, SDB is clearly associatedwith male gender [5], older age [39] and obesity [40]. Suchrelationships are less evident in ESRD-related SDB, andfindings from previous studies have been controversial[6,25,41]. In our study, the majority of patients wereyoung, which could have contributed to a lower prevalenceof changes in relation to similar studies. SDB is also asso-ciated with diabetes [42], cardiac disorders [43] and pul-monary diseases [44]. In our study, patients with thesediagnoses were excluded to avoid confounding factors thatcould be causes of sleep disturbances.

In our study, AHI declined in most subjects with pre-transplant SDB while it increased in some subjects withoutpre-transplant SDB. Of the nine individuals with SDB be-fore kidney transplantation, three persisted with alterationsafter transplantation, and four others showed SDB only inthe second phase of the study. The results of our study con-firm that the prevalence of SDB still persists at a high levelafter kidney transplantation. In fact, twelve patients hadeven higher indices than during chronic haemodialysis.The heterogeneous distribution of the changes reinforcesthe possibility of multifactorial mechanisms in which dif-ferent factors may be involved in each situation.

It is well known that conventional haemodialysis doesnot reduce the prevalence or severity of SDB in ESRD pa-tients, but previous studies have described improvementsin subjects undergoing nocturnal haemodialysis [45] andcycle-assisted peritoneal dialysis [46]. The authors of theaforementioned studies and a recent review of the associ-ation between SDB and peritoneal dialysis [47] did consid-er that such reduction of sleep disturbances could berelated to a better clearance of uraemic toxins, supportinga direct effect of uraemia on respiratory control, or to abetter fluid clearance. Recent studies have demonstrateda high prevalence of SDB in non-dialysed chronic renalfailure patients [48,49]. Other factors such as metabolic ac-idosis, uraemic myopathy or neuropathy, anaemia, hor-monal imbalance, fluid overload, inflammatory cytokinesand the dialytic process itself have been considered as pos-sibly associated with the high prevalence of SDB in ESRDpatients [6,10,12,50]. Several of these factors persist aftertransplantation and should be considered as possible con-tributors to the high frequency of SDB.

On the other hand, other factors typically associatedwith SDB appear with kidney transplant. SDB and dis-rupted sleep have been described as being related toCushing's disease and to corticosteroid effects [51], so acontribution of immunosuppressive drugs to the high fre-quency of SDB in our study cannot be excluded. A recentItalian study compared polysomnographic data of 163kidney transplant patients with two control groups [16].In the first case, the data utilized were from pulse oxime-try of individuals matched by weight, age and sex. Alsocompared were data from the Wisconsin study cohortwhich included 602 North Americans. In both cases, theauthors did not find any differences in prevalence of SDBin relation to the control groups. There are no data ofpolysomnographic studies before transplantation that al-

low the comparison of the development of changes. Theauthors concluded that the prevalence of SDB in trans-planted patients did not differ from that in the generalpopulation. The high prevalence of SDB in transplantedpatients could be associated to weight gain. In fact, inour study, there was substantial weight gain after kidneytransplantation. Although we did not find any associationbetween changes in BMI and in AHI, the possible contri-bution of weight gain after kidney transplantation cannotbe excluded and warrants better future investigations.

Considering the important association of SDB with car-diovascular events and high cardiovascular mortality inkidney transplant patients, new studies are needed to de-termine which factors are involved in the persistence ofSDB in this population.

Acknowledgements. This work was supported by the State of São PauloResearch Foundation/“FAPESP” (grant no. 99/04460-7) and the NationalCouncil for Scientific and Technological Development/“CNPQ”—Brazil.

Conflict of interest statement. None declared.

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Received for publication: 5.9.09; Accepted in revised form: 11.12.09

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