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Nephrol Dial Transplant (2010) 25: 181–186 doi: 10.1093/ndt/gfp403 Advance Access publication 12 August 2009
Prevalence of chronic kidney disease in patients with suspected sleep apnoea Georg Fleischmann1 , Gundula Fillafer1 , Heike Matterer1 , Falko Skrabal1 and Peter Kotanko1,2 1
Department of Internal Medicine, Krankenhaus der Barmherzigen Br¨uder, Graz, Austria and 2 Renal Research Institute, New York, NY, USA Correspondence and offprint requests to: Peter Kotanko; E-mail:
[email protected]
Abstract Background. Little is known about the epidemiology of chronic kidney disease (CKD) in patients with suspected sleep apnoea (SA). Methods. Glomerular filtration rate (eGFR) was calculated in consecutive patients referred for full-night observed inhospital polysomnography. SA was defined as the respiratory disturbance index (RDI) > 5. Results. One hundred and fifty-eight patients were studied. The age (mean ± SD) was 61.2 ± 12.7 years, body mass index 29.5 ± 5.9 kg/m2 and eGFR 86.1 ± 21.7 mL/min/1.73 m2 . SA was present in 133 patients (85%). The eGFR was 94.6 7 mL/min/1.73 m2 in patients without SA and 84.5 7 mL/min/1.73 m2 in patients with SA [mean difference (95% confidence interval) 10.0 (0.6– 19.4) mL/min/1.73 m2 ; P = 0.037]. Seventy patients had eGFR ≥ 90 mL/min/1.73 m2 (group 1), and 70 patients had between 60 and 89 mL/min/1.73 m2 (group 2), and 18 patients had 30–59 mL/min/1.73 m2 (CKD 3). Although the prevalence of SA did not differ among the groups (group 1: 80%; group 2: 86%; CKD 3: 94%), the number of central sleep apnoeas (CSA) per hour was 5.9 ± 12.2 in CKD 3, six times greater compared to patients with eGFR ≥ 60 mL/min/1.73 m2 (1.0 ± 2.1; P = 0.01). The prevalence of obstructive SA did not differ between the groups. After adjustment for age, gender, BMI, hypertension, diabetes mellitus and smoking status, CKD 3 (P = 0.0004) and New York Heart Association class ≥3 (P = 0.0001) remained predictive of CSA events per hour. Conclusions. eGFR is reduced in patients with SA, particularly in those with episodes of CSA.
Keywords: cardiac insufficiency; central sleep apnoea; chronic kidney disease; CKD 3; sleep apnoea
Introduction Sleep apnoea (SA) occurs in 2–4% of the general population [1]. Obesity, male gender, congestive heart failure (CHF), cerebrovascular disease and neurodegenerative disorders are major risk factors for SA. SA syndrome is prominent among the many sequelae affecting chronic dialysis patients, and it is a recognized cause of cardiovascular disease. During episodes of SA, hypoxia triggers brisk sympathetic activation that may result in sympathetic overactivity and hypertension [2]. In chronic dialysis patients, SA frequency has been reported as high as 50% [3]. The reasons for this 10- to 20-fold higher SA prevalence in dialysis patients compared to the general population are not entirely clear. It has been speculated that uraemic toxins, overhydration and comorbidities such as hypertension and CHF may play essential roles [4]. This notion is supported by results from a recent study showing that SA is reversed in renal transplant recipients [5]. In this cross-sectional study, we aimed to test the hypothesis that CKD is more prevalent in patients with SA. Methods Study population In this cross-sectional study, we investigated the prevalence of CKD in consecutive patients referred to standardized full night observed inhospital polysomnography for suspected SA. All patients referred between January 2004 and April 2007 in whom serum creatinine determinations
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182 were available within 4 weeks of polysomnography were enrolled in this study. Prior to polysomnography, the patients answered standardized questionnaires, with the assistance of a physician, regarding their medication use (number and class of antihypertensive drugs; use of benzodiazepines; drugs for pharmacologic treatment of Parkinson’s disease), sleep disturbances, snoring, subjective sleep quality, daytime fatigue, pre-existing illnesses and surgery. Serum creatinine was determined with a standardized serum creatinine assay. Glomerular filtration rate (eGFR; expressed in mL/min/1.73 m2 ) was calculated with the abbreviated MDRD equation [6]. The patients were stratified by eGFR into three groups: group 1 (eGFR ≥90); group 2 (eGFR 60–89) and group 3 with CKD stage 3 as defined by an eGFR between 30 and 59 mL/min/1.73 m2 [7]. Since urinalysis was available only in a minority of patients, the presence or absence of CKD in patients in groups 1 and 2 was undetermined. Body mass index (BMI) was calculated as weight (kg) divided by height (m) squared.
Polysomnography Polysomnography employed the Alice 4 system (Respironics Inc., Switzerland). Recordings included electroencephalogram, electro-oculogram, submental electromyogram, bilateral anterior tibial electromyogram, electrocardiogram, chest and abdominal wall movement by inductance plethysmography. Airflow was measured with nasal and oral pressure transducer and capillary oxygen was measured by finger pulse oximetry. Sleep stages were scored from 1 to 4 using the Rechtshaffen and Kales criteria [8] with arousals scored using the American Sleep Disorders Association (ASDA) criteria [9]. Hypopnoea was defined as a reduction of nasal pressure airflow of at least 10 s associated with a drop in oxygen saturation of ≥4% and/or arousal from sleep. Obstructive SA (OSA) was defined by the absence of nasal and oral airflow ≥10 s in the presence of thoracic and/or abdominal breathing efforts. Central SA (CSA) was defined as the absence of nasal and oral airflow in combination with no evidence of both abdominal and thoracic breathing effort. Cheyne–Stokes breathing (CSB) with CSA was defined as a form of periodic breathing in which apnoeas and hypopnoeas alternate with prolonged ventilatory periods characterized by a cyclic crescendo– decrescendo respiratory effort and airflow during wakefulness or sleep, without upper airway obstruction. The frequency of respiratory events was expressed as the number of events per hour. The respiratory disturbance index (RDI) was defined by dividing the sum of central, obstructive and mixed apnoeas and hypopnoeas by the number of hours of sleep. The arousal index was defined as the number of abrupt changes from sleep to wakefulness per hour. The desaturation index was defined as the occurrences of oxygen desaturation
