INTRODUCTION AND AIMS: Autosomal dominant polycystic kidney disease (ADPKD), the most common inherited renal cystic disease, is characterized by progressive cyst growth in the kidney and other organs and hypertension. Cyst expansion leads to focal areas of renal ischemia Increased activity of the renin-angiotensin system (RAS) secondary to ischemia seem to play an important role in the rise in blood pressure. Hypoxia stimulates RAS activation. This activation leads to local inflammation in the carotid body which plays a pathogenic role in sleep apnea. In this study, we investigated the frequency of obstructive sleep apnea syndrome ( OSAS) in ADPKD patients either with chronic kidney disease (CKD) or not. We also compared frequency of OSAS between ADPKD patients and a control group with normal kidney function and normal blood pressure. We also aimed to see effect of RAS blockage on obstructive sleep apnea.

METHODS: We recruited 36 ADPKD patients for the study. Presence of normal ear, nose and throat examination was a criteria for patient selection. Moreover, none of these patients had neither hypothyroidism or acromegaly. Pulmonary function tests were performed to all patients. Additionally, presence of sleep apnea syndrome symptoms were asked to all participants. Finally, 28 patients agreed to participate polysomnography study. Patients with apnea hypopnea index(AHI) score higher than 5 were accepted as having OSAS. Patients with eGFR values below 60 ml/min were accepted as CKD patients. We matched the patients and controls. Data of groups were compared using independent sample t test and chi-square test. P values of <0.05 were considered significant.

RESULTS: All participants were evaluated with clinical and biochemical examinations (Table 1). Mean FEV1%, FVC% and FEV1/FVC% were 101,8 ± 13,8; 106 ± 12,5; 80,9 ± 7,1, respectively. Most seen OSAS symptom was snoring (23/36;63,8%). Frequency of OSAS in patients with eGFR levels below 60 ml/min were significantly higher than individuals with eGFR levels above 60 ml/min( 10/10(100%); 9/18(50%), respectively, p:0,000). Comparison of ADPKD patients and control group was shown in Table 2. Regarding effect of RAS blockage on frequency of OSAS in all patients, individuals using ACE-I/ARB had significantly lower rate of OSAS compare to patients not using RAS blockers ( 14/21(66,6%) ,5/7(71,4%), respectively; p:0,000).

CONCLUSIONS: It is well known that CKD is associated with sleep disorders. Therefore, patients with CKD had higher rate of OSAS compare to non-CKD patients. On the other hand, use of RAS blockers may seem to decline frequency of OSAS in patients with ADPKD. In terms of limitation of this study, this is an ongoing study and these are preliminary results with limited number of patients.

Table 1: Clinical and laboratory findings of patients

Findingsn(%)
Age(year)50,7± 13,9
Gender(M/F)17/19
BMI29±3,5
Creatinine(mg/dl)1,51±0,96
e-GFR(ml/min)64,2±33,2
GFR>60 ml/min21/36(58,3%)
Presence of Hypertension30/36(83,3%)
Use of ACE-I/ARB25/30(83,3%)
Presence of OSAS19/28(67,8%)
Findingsn(%)
Age(year)50,7± 13,9
Gender(M/F)17/19
BMI29±3,5
Creatinine(mg/dl)1,51±0,96
e-GFR(ml/min)64,2±33,2
GFR>60 ml/min21/36(58,3%)
Presence of Hypertension30/36(83,3%)
Use of ACE-I/ARB25/30(83,3%)
Presence of OSAS19/28(67,8%)

Table 1: Clinical and laboratory findings of patients

Findingsn(%)
Age(year)50,7± 13,9
Gender(M/F)17/19
BMI29±3,5
Creatinine(mg/dl)1,51±0,96
e-GFR(ml/min)64,2±33,2
GFR>60 ml/min21/36(58,3%)
Presence of Hypertension30/36(83,3%)
Use of ACE-I/ARB25/30(83,3%)
Presence of OSAS19/28(67,8%)
Findingsn(%)
Age(year)50,7± 13,9
Gender(M/F)17/19
BMI29±3,5
Creatinine(mg/dl)1,51±0,96
e-GFR(ml/min)64,2±33,2
GFR>60 ml/min21/36(58,3%)
Presence of Hypertension30/36(83,3%)
Use of ACE-I/ARB25/30(83,3%)
Presence of OSAS19/28(67,8%)

Table 2: Comparison of two groups

Patients(n:36)Controls(n:37)P
Age50,9±13,846±70,065
Gender(M/F)17/19(47,2%)19/18(51,3%)0,23
BMI29± 3,528,5±4,60,612
Presence of OSAS19/28(67,8%)18/37(48,6%)0,000
Patients(n:36)Controls(n:37)P
Age50,9±13,846±70,065
Gender(M/F)17/19(47,2%)19/18(51,3%)0,23
BMI29± 3,528,5±4,60,612
Presence of OSAS19/28(67,8%)18/37(48,6%)0,000

Table 2: Comparison of two groups

Patients(n:36)Controls(n:37)P
Age50,9±13,846±70,065
Gender(M/F)17/19(47,2%)19/18(51,3%)0,23
BMI29± 3,528,5±4,60,612
Presence of OSAS19/28(67,8%)18/37(48,6%)0,000
Patients(n:36)Controls(n:37)P
Age50,9±13,846±70,065
Gender(M/F)17/19(47,2%)19/18(51,3%)0,23
BMI29± 3,528,5±4,60,612
Presence of OSAS19/28(67,8%)18/37(48,6%)0,000

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