Abstract
Background: Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for cardiovascular morbidity and mortality, and it has a detrimental effect on renal function. Obesity is the major risk factor for OSAS, and represents a risk factor for chronic kidney disease. Continuous positive airway pressure (CPAP) is the suggested therapy for moderate-to-severe OSAS. We designed this study to evaluate the effect of CPAP on estimated glomerular filtration rate (e-GFR) in a cohort of obese patients with moderate-to-severe OSAS and normal renal function.Methods: We enrolled 198 obese subjects, divided into two groups (OSAS+ and OSAS–), on the basis of cardiorespiratory monitoring; mild OSAS patients (n = 33) were excluded from the study, thus the analyses were conducted on 165 patients. Comparisons between groups were made by Student t-test or χ2 test as appropriate. Linear regression analyses were used to assess the relationship between baseline e-GFR and different covariates and, in the OSAS+ group, between Δe-GFR and different covariates. A multivariate regression analysis was performed to determinate the independent predictor of the Δe-GFR.Results: OSAS+ subjects showed significantly increased values of systolic blood pressure, HOMA, pulse wave velocity, high-sensitivity C reactive protein and uric acid compared with OSAS– group. OSAS+ group showed significantly lower values of e-GFR and increased values of microalbuminuria. At linear regression analysis e-GFR resulted significantly and inversely related to AHI in the whole study population and in the two groups. After 6 months of CPAP therapy, OSAS+ subjects showed an improvement in respiratory parameters, as well as a significant increase in e-GFR values (104.2 + 19.0 vs. 84.0 + 13.1 ml/min/1.73 m2, P < 0.0001). At multiple regression analysis, Δ apnea/hypopnea index (AHIa) resulted the main independent predictor of Δe-GFR explaining 22% of its variation.Conclusions: Obese OSAS patients show significantly lower values of e-GFR, even if in the normal range, compared with obese non-OSAS subjects. After 6 months of CPAP, e-GFR significantly improved (+20 ml/min/1.73 m2) and ΔAHIa resulted the most important independent predictor of Δe-GFR.
Highlights
In the last years obstructive sleep apnea syndrome (OSAS) has been considered as an independent risk factor for cardiovascular (CV) morbidity and mortality, to other classical risk factors such as obesity, diabetes mellitus (DM), and hypertension [1]
It has been hypothesized that chronic kidney disease (CKD) shares common pathogenetic mechanisms with OSAS, such as increased oxidative stress, metabolic alterations and sympathetic activation, which could explain the link between OSAS and renal function decline [10]
The relationship between OSAS and renal function decline needs to be further elucidated; it is well-known that OSAS is highly prevalent among individuals with end-stage renal disease (ESRD) [13] and that patients with early stages of CKD show an increased risk of OSAS compared to subjects with normal renal function [14], but the cause-effect link between these conditions has not yet been clearly explained
Summary
In the last years obstructive sleep apnea syndrome (OSAS) has been considered as an independent risk factor for cardiovascular (CV) morbidity and mortality, to other classical risk factors such as obesity, diabetes mellitus (DM), and hypertension [1]. Renal function decline, evaluated by estimated glomerular filtration rate (e-GFR), is associated with increased CV morbidity and mortality in the general population as well as in various settings of patients [7,8,9], and mild-to-moderate renal insufficiency has emerged as a major public and clinical health problem. Obstructive sleep apnea syndrome (OSAS) is an independent risk factor for cardiovascular morbidity and mortality, and it has a detrimental effect on renal function. We designed this study to evaluate the effect of CPAP on estimated glomerular filtration rate (e-GFR) in a cohort of obese patients with moderate-to-severe OSAS and normal renal function
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