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      Correlation between obesity and chronic kidney disease: is obstructive sleep apnea an interfering factor?

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          Abstract

          Dear editor The increasing prevalence of obesity can be considered an alarming issue throughout the world.1 In only 4 years, for example, the People’s Republic of China has experienced an increase in the overweight population from 29.1% to 34.4%.2 Therefore, we would like to congratulate Xu et al3 for conducting an elegant study on a less explored topic: the accumulation of visceral fat in kidney disease. The rise in obesity may result, at least in part, from changes in lifestyle, currently characterized by sedentary, poor eating, and sleep habits. The reduction in sleep duration is known to predispose individuals to obesity by increasing the white adipose tissue deposits such as visceral fat.4,5 Of note, obesity and visceral fat accumulation are etiopathological factors for both chronic kidney disease (CKD) and sleep disorders.6,7 A sleep disorder that is closely related to obesity and CKD is obstructive sleep apnea (OSA).8,9 OSA is characterized by partial or complete obstruction of the pharyngeal airway during sleep, leading to repeated breathing pauses, oxygen desaturation, and arousals.10 It is known that 70% of patients with OSA are overweight and have higher intra-abdominal visceral fat accumulation11 and 40% of obese people have OSA.7 In CKD, the situation may be worse as OSA affects up to 94% of these patients.12 In obese people, the obstruction of pharyngeal airway becomes more frequent during sleep due to the local accumulation of fat in the neck region, which anatomically blocks the airways in the lying position.9 In CKD, this occurs also due to the accumulation of body liquids and its shift to the neck region, which compresses the pharynx, leading to apneas.13 It is important to consider that OSA and visceral fat accumulation represent risk factors for the development and progression of CKD.14 In this context, we believe that OSA screening in individuals with visceral fat accumulation can be very relevant to predict the decline in glomerular filtration rate. As indicated by the authors, visceral fat accumulation acts as a predictive factor for CKD; thus, evaluation of OSA may be relevant since it has been considered as a new risk factor for CKD. There are some questionnaires that evaluate sleep-disordered breathing risk subjectively, and, in addition, there is the polysomnography, the gold standard examination for diagnosis of OSA. In conclusion, we believe that implementing OSA screening in clinical practice when dealing with obesity and CKD is very important and may help future research in acquiring evidence for complementary therapeutic treatments based on sleep, since OSA can act as a possible aggravating factor in CKD.

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          Most cited references 12

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          Sleep apnea and daytime sleepiness and fatigue: relation to visceral obesity, insulin resistance, and hypercytokinemia.

          Sleep apnea and associated daytime sleepiness and fatigue are common manifestations of mainly obese middle-aged men. The onset of sleep apnea peaks in middle age, and its morbid and mortal sequelae include complications from accidents and cardiovascular events. The pathophysiology of sleep apnea remains obscure. The purpose of this study was to test three separate, albeit closely related, hypotheses. 1) Does sleep apnea contribute to the previously reported changes of plasma cytokine (tumor necrosis factor-alpha and interleukin-6) and leptin levels independently of obesity? 2) Among obese patients, is it generalized or visceral obesity that predisposes to sleep apnea? 3) Is apnea a factor independent from obesity in the development of insulin resistance? Obese middle-aged men with sleep apnea were first compared with nonapneic age- and body mass index (BMI)-matched obese and age-matched lean men. All subjects were monitored in the sleep laboratory for 4 consecutive nights. We obtained simultaneous indexes of sleep, sleep stages, and sleep apnea, including apnea/hypopnea index and percent minimum oxygen saturation. The sleep apneic men had higher plasma concentrations of the adipose tissue-derived hormone, leptin, and of the inflammatory, fatigue-causing, and insulin resistance-producing cytokines tumor necrosis factor-alpha and interleukin-6 than nonapneic obese men, who had intermediate values, or lean men, who had the lowest values. Because these findings suggested that sleep apneics might have a higher degree of insulin resistance than the BMI-matched controls, we studied groups of sleep-apneic obese and age- and BMI-matched nonapneic controls in whom we obtained computed tomographic scan measures of total, sc, and visceral abdominal fat, and additional biochemical indexes of insulin resistance, including fasting plasma glucose and insulin. The sleep apnea patients had a significantly greater amount of visceral fat compared to obese controls (<0.05) and indexes of sleep disordered breathing were positively correlated with visceral fat, but not with BMI or total or sc fat. Furthermore, the biochemical data confirmed a higher degree of insulin resistance in the group of apneics than in BMI-matched nonapneic controls. We conclude that there is a strong independent association among sleep apnea, visceral obesity, insulin resistance and hypercytokinemia, which may contribute to the pathological manifestations and somatic sequelae of this condition.
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            Obesity and obstructive sleep apnea: pathogenic mechanisms and therapeutic approaches.

            Obstructive sleep apnea is a common disorder whose prevalence is linked to an epidemic of obesity in Western society. Sleep apnea is due to recurrent episodes of upper airway obstruction during sleep that are caused by elevations in upper airway collapsibility during sleep. Collapsibility can be increased by underlying anatomic alterations and/or disturbances in upper airway neuromuscular control, both of which play key roles in the pathogenesis of obstructive sleep apnea. Obesity and particularly central adiposity are potent risk factors for sleep apnea. They can increase pharyngeal collapsibility through mechanical effects on pharyngeal soft tissues and lung volume, and through central nervous system-acting signaling proteins (adipokines) that may affect airway neuromuscular control. Specific molecular signaling pathways encode differences in the distribution and metabolic activity of adipose tissue. These differences can produce alterations in the mechanical and neural control of upper airway collapsibility, which determine sleep apnea susceptibility. Although weight loss reduces upper airway collapsibility during sleep, it is not known whether its effects are mediated primarily by improvement in upper airway mechanical properties or neuromuscular control. A variety of behavioral, pharmacologic, and surgical approaches to weight loss may be of benefit to patients with sleep apnea, through distinct effects on the mass and activity of regional adipose stores. Examining responses to specific weight loss strategies will provide critical insight into mechanisms linking obesity and sleep apnea, and will help to elucidate the humoral and molecular predictors of weight loss responses.
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              The dual roles of obesity in chronic kidney disease: a review of the current literature.

              Obesity is a major risk factor for the development of de novo chronic kidney disease (CKD). However, once kidney disease is acquired, obesity is paradoxically linked with greater survival, especially in those with advanced CKD. This review examines current evidence for obesity as a risk factor for incident CKD, studies of obesity and mortality across various CKD populations, and potential mechanisms underlying the 'obesity paradox' in kidney disease.
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                Author and article information

                Journal
                Ther Clin Risk Manag
                Ther Clin Risk Manag
                Therapeutics and Clinical Risk Management
                Therapeutics and Clinical Risk Management
                Dove Medical Press
                1176-6336
                1178-203X
                2016
                11 July 2016
                : 12
                : 1093-1094
                Affiliations
                Department of Psychobiology, Universidade Federal de São Paulo, São Paulo, Brazil
                Author notes
                Correspondence: Camila Hirotsu, Department of Psychobiology, Universidade Federal de São Paulo, Rua Napoleão de Barros, 925 Zipcode 04024-002 - 1st florr, São Paulo, Brazil, Tel +55 11 5908 7193, Fax +55 11 5572 5092, Email milahirotsu@ 123456gmail.com
                Article
                tcrm-12-1093
                10.2147/TCRM.S112442
                4946848
                27468237
                © 2016 Santos-Camilo et al. This work is published and licensed by Dove Medical Press Limited

                The full terms of this license are available at https://www.dovepress.com/terms.php and incorporate the Creative Commons Attribution – Non Commercial (unported, v3.0) License ( http://creativecommons.org/licenses/by-nc/3.0/). By accessing the work you hereby accept the Terms. Non-commercial uses of the work are permitted without any further permission from Dove Medical Press Limited, provided the work is properly attributed.

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                Letter

                Medicine

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