Background. Previous studies have found an association between obstructive sleep apnea (OSA) and chronic kidney disease (CKD). However, subjects with confounding factors such as diabetes and hypertension were not excluded. The purpose of the present study was to determine whether patients with OSA without meeting criteria for diabetes or hypertension would also show increased likelihood of CKD. Methods. We prospectively enrolled adult patients with a chief complaint of habitual snoring. Overnight polysomnography, fasting blood triglyceride, cholesterol, glucose, insulin, creatinine, albumin and hemoglobin A1c, and first voiding urine albumin and creatinine were examined. Estimated glomerular filtration rate (eGFR), urine albumin-to-creatinine ratio (UACR), homeostatic model assessment–insulin resistance and percentage of CKD were calculated. Results. The final analyses involved 40 patients who were middle-aged [44.8 (8.6) years] predominantly male (83%), obese [body mass index, 28.2 (5.1) kg/m²] and more severe OSA, with an apnea–hypopnea index (AHI) of 51.6 (39.2)/h. The mean eGFR and UACR were 85.4 (18.3) mL/min/1.73m² and 13.4 (23.4) mg/g, respectively. The prevalence of CKD in severe OSA subjects is 18%. With stepwise multivariate linear regression analysis, AHI and desaturation index were the only independent predictor of UACR (β = 0.26, P = 0.01, R² = 0.17) and eGFR (β = 0.32, P < 0.01, R² = 0.32), respectively. Conclusions. High prevalence of CKD is present in severe OSA patients without hypertension or diabetes. Significantly positive correlations were found between severity of OSA and renal function impairment.

Backgrounds Obstructive sleep apnea (OSA) is common in patients on hemodialysis, but its correlation with chronic kidney disease (CKD) is not clear. We aimed to clarify the relationship between OSA without hypertension or diabetes and incidence of CKD in Taiwan. Methods This population-based cohort study consisted of patients with newly diagnosed OSA between 2000 and 2009. The comparison cohort was matched for age, sex, diabetes mellitus, and hypertension. All subjects previously diagnosed with acute or chronic kidney disease were excluded. The primary end point was newly diagnosed CKD. Results We identified 6866 subjects with OSA during the 10-year study period. The median duration until development of CKD in the OSA cohort was 3.2 years, 2.5 months earlier than that in the non-OSA cohort. After exclusion of hypertension and diabetes, 4319 OSA patients was identified and the hazard ratio (HR) of CKD with OSA was 1.37 (95 % confidence interval [CI], 1.05–1.77; p = 0.019). In the subgroup analysis, an increased incidence of CKD in OSA was observed in women (HR, 1.41; 95 % CI, 1.12–1.78; p = 0.0036). Conclusions This longitudinal population-based cohort study provides evidence that patients with OSA even without diabetes or hypertension are at higher risk of developing CKD over the next 3 years and nearly 2.5 months earlier than the non-OSA cohort, particularly women.

The impact of the outbreak of severe acute respiratory syndrome (SARS) was enormous, but few studies have focused on the infectious and general health status of healthcare workers (HCWs) who treated patients with SARS. We prospectively evaluated the general health status of HCWs during the SARS epidemic.The Medical Outcome Study Short-Form 36 Survey was given to all HCWs immediately after caring for patients with SARS and 4 weeks after self-quarantine and off-duty shifts. Tests for detection of SARS Coronavirus antibody were performed for HCWs at these 2 time points and for control subjects during the SARS epidemic. Tertiary care referral center in Taipei, Taiwan. Ninety SARS-care task force members (SARS HCWs) and 82 control subjects. All serum specimens tested negative for SARS antibody. Survey scores for SARS HCWs immediately after care were significantly lower than those for the control group (P < .05 by the t test) in 6 categories. Vitality, social functioning, and mental health immediately after care and vitality and mental health after self-quarantine and off-duty shifts were among the worst subscales. The social functioning, role emotional, and role physical subscales significantly improved after self-quarantine and off-duty shifts (P < .05, by paired t test). The length of contact time (mean number of contact-hours per day) with patients with SARS was associated with some subscales (role emotional, role physical, and mental health) to a mild extent. The total number of contact-hours with symptomatic patients with SARS was a borderline predictor (adjusted R² = 0.069; P = .038) of mental health score. The impact of the SARS outbreak on SARS HCWs was significant in many dimensions of general health. The vitality and mental health status of SARS HCWs 1 month after self-quarantine and off-duty shifts remained inferior to those of the control group.

The relationship between inflammatory bowel disease and sleep disturbances is complicated and of increasing interest. We investigated the inflammatory and immunological consequences of EA in sleep-deprived colitis and found that dextran sulfate sodium (DSS)-induced colitis in sleep-fragmented (SF) mice was more severe than that in mice with normal sleep. This increase in the severity of colitis was accompanied by reduced body weight, shortened colon length, and deteriorated disease activity index. DSS with SF mice presented obvious diminished intestinal tight junction proteins (claudin-1 and occludin), elevated proinflammatory cytokines (CRP, IFN-γ, IL-6), lowered melatonin and adiponectin levels, downregulated vasoactive intestinal peptide (VIP) type 1 and 2 receptor (VPAC1, VPAC2) expression, and decreased diversity of gut bacteria. EA ameliorated colitis severity and preserved the performance of the epithelial tight junction proteins and VIP receptors, especially VPAC2. Meanwhile, the innate lymphoid cells-derived cytokines in both group 2 (IL-4, IL5, IL-9, IL-13) and group 3 (IL-22, GM-CSF) were elevated in mice colon tissue. Furthermore, dysbiosis was confirmed in the DSS group with and without SF, and EA could maintain the species diversity. Firmicutes could be restored, such as Lachnospiraceae, and Proteobacteria become rebalanced, mainly Enterobacteriaceae, after EA intervention. On the other hand, SF plays different roles in physiological and pathological conditions. In normal mice, interrupted sleep did not affect the expression of claudin-1 and occludin. But VPAC1, VPAC2, and gut microbiota diversity, including Burkholderiaceae and Rhodococcus, were opposite to mice in an inflamed state.

Older age, obesity, and obstructive sleep apnea syndrome (OSAS) are known to increase the risk of hypertension in adults. However, data for children are scarce. This study aimed to investigate the relationships between hypertension, age, weight status, and disease severity in 396 children with OSAS. The prevalence rates of hypertension, obesity, and severe OSAS (apnea-hypopnea index ≥10) were 27.0%, 28.0%, and 42.9%, respectively. Weight z-score and apnea-hypopnea index were independently correlated with systolic blood pressure z-score, and minimal blood oxygen saturation (SpO₂) was independently associated with diastolic blood pressure z-score. Overall, late childhood/adolescence (odds ratio (OR) = 1.72, 95% CI = 1.05–2.81), obesity (OR, 2.58, 95% CI = 1.58–4.22), and severe OSAS (OR = 2.38, 95% CI = 1.48–3.81) were independent predictors of pediatric hypertension. Furthermore, late childhood/adolescence (OR = 2.50, 95% CI = 1.10–5.71) and abnormal SpO₂ (mean SpO₂ < 95%; OR = 4.91, 95% CI = 1.81–13.27) independently predicted hypertension in obese children, and severe OSAS (OR = 2.28, 95% CI = 1.27–4.10) independently predicted hypertension in non-obese children. In conclusion, obesity, OSAS severity, and abnormal SpO₂ are potentially modifiable targets to improve hypertension while treating children with OSAS.