Longer time spent in bed attempting to sleep is associated with rapid renal function decline: the Dongfeng–Tongji cohort study

<p><b>Introduction:</b> Prospective evidence on the relation between time in bed and renal dysfunction remains limited. We aimed to investigate the association of time spent in bed attempting to sleep (TSBS) with renal function decline in a middle-aged and elderly Chinese population.</p> <p><b>Methods:</b> About 16,733 eligible participants with a mean age of 62.3 years at baseline were included. Rapid renal function decline was defined as (baseline eGFR − revisit eGFR)/years of follow-up ≥5 mL/min per 1.73 m²/year. A total of 1738 study participants experienced rapid renal function decline after a median 4.6-year follow-up. Logistic regression models were used for multivariate analyses.</p> <p><b>Results:</b> The adjusted odds ratio (OR) of rapid renal function decline was 1.18 (95% CI: 1.02, 1.37) for TSBS ≥9 h/night compared with TSBS 7 to <8 h/night. This association remained significant (OR = 1.19, 95% CI: 1.03, 1.38) after further adjustment for sleep quality, midday napping and usage of sleeping pills. Particularly, the association appeared to be prominent in individuals with diabetes.</p> <p><b>Conclusions:</b> Longer TSBS (≥9 h) was independently associated with an increased risk of rapid renal function decline. Our findings emphasized the importance to have optimal TSBS.Key messages</p><p>Our study firstly investigated the association between time spent in bed attempting to sleep (TSBS) and renal dysfunction in Chinese adults.</p><p>Compared with individuals TSBS 7 to <8 h, individuals with TSBS ≥9 h had 19% increased risk for rapid renal function decline after adjustment for multivariate confounders.</p><p>The association appeared to be prominent in individuals with diabetes.</p><p></p> <p>Our study firstly investigated the association between time spent in bed attempting to sleep (TSBS) and renal dysfunction in Chinese adults.</p> <p>Compared with individuals TSBS 7 to <8 h, individuals with TSBS ≥9 h had 19% increased risk for rapid renal function decline after adjustment for multivariate confounders.</p> <p>The association appeared to be prominent in individuals with diabetes.</p

Association of plasma IL-6 with HRV by urinary PAHs metabolites in coke oven workers^*.

<p>1-OHP, 1-hydroxypyrene; 2-OHPh, 2-hydroxyphenanthrene; ΣOH-PAHs, total concentration of all PAHs metabolites.</p><p>*HRV indices were natural log transformed and presented as multivariate adjusted means and SE.</p>a<p>IL-6 tertile were defined as less than or equal to 1.52 pg/ml, 1.52 to 2.95 pg/ml, and greater than 2.95 pg/ml, respectively. ^bMultivariate linear regression for the trend of HRV with IL-6 levels with adjustment for age, sex, length of work, smoking status, alcohol use, BMI, physical activity, working sites, workshift and weekday. ^cGeneral linear models for the interaction between IL-6 and PAHs metabolites on HRV. ^dΣOH-PAHs: Low≤8.84 μg/mmol creatinine, High>8.84 μg/mmol creatinine. ^e1-OHP: Low≤2.20 μg/mmol creatinine, High>2.20 μg/mmol creatinine. ^f2-OHPh: Low≤0.21 μg/mmol creatinine, High>0.21 μg/mmol creatinine.</p

Association of urinary PAHs metabolites quartiles and ln-transformed IL-6.

<p><i>P</i>_trend was calculated from the regression models, adjusting for age, sex, length of work, smoking status, alcohol use, BMI, physical activity, working sites, workshift and weekday. 1-OHNa: Q1 (≤0.92 μg/mmol creatinine), Q2 (0.92–1.57 μg/mmol creatinine), Q3 (1.57–2.80 μg/mmol creatinine), Q4 (>2.80 μg/mmol creatinine); 1-OHPh: Q1 (≤0.40 μg/mmol creatinine), Q2 (0.40–0.84 μg/mmol creatinine), Q3 (0.84–1.55 μg/mmol creatinine), Q4 (>1.55 μg/mmol creatinine); 9-OHPh: Q1 (≤0.39 μg/mmol creatinine), Q2 (0.39–0.70 μg/mmol creatinine), Q3 (0.70–1.35 μg/mmol creatinine), Q4 (>1.35 μg/mmol creatinine); 1-OHP: Q1 (≤1.86 μg/mmol creatinine), Q2 (1.86–3.29 μg/mmol creatinine), Q3 (3.29–6.11 μg/mmol creatinine), Q4 (>6.11 μg/mmol creatinine).</p

Values for natural log transformed TP (A) and LF (B) by quartiles of IL-6.

<p><i>P</i>_trend was calculated from the regression models, adjusting for age, sex, length of work, smoking status, alcohol use, BMI, physical activity, working sites, workshift and weekday. Box plots indicate the 10th quartile, 25th quartile, median, 75th quartile, and 90th quartile for each group. IL-6: Q1 (≤1.25 pg/ml), Q2 (1.25–2.13 pg/ml), Q3 (2.13–3.71 pg/ml), Q4 (>3.71 pg/ml).</p

General characteristics of the workers by urinary total OH-PAHs levels^*.

<p>BMI, body mass index; HF, high frequency; HRV, heart rate variability; Hsp70, heat shock protein 70; IL-6, interleukin-6; LF, low frequency; RMSSD, root mean square of successive differences in adjacent NN intervals; SDNN, standard deviation of NN intervals; TP, total power.</p><p>*Values are presented as mean ± SD, n (%), or median (25th, 75th quartile) unless otherwise indicated.</p>a<p>ΣOH-PAHs was dichotomized at the 33th percentile as either low (≤8.84 μg/mmol creatinine) or high (>8.84 μg/mmol creatinine). ^b<i>P-</i>values were calculated by χ² test for categorical variables, and t-test for continuous variables. ^c HRV indices were natural log transformed.</p

Direct, indirect and total bilirubin and risk of incident coronary heart disease in the Dongfeng-Tongji cohort

<p><b>Background:</b> Total bilirubin (TBIL) is known to be inversely associated with coronary heart disease (CHD) risk, however, whether this association is dose-response remains inconsistent and it is unclear which subtype of bilirubin is responsible for the potential protective effect.</p> <p><b>Methods:</b> We included 12,097 participants who were free of CHD, stroke, cancer and potential liver, biliary and renal diseases at baseline from September 2008 to June 2010 and were followed-up until October 2013. Cox proportional hazards models were used to assess the hazard ratios (HR) and 95% confidence interval (95% CI) of bilirubin with incident CHD risk.</p> <p><b>Results:</b> The adjusted HRs for incident CHD increased with increasing direct bilirubin (DBIL) (<i>p</i> for trend = .013). Participants within the highest quintile of DBIL had 30% higher risk of incident CHD compared to those in the lowest quintile (95% CI: 1.07, 1.58). In contrast, compared with subjects in the lowest quintile of TBIL, those in the third quintile had the lowest of 24% risk for CHD incidence (95% CI: 0.63, 0.92), which showed a U-shaped association (<i>p</i> for quadratic trend = .040).</p> <p><b>Conclusions:</b> DBIL was associated with a dose-response increased risk for CHD incidence. However, a U-shaped association existed between TBIL, indirect bilirubin and incident CHD risk.Key messages</p><p>Direct bilirubin is independently associated with incident coronary heart disease (CHD) in a dose-response manner.</p><p>A similarly consistent U-shaped association was found between total bilirubin, indirect bilirubin and incident CHD.</p><p>The potential protective effect of total bilirubin within the normal range on incident CHD should be mainly attributed to mild-to moderate elevated levels of indirect bilirubin.</p><p></p> <p>Direct bilirubin is independently associated with incident coronary heart disease (CHD) in a dose-response manner.</p> <p>A similarly consistent U-shaped association was found between total bilirubin, indirect bilirubin and incident CHD.</p> <p>The potential protective effect of total bilirubin within the normal range on incident CHD should be mainly attributed to mild-to moderate elevated levels of indirect bilirubin.</p