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Objective: To investigate the relationship between endogenous estrogen exposure and renal function, the association of female reproductive life span duration (RLD) and chronic kidney disease (CKD) was analyzed in postmenopausal women. Patients and Methods: Data were retrieved from the Korean Genome and Epidemiology Study, which was constructed from May 1, 2001, through December 25, 2017. A total of 50,338 and 3155 postmenopausal women were each included in the cross-sectional and longitudinal analyses. The RLD was determined by subtracting the age at menarche from the age at menopause. Participants were grouped into RLD quartiles. Participants with estimated glomerular filtration rates less than 60 mL/min/1.73 m 2 were regarded to have CKD. Results: In the cross-sectional analysis, mean AE SD age and estimated glomerular filtration rate were 56.3AE4.9 years and 93.1AE13.6 mL/min/1.73 m 2 , respectively. Mean AE SD RLD was 34.2AE4.0 years. A total of 765 of 50,338 (1.52%) women were found to have CKD. Logistic regression analysis revealed that the odds ratio for CKD was lower in groups with longer RLDs as compared with the shortest RLD group. In longitudinal analysis, postmenopausal women with normal kidney function were followed up for 9.7 years and incident CKD occurred in 221 of 3155 (7.00%) participants. Cox analysis revealed that the risk for CKD development was significantly lower in longer RLD groups. This finding was significant even after adjustments for confounding factors. Conclusion: The risk for CKD was lower in women with longer RLDs. The amount of endogenous estrogen exposure could be a determining factor for renal function in postmenopausal women.

Statin use in end-stage kidney disease (ESKD) patients are not encouraged due to low cardioprotective effects. Although the risk of hepatocellular carcinoma (HCC), a frequently occurring cancer in East Asia, is elevated in ESKD patients, the relationship between statins and HCC is not known despite its possible chemopreventive effect. The relationship between statin use and HCC development in ESKD patients with chronic hepatitis was evaluated. In total, 6165 dialysis patients with chronic hepatitis B or C were selected from a national health insurance database. Patients prescribed with ≥ 28 cumulative defined daily doses of statins during the first 3 months after dialysis commencement were defined as statin users, while those not prescribed with statins were considered as non-users. Primary outcome was the first diagnosis of HCC. Sub-distribution hazard model with inverse probability of treatment weighting was used to estimate HCC risk considering death as competing risk. During a median follow-up of 2.8 years, HCC occurred in 114 (3.2%) statin non-users and 33 (1.2%) statin users. The HCC risk was 41% lower in statin users than in non-users (sub-distribution hazard ratio, 0.59; 95% confidence interval [CI], 0.42–0.81). The weighted incidence rate of HCC was lower in statin users than in statin non-users (incidence rate difference, − 3.7; 95% CI − 5.7 to − 1.7; P < 0.001). Incidence rate ratio (IRR) was also consistent with other analyses (IRR, 0.56; 95% CI, 0.41 to 0.78; P < 0.001). Statin use was associated with a lower risk of incident HCC in dialysis patients with chronic hepatitis B or C infection.

Background: Alzheimer disease (AD) and depressive disorder (DD) are prevalent among elderly end-stage kidney disease (ESKD) patients. However, whether preexisting mental health disorders increase the risk of ESKD is not well understood. The risk of incident ESKD in patients with or without underlying AD or DD was evaluated in a nationwide cohort of elderly people in Republic of Korea. Methods: This study used data from the National Health Insurance Service-Senior cohort in Republic of Korea. Among the 558,147 total subjects, 49,634 and 54,231 were diagnosed with AD (AD group) or DD (DD group), respectively, during the follow-up period. Propensity score matching was conducted to create non-AD and non-DD groups of subjects. AD and DD diagnoses were analyzed as time-varying exposures, and the study outcome was development of ESKD. Results: The incidence rates of ESKD were 0.36 and 1.17 per 1,000 person-years in the non-AD and AD groups, respectively. After adjustment for clinical variables and competing risks of death, the risk of incident ESKD was higher in the AD group than in the non-AD group (hazard ratio [HR], 1.67; 95% confidence interval [CI], 1.34-2.08). The incidence rates of ESKD in the non-DD and DD groups were 0.36 and 0.91 per 1,000 person-years, respectively. The risk of ESKD development was also higher in the DD group than the non-DD group (HR, 1.44; 95% CI, 1.19-1.76). Conclusion:The risk of ESKD development was higher in subjects diagnosed with AD or DD, suggesting that central nervous system diseases can adversely affect kidney function in elderly people.

Sleep apnea (SA) is a sleep disorder characterized by repeated episodes of shallow breathing or temporary pauses of breathing during sleep. SA is associated with increased risks of numerous health issues. SA causes sleep fragmentation and intermittent hypoxemia, consequently, people with SA can have excessive daytime sleepiness (EDS), impaired alertness, and decreased quality of life. 1,2 Furthermore, SA is associated with increased risks of cardiovascular and neurocognitive diseases in both the general population and endstage kidney disease (ESKD) patients. [3][4][5][6] Compared with the general population, prevalence of SA is reportedly much higher in ESKD patients. 7,8 The pathophysiological association between ESKD and SA has been investigated to determine why SA is more common in ESKD patients. Recently, overnight rostral fluid shift and fluid overload were suggested as pathophysiological links between ESKD and SA. 9,10 In a previous study, body water overload reportedly influenced overnight rostral fluid shift and worsened SA severity in patients receiving hemodialysis (HD). 11In another study, fluid removal was shown to attenuate the severity of SA in HD patients, independent of their uremic or metabolic status. 12