ABSTRACT
Despite efforts to treat critically ill patients who require continuous renal replacement therapy (CRRT) due to acute kidney injury (AKI), their mortality risk remains high. This condition may be attributable to complications of CRRT, such as arrhythmias. Here, we addressed the occurrence of ventricular tachycardia (VT) during CRRT and its relationship with patient outcomes. Methods: This study retrospectively enrolled 2,397 patients who started CRRT due to AKI from 2010 to 2020 at Seoul National University Hospital in Korea. The occurrence of VT was evaluated from the initiation of CRRT until weaning from CRRT. The odds ratios (ORs) of mortality outcomes were measured using logistic regression models after adjustment for multiple variables. Results: VT occurred in 150 patients (6.3%) after starting CRRT. Among them, 95 cases were defined as sustained VT (i.e., lasting ≥30 seconds), and the other 55 cases were defined as non-sustained VT (i.e., lasting <30 seconds). The occurrence of sustained VT was associated with a higher mortality rate than a nonoccurrence (OR, 2.04 and 95% confidence interval [CI], 1.23–3.39 for the 30- day mortality; OR, 4.06 and 95% CI, 2.04–8.08 for the 90-day mortality). The mortality risk did not differ between patients with non-sustained VT and nonoccurrence. A history of myocardial infarction, vasopressor use, and certain trends of blood laboratory findings (such as acidosis and hyperkalemia) were associated with the subsequent risk of sustained VT. Conclusion: Sustained VT occurrence after starting CRRT is associated with increased patient mortality. The monitoring of electrolytes and acid-base status during CRRT is essential because of its relationship with the risk of VT.
ABSTRACT
Background@#An inverse observational association between alcohol use and the risk of chronic kidney disease (CKD) or end-stage kidney disease (ESKD) has been reported. The causal effect of alcohol use on the risk of ESKD warrants additional investigation. @*Methods@#The study was an observational cohort study investigating the UK Biobank and performed Mendelian randomization (MR) analysis. Amounts of alcohol use were collected using a touchscreen questionnaire. In the observational analysis, 212,133 participants without prevalent ESKD were studied, and the association between alcohol use and the risk of prevalent CKD or incident ESKD was investigated. The genetic analysis included 337,138 participants of white British ancestry. For one-sample MR, an analysis based on a polygenic risk score (PRS) was conducted with genetically predicted alcohol intake. The MR analysis investigated ESKD outcome and related comorbidities. @*Results@#Lower alcohol use was observationally associated with a higher risk of prevalent CKD or incident ESKD. However, the genetic risk of CKD was significantly associated with lower alcohol use, suggesting reverse causation. A higher PRS for alcohol use was significantly associated with a higher risk of ESKD (per units of one phenotypical alcohol drink; adjusted odds ratio of 1.16 [95% confidence interval, 1.02–1.31]) and related comorbidities, including hypertension, diabetes mellitus, obesity, and central obesity. @*Conclusion@#The inverse observational association between alcohol use and the risk of CKD or ESKD may have been affected by reverse causation. Our study supports a causal effect of alcohol use on a higher risk of ESKD and related predisposing comorbidities.
ABSTRACT
Background@#An inverse observational association between alcohol use and the risk of chronic kidney disease (CKD) or end-stage kidney disease (ESKD) has been reported. The causal effect of alcohol use on the risk of ESKD warrants additional investigation. @*Methods@#The study was an observational cohort study investigating the UK Biobank and performed Mendelian randomization (MR) analysis. Amounts of alcohol use were collected using a touchscreen questionnaire. In the observational analysis, 212,133 participants without prevalent ESKD were studied, and the association between alcohol use and the risk of prevalent CKD or incident ESKD was investigated. The genetic analysis included 337,138 participants of white British ancestry. For one-sample MR, an analysis based on a polygenic risk score (PRS) was conducted with genetically predicted alcohol intake. The MR analysis investigated ESKD outcome and related comorbidities. @*Results@#Lower alcohol use was observationally associated with a higher risk of prevalent CKD or incident ESKD. However, the genetic risk of CKD was significantly associated with lower alcohol use, suggesting reverse causation. A higher PRS for alcohol use was significantly associated with a higher risk of ESKD (per units of one phenotypical alcohol drink; adjusted odds ratio of 1.16 [95% confidence interval, 1.02–1.31]) and related comorbidities, including hypertension, diabetes mellitus, obesity, and central obesity. @*Conclusion@#The inverse observational association between alcohol use and the risk of CKD or ESKD may have been affected by reverse causation. Our study supports a causal effect of alcohol use on a higher risk of ESKD and related predisposing comorbidities.
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Background@#Metabolic syndrome (MetS) is linked to various chronic comorbidities, including chronic kidney disease (CKD). However, few large studies have addressed whether recovery from MetS is associated with reduction in the risks of such comorbidities. @*Methods@#This nationwide population-based study in Korea screened 10,664,268 people who received national health screening ≥ 3 times between 2012 and 2016. Those with a history of major cardiovascular events or preexisting CKD were excluded. We classified study groups into four, according to the course of MetS state, as defined by the harmonizing criteria. The main study outcome was incidental CKD (estimated glomerular filtration rate < 60 mL/min/1.73 m2 which was persistent until the last health exams). The study outcomes were investigated using multivariable logistic regression analysis, which was adjusted for clinical variables and the previous severity of MetS. @*Results@#Four study groups included 6,315,301 subjects: 4,537,869 people without MetS, 1,034,605 with chronic MetS, 438,287 who developed MetS, and 304,540 who recovered from preexisting MetS. Those who developed MetS demonstrated higher risk of CKD (adjusted odds ratio [OR], 1.26 [1.23-1.29]) than did those who did not develop MetS. In contrast, MetSrecovery was associated with decreased risk of CKD (adjusted OR, 0.84 [0.82-0.86]) than that in people with chronic MetS. Among the MetS components, change in hypertension was associated with the largest difference in CKD risk. @*Conclusion@#Reducing or preventing MetS may reduce the burden of CKD on a population-scale. Clinicians should consider the clinical importance of altering MetS status for risk of CKD.
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Objective@#Little is known about percutaneous coronary intervention (PCI) and its benefits in elderly patients with out-of-hospital cardiac arrest (OHCA). This study compared the survival to discharge and the neurological outcomes across the age groups of patients with OHCA. @*Methods@#Using the national cardiac arrest registry, OHCA patients with a return of spontaneous circulation from 2013 to 2017 were included in this study. The PCI history of the patients was obtained from their medical records. The outcomes were cerebral performance category (CPC) 1 and 2 and survival to discharge. Multivariable logistic regression analysis was performed, and an interaction term was evaluated to compare the effects of PCI across the age groups. @*Results@#This study included 22,320 patients. In the interaction term, the adjusted odds ratio (AOR) (95% confidence interval [CI]) for a good CPC was 2.84 (2.43-3.32) for the age group of 18-64 years, 3.26 (2.53-4.21) for the age group of 65-74 years, 3.37 (2.33-4.88) for the age group of 75-84 years, and 2.54 (0.92-7.01) for the age group of 85-106 years. The AOR (95% CI) for survival to hospital discharge was 3.31 (2.82-3.88) for the age group of 18-64 years, 2.65 (2.09-3.35) for the age group of 65-74 years, 2.20 (1.61-3.02) for the age group of 75-84 years, and 1.64 (0.73-3.67) for the age group of 85-106 years. @*Conclusion@#In the OHCA patients, the PCI group had more good outcomes (good CPC, survival to discharge) than the non-PCI group, but this benefit was not shown in those aged over 85 years. On the other hand, it could not explain why PCI should not be performed in the elderly, suggesting that age alone should not be used to make decisions regarding early invasive strategies.
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Objective@#We aimed to compare the multi-marker strategy (copeptin and high-sensitivity cardiac troponin I [hs-cTnI]) with serial hs-cTnI measurements to rule out acute myocardial infarction (AMI) in patients with chest pain. @*Methods@#This prospective observational study was performed in a single emergency department. To test the non-inferiority margin of 4% in terms of negative predictive value (NPV) between the multi-marker strategy (0 hour) and serial hs-cTnI measurements (0 and 2 hours), 262 participants were required. Samples for copeptin and hs-cTnI assays were collected at presentation (0 hour) and after 2 hours. The measured biomarkers were considered abnormal when hs-cTnI was >26.2 ng/L and when copeptin was >10 pmol/L. @*Results@#AMI was diagnosed in 28 patients (10.7%). The NPV of the multi-marker strategy was 100% (160/160; 95% confidence interval [CI], 97.7% to 100%), which was not inferior to that of serial hs-cTnI measurements (201/201; 100%; 95% CI, 98.2% to 100%). The sensitivity, specificity, and positive predictive value of the multi-marker strategy were 100% (95% CI, 87.7% to 100%), 68.1% (95% CI, 61.7% to 74.0%), and 27.2% (95% CI, 18.9% to 36.8%), respectively. The sensitivity, specificity, and positive predictive value of serial hs-cTnI measurements were 100% (95% CI, 87.7% to 100%), 85.5% (95% CI, 80.4% to 89.8%), and 45.2% (95% CI, 32.5% to 58.3%), respectively. @*Conclusion@#The multi-marker strategy (copeptin and hs-cTnI measurement) was not inferior to serial hs-cTnI measurements in terms of NPV for AMI diagnosis, with a sensitivity and NPV of 100%. Copeptin may help in the early rule-out of AMI in patients with chest pain.
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BACKGROUND: Cancer risk and epidemiology in pre-dialysis chronic kidney disease (CKD) warrant further investigation in a large-scale cohort. METHODS: We performed a nationwide population-based study using the national health insurance database of Korea. We screened records from 18,936,885 individuals who received a national health examination ≥ 2 times from 2009 to 2016. Pre-dialysis CKD was identified based on serum creatinine and dipstick albuminuria results. Individuals with preexisting cancer history, renal replacement therapy, or transient CKD were excluded. A control group without evidence of kidney function impairment and matched for age, sex, low-income status, and smoking history was included. Risk of cancers, as identified in the claims database, was investigated using a multivariable Cox regression model including matched variables and other unmatched clinical characteristics as covariates. RESULTS: A total of 471,758 people with pre-dialysis CKD and the same number of matched controls were included. Urinary (adjusted hazard ratio [HR], 1.97; 95% confidence interval [95% CI], 1.82–2.13) and hematopoietic (adjusted HR, 1.53; 95% CI, 1.38–1.68) malignancy risk was increased in pre-dialysis CKD and all CKD stages. However, the risk of digestive cancer was lower in the pre-dialysis CKD group (adjusted HR, 0.89; 95% CI, 0.87–0.92). The risk of digestive, respiratory, thyroid, and prostate malignancy demonstrated a non-linear association with CKD stage, with stage 1 or stage 4/5 CKD without dialysis demonstrating relatively lower risk. CONCLUSION: Cancer risk varied in pre-dialysis CKD compared to controls, and the association between cancer risk and CKD stage varied depending on the cancer type.