observational cohort
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2022 ◽  
Vol 77 ◽  
pp. 110598
Author(s):  
Jean-Noël Evain ◽  
Zoé Durand ◽  
Kelly Dilworth ◽  
Sarah Sintzel ◽  
Aurélien Courvoisier ◽  
...  

2022 ◽  
Vol 77 ◽  
pp. 110633
Author(s):  
Barak Cohen ◽  
Eva Rivas ◽  
Xuan Pu ◽  
Kamal Maheshwari ◽  
Jorge A. Araujo-Duran ◽  
...  

Author(s):  
Anne-Laure Couderc ◽  
Pascale Tomasini ◽  
Laurent Greillier ◽  
Emilie Nouguerède ◽  
Dominique Rey ◽  
...  

PLoS ONE ◽  
2022 ◽  
Vol 17 (1) ◽  
pp. e0261142
Author(s):  
Katie Bechman ◽  
Mark Yates ◽  
Kirsty Mann ◽  
Deepak Nagra ◽  
Laura-Jane Smith ◽  
...  

Background The Covid-19 pandemic in the United Kingdom has seen two waves; the first starting in March 2020 and the second in late October 2020. It is not known whether outcomes for those admitted with severe Covid were different in the first and second waves. Methods The study population comprised all patients admitted to a 1,500-bed London Hospital Trust between March 2020 and March 2021, who tested positive for Covid-19 by PCR within 3-days of admissions. Primary outcome was death within 28-days of admission. Socio-demographics (age, sex, ethnicity), hypertension, diabetes, obesity, baseline physiological observations, CRP, neutrophil, chest x-ray abnormality, remdesivir and dexamethasone were incorporated as co-variates. Proportional subhazards models compared mortality risk between wave 1 and wave 2. Cox-proportional hazard model with propensity score adjustment were used to compare mortality in patients prescribed remdesivir and dexamethasone. Results There were 3,949 COVID-19 admissions, 3,195 hospital discharges and 733 deaths. There were notable differences in age, ethnicity, comorbidities, and admission disease severity between wave 1 and wave 2. Twenty-eight-day mortality was higher during wave 1 (26.1% versus 13.1%). Mortality risk adjusted for co-variates was significantly lower in wave 2 compared to wave 1 [adjSHR 0.49 (0.37, 0.65) p<0.001]. Analysis of treatment impact did not show statistically different effects of remdesivir [HR 0.84 (95%CI 0.65, 1.08), p = 0.17] or dexamethasone [HR 0.97 (95%CI 0.70, 1.35) p = 0.87]. Conclusion There has been substantial improvements in COVID-19 mortality in the second wave, even accounting for demographics, comorbidity, and disease severity. Neither dexamethasone nor remdesivir appeared to be key explanatory factors, although there may be unmeasured confounding present.


Author(s):  
Gianmarco Lombardi ◽  
Giovanni Gambaro ◽  
Pietro Manuel Ferraro

Introduction Electrolytes disorders are common findings in kidney diseases and might represent a useful biomarker preceding kidney injury. Serum potassium [K+] imbalance is still poorly investigated for association with acute kidney injury (AKI) and most evidence come from intensive care units (ICU). The aim of our study was to comprehensively investigate this association in a large, unselected cohort of hospitalized patients. Methods: We performed a retrospective observational cohort study on the inpatient population admitted to Fondazione Policlinico Universitario A. Gemelli IRCCS between January 1, 2010 and December 31, 2014 with inclusion of adult patients with at least 2 [K+] and 3 serum creatinine (sCr) measurements who did not develop AKI during an initial 10-day window. The outcome of interest was in-hospital AKI. The exposures of interest were [K+] fluctuations and hypo (HoK) and hyperkalemia (HerK). [K+] variability was evaluated using the coefficient of variation (CV). Cox proportional hazards regression models were used to obtain hazard ratios (HRs) and 95% confidence intervals (CIs) of the association between the exposures of interest and development of AKI. Results: 21,830 hospital admissions from 18,836 patients were included in our study. During a median follow-up of 5 (interquartile range [IQR] 7) days, AKI was observed in 555 hospital admissions (2.9%); median time for AKI development was 5 (IQR 7) days. Higher [K+] variability was independently associated with increased risk of AKI with a statistically significant linear trend across groups (p-value = 0.012). A significantly higher incidence of AKI was documented in patients with HerK compared with normokalemia. No statistically significant difference was observed between HoK and HerK (p-value = 0.92). Conclusion: [K+] abnormalities including fluctuations even within the normal range are associated with development of AKI.


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