Summary Background Acute kidney injury often goes unrecognised in its early stages when effective treatment options might be available. We aimed to determine whether an automated electronic alert for acute kidney injury would reduce the severity of such injury and improve clinical outcomes in patients in hospital. Methods In this investigator-masked, parallel-group, randomised controlled trial, patients were recruited from the hospital of the University of Pennsylvania in Philadelphia, PA, USA. Eligible participants were adults aged 18 years or older who were in hospital with stage 1 or greater acute kidney injury as defined by Kidney Disease Improving Global Outcomes creatinine-based criteria. Exclusion criteria were initial hospital creatinine 4·0 mg/dL (to convert to μmol/L, multiply by 88·4) or greater, fewer than two creatinine values measured, inability to determine the covering provider, admission to hospice or the observation unit, previous randomisation, or end-stage renal disease. Patients were randomly assigned (1:1) via a computer-generated sequence to receive an acute kidney injury alert (a text-based alert sent to the covering provider and unit pharmacist indicating new acute kidney injury) or usual care, stratified by medical versus surgical admission and intensive care unit versus non-intensive care unit location in blocks of 4–8 participants. The primary outcome was a composite of relative maximum change in creatinine, dialysis, and death at 7 days after randomisation. All analyses were by intention to treat. This study is registered with ClinicalTrials.gov, number NCT01862419. Findings Between Sept 17, 2013, and April 14, 2014, 23 664 patients were screened. 1201 eligible participants were assigned to the acute kidney injury alert group and 1192 were assigned to the usual care group. Composite relative maximum change in creatinine, dialysis, and death at 7 days did not differ between the alert group and the usual care group (p=0·88), or within any of the four randomisation strata (all p>0·05). At 7 days after randomisation, median maximum relative change in creatinine concentrations was 0·0% (IQR 0·0–18·4) in the alert group and 0·6% (0·0–17·5) in the usual care group (p=0·81); 87 (7·2%) patients in the alert group and 70 (5·9%) patients in usual care group had received dialysis (odds ratio 1·25 [95% CI 0·90–1·74]; p=0·18); and 71 (5·9%) patients in the alert group and 61 (5·1%) patients in the usual care group had died (1·16 [0·81–1·68]; p=0·40). Interpretation An electronic alert system for acute kidney injury did not improve clinical outcomes among patients in hospital. Funding Penn Center for Healthcare Improvement and Patient Safety.

In a large health system in the United States, investigators examined whether mortality, receipt of mechanical ventilation, and patient acuity changed over time among adult patients with COVID-19–related critical illness admitted to intensive care units.

More than 1 million heart failure hospitalizations occur annually, and congestion is the predominant cause. Rehospitalizations for recurrent congestion portend poor outcomes independently of age and renal function. Persistent congestion trumps serum creatinine increases in predicting adverse heart failure outcomes. No decongestive pharmacological therapy has reduced these harmful consequences. Simplified ultrafiltration devices permit fluid removal in lower-acuity hospital settings, but with conflicting results regarding safety and efficacy. Ultrafiltration performed at fixed rates after onset of therapy-induced increased serum creatinine was not superior to standard care and resulted in more complications. In contrast, compared with diuretic agents, some data suggest that adjustment of ultrafiltration rates to patients’ vital signs and renal function may be associated with more effective decongestion and fewer heart failure events. Essential aspects of ultrafiltration remain poorly defined. Further research is urgently needed, given the burden of congestion and data suggesting sustained benefits of early and adjustable ultrafiltration.

Background Home hemodialysis (HHD) is associated with improved clinical and quality of life outcomes compared with in-center hemodialysis but remains an underused modality in the United States. Discontinuation from HHD may be an important contributor to the low utilization of this modality. This study aimed to describe the rate and timing of HHD discontinuation, or technique failure, and identify contributing factors. Study Design Retrospective cohort study Setting & Participants Using data from a large dialysis provider, we identified a nationally representative cohort of patients who initiated HHD from 2007 – 2009 (N=2840). Factors Demographics, ESRD duration, kidney transplant listing status, co-morbid conditions, level of urbanization or rurality based on residence zip code, socioeconomic status based on residence zip code, and dialysis facility factors. Outcomes Discontinuation from HHD, defined as ≥60 days with no HHD treatments. Measurements Competing risk models were used to produce cumulative incidence plots and to identify socio-demographic and clinical variables associated with HHD discontinuation. Transplantation and death were treated as competing risks for HHD discontinuation. Results The 1-year incidence of discontinuation was 24.9% and the 1-year mortality estimate was 7.6%. Median ESRD duration prior to initiating HHD was 2.1 years. Diabetes and smoking/alcohol/drug use were associated with increased risk of HHD discontinuation (HRs of 1.34 [95% CI, 1.07–1.68] and 1.34 [95% CI, 1.01–1.78], respectively). Listing for kidney transplant and rural residence (rural-urban commuting area ≥ 7) were associated with decreased risk of HHD discontinuation (HRs of 0.73 [95% CI, 0.61–0.87] and 0.78 [95% CI, 0.59–1.02], respectively). Limitations Limited to variables available within the DaVita dialysis and US Renal Data System datasets. Conclusions A substantial proportion of patients discontinue HHD within the first 12 months of use of the modality. Patients with diabetes, substance use, non-listing for kidney transplant, and urban residence are at greater risk for discontinuation. Targeting high-risk patients for increased support from clinical teams is a potential strategy for reducing HHD discontinuation and increasing technique survival.

Background and objectives Use of small changes in serum creatinine to diagnose AKI allows for earlier detection but may increase diagnostic false-positive rates because of inherent laboratory and biologic variabilities of creatinine.Design, setting, participants, & measurements We examined serum creatinine measurement characteristics in a prospective observational clinical reference cohort of 2267 adult patients with AKI by Kidney Disease Improving Global Outcomes creatinine criteria and used these data to create a simulation cohort to model AKI false-positive rates. We simulated up to seven successive blood draws on an equal population of hypothetical patients with unchanging true serum creatinine values. Error terms generated from laboratory and biologic variabilities were added to each simulated patient's true serum creatinine value to obtain the simulated measured serum creatinine for each blood draw. We determined the proportion of patients who would be erroneously diagnosed with AKI by Kidney Disease Improving Global Outcomes creatinine criteria.Results Within the clinical cohort, 75.0% of patients received four serum creatinine draws within at least one 48-hour period during hospitalization. After four simulated creatinine measurements that accounted for laboratory variability calculated from assay characteristics and 4.4% of biologic variability determined from the clinical cohort and publicly available data, the overall false-positive rate for AKI diagnosis was 8.0% (interquartile range =7.9%-8.1%), whereas patients with true serum creatinine $1.5 mg/dl (representing 21% of the clinical cohort) had a false-positive AKI diagnosis rate of 30.5% (interquartile range =30.1%-30.9%) versus 2.0% (interquartile range =1.9%-2.1%) in patients with true serum creatinine values ,1.5 mg/dl (P,0.001).Conclusions Use of small serum creatinine changes to diagnose AKI is limited by high false-positive rates caused by inherent variability of serum creatinine at higher baseline values, potentially misclassifying patients with CKD in AKI studies.