Automated, electronic alerts for acute kidney injury: a single-blind, parallel-group, randomised controlled trial

Abstract

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.

Recognition and management of acute kidney injury in hospitalised patients can be partially improved with the use of a care bundle

“…The first randomised controlled trial to examine the effect of an AKI e-alert showed no difference in maximum increase in serum creatinine, need for dialysis or mortality. 18 Our hospital is currently in the process of implementing an e-alert via the electronic patient record system. Future audits and evaluations will inform whether this initiative, in combination with ongoing educational projects and changes in clinical practice, has a role in improving the management and outcome of AKI.…”

Service evaluation of the implementation of a digitally-enabled care pathway for the recognition and management of acute kidney injury

“…The ‘Think Kidneys’ NHS England National programme has provided best practice examples of how AKI alerts may be clinically deployed 13 . However, simply alerting a clinician to the presence of a possible AKI incident may be insufficient to improve outcomes 14 . A much richer clinical dataset is required to help clinicians prioritise, diagnose and manage patients.…”

False-Positive Rate of AKI Using Consensus Creatinine–Based Criteria

“…However, randomized trials attempting to intervene on early AKI have been largely unsuccessful (6)(7)(8)(9). This may, in part, result from misclassification of AKI under frameworks that do not reflect true GFR reduction.…”

“…Factors predisposing to FP AKI diagnoses could include a higher degree of variation in laboratory measurement of SCr, a higher degree of biologic variation in creatinine levels (1)(2)(3)(4)(5)11,12), and a higher number of creatinine assays performed. Like all laboratory tests, SCr measurements are affected by within-and between-sample coefficients of variation (CoVs), which for the widely used modified Jaffe rate reaction (5-9,13), range from 0.6% to as high as 9% depending on the true SCr concentration and assay characteristics (6)(7)(8)(9)14). SCr measurements are also associated with intraindividual biologic variation and can be affected by changes in volume status, medications, and creatinine generation during critical illness (1)(2)(3)(4)10,11,15,16).…”