Background Early recognition of hospital-acquired Acute Kidney Injury (AKI) may improve patient management and outcomes. Methods This multicentre study was conducted at three hospitals (H1–intervention; H2 & H3 –controls) served by a single laboratory. The intervention bundle (an interruptive aAlert showing AKI stage and baseline creatinine in the eMR, a management guide and junior medical staff education) was implemented only at H1. Outcome variables included length of stay (LOS), all-cause in-hospital mortality and management quality. Results Over 6 months, 639 patients developed AKI (265 at H1, and 374 at controls), with 94.7% in general wards; 537 (84%) patients developed stage 1, 58 (9%) stage 2 and 43 (7%) stage 3 AKI. Median LOS was 9 days (IQR 4–17) and not different between intervention and controls. However, patients with AKI stage 1 had shorter LOS at H1 (median 8 versus 10 days (p = 0.021). Serum creatinine had risen prior to admission in most patients. Documentation of AKI was better in H1 (94.8% vs 83.4%; p = 0.001), with higher rates of nephrology consultation (25% vs 19%; p = 0.04) and cessation of nephrotoxins (25.3 vs 18.8% p = 0.045). There was no difference in mortality between H1 vs Controls (11.7% vs 13.0%; p = 0.71). Conclusions Most hospitalised patients developed stage 1 AKI and developed AKI in the community and remained outside the ICU. The AKI eAlert bundle reduced LOS in most patients with AKI and increased AKI documentation, nephrology consultation rate and cessation of nephrotoxic medications.
Background: Urine tissue inhibitor of metalloproteinases-2/insulin-like growth factor-binding protein 7 (TIMP-2/IGFBP7) (NephroCheck, Ortho Clinical Diagnostics, Raritan, NJ, USA) is a US Food and Drug Administration-approved biomarker for risk assessment of acute kidney injury (AKI) in critically ill adult patients in intensive care units; however, its clinical impact in the emergency department (ED) remains unproven. We evaluated the utility of NephroCheck for predicting AKI development and short-term mortality in the ED.Methods: This was a prospective, observational, five-center international study. We consecutively enrolled ED patients admitted with ≥ 30% risk of AKI development (assessed by ED physician: ED score) or acute diseases. Serum creatinine was tested on ED arrival (T0), day 1, and day 2 (T48); urine for NephroCheck was collected at T0 and T48. We performed ROC curve and reclassification analyses.Results: Among the 529 patients enrolled (213 females; median age, 65 years), AKI developed in 59 (11.2%) patients. The T0 NephroCheck value was higher in the AKI group than in the non-AKI group (median 0.77 vs. 0.29 (ng/m) 2 /1,000, P = 0.001), and better predicted AKI development than the ED score (area under the curve [AUC], 0.64 vs. 0.53; P = 0.04). In reclassification analyses, adding NephroCheck to the ED score improved the prediction of AKI development (P < 0.05). The T0 NephroCheck value predicted 30-day mortality (AUC, 0.68; P < 0.001).Conclusions: NephroCheck can predict both AKI development and short-term mortality in at-risk ED patients. NephroCheck would be a useful biomarker for early ruling-in or rulingout of AKI in the ED.
Aim: Kinetic estimated Glomerular Filtration Rate (KeGFR) approximates GFR under non-steady-state conditions. We investigated whether the ratio of KeGFR difference to baseline eGFR could predict acute kidney injury (AKI) earlier than a creatininebased algorithm that triggered an AKI electronic Alert (eAlert).Methods: This retrospective, single-centre, proof-of-concept cohort study assessed all patients diagnosed with AKI by an automated serum creatinine-based eAlert. The kinetic eGFR, the kinetic eGFR difference from baseline and the ratio of difference to baseline was calculated in subjects with at least two serum creatinine (sCr) measurements within 72 h of AKI.Results: Patients in the AKI cohort (n = 140) had a significant decline in KeGFR ratio (AKI: 17% IQR 7% to 29%, Non-AKI: 0 IQR À12% to 9%; P-value <.0001). A decrease of the ratio greater than 10% predicted AKI with a sensitivity of 66%, a specificity of 77%, a positive predictive value of 63%, and negative predictive value of 80%. The median lead time between KeGFR ratio decrease and AKI was 24 h (IQR: 19-27 h).Conclusions: KeGFR ratio is a cheap, simple method that predicted AKI 24 h before laboratory detection. KeGFR may facilitate triaging patients to increased monitoring or intervention.
Normalisation to standard reference gene(s) is essential for quantitative real-time polymerase chain reaction (RT-qPCR) to obtain reproducible and comparable results of a gene of interest (GOI) between subjects and under varying experimental conditions. There is limited evidence to support selection of the commonly used reference genes in rat ischaemic and toxicological kidney models. Employing these models, we determined the most stable reference genes by comparing 4 standard methods (NormFinder, qBase+, BestKeeper and comparative ΔCq) and developed a new 3-way linear mixed-effects model for evaluation of reference gene stability. This new technique utilises the intra-class correlation coefficient as the stability measure for multiple continuous and categorical covariates when determining the optimum normalisation factor. The model also determines confidence intervals for each candidate normalisation gene to facilitate selection and allow sample size calculation for designing experiments to identify reference genes. Of the 10 candidate reference genes tested, the geometric mean of polyadenylate-binding nuclear protein 1 (PABPN1) and betaactin (ACTB) was the most stable reference combination. In contrast, commonly used ribosomal 18S and glyceraldehyde 3-phosphate dehydrogenase (GAPDH) were the most unstable. We compared the use of PABPN1×ACTB and 2 commonly used genes 18S and GAPDH on the expression of 4 genes of interest know to vary after renal injury and expressed by different kidney cell types (KIM-1, HIF1α, TGFβ1 and PECAM1). The less stable reference genes gave varying patterns of GOI expression in contrast to the use of the least unstable reference PABPN1×ACTB combination; this improved detection of differences in gene expression between experimental groups. Reduced within-group variation of the now more accurately normalised GOI may allow for reduced experimental group size particularly for comparison between various models. This objective selection of stable reference genes increased the reliability of comparisons within and between experimental groups.
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