Dataset Information

Acute Kidney Injury in the Era of the AKI E-Alert.

ABSTRACT: Our aim was to use a national electronic AKI alert to define the incidence and outcome of all episodes of community- and hospital-acquired adult AKI.A prospective national cohort study was undertaken in a population of 3.06 million. Data were collected between March of 2015 and August of 2015. All patients with adult (?18 years of age) AKI were identified to define the incidence and outcome of all episodes of community- and hospital-acquired AKI in adults. Mortality and renal outcomes were assessed at 90 days.There was a total of 31,601 alerts representing 17,689 incident episodes, giving an incidence of AKI of 577 per 100,000 population. Community-acquired AKI accounted for 49.3% of all incident episodes, and 42% occurred in the context of preexisting CKD (Chronic Kidney Disease Epidemiology Collaboration eGFR); 90-day mortality rate was 25.6%, and 23.7% of episodes progressed to a higher AKI stage than the stage associated with the alert. AKI electronic alert stage and peak AKI stage were associated with mortality, and mortality was significantly higher for hospital-acquired AKI compared with alerts generated in a community setting. Among patients who survived to 90 days after the AKI electronic alert, those who were not hospitalized had a lower rate of renal recovery and a greater likelihood of developing an eGFR<60 ml/min per 1.73 m2 for the first time, which may be indicative of development of de novo CKD.The reported incidence of AKI is far greater than the previously reported incidence in studies reliant on clinical identification of adult AKI or hospital coding data. Although an electronic alert system is Information Technology driven and therefore, lacks intelligence and clinical context, these data can be used to identify deficiencies in care, guide the development of appropriate intervention strategies, and provide a baseline against which the effectiveness of these interventions may be measured.

SUBMITTER: Holmes J

PROVIDER: S-EPMC5142071 | biostudies-other | 2016 Dec

REPOSITORIES: biostudies-other

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Acute Kidney Injury in the Era of the AKI E-Alert.

Holmes Jennifer J Rainer Timothy T Geen John J Roberts Gethin G May Kate K Wilson Nick N Williams John D JD Phillips Aled O AO

Clinical journal of the American Society of Nephrology : CJASN 20161028 12

<h4>Background and objectives</h4>Our aim was to use a national electronic AKI alert to define the incidence and outcome of all episodes of community- and hospital-acquired adult AKI.<h4>Design, setting, participants, & measurements</h4>A prospective national cohort study was undertaken in a population of 3.06 million. Data were collected between March of 2015 and August of 2015. All patients with adult (≥18 years of age) AKI were identified to define the incidence and outcome of all episodes of ...[more]

PMID: 27793961

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Project description:Renal hypoxia is widespread in acute kidney injury (AKI) of various aetiologies. Hypoxia adaptation, conferred through the hypoxia-inducible factor (HIF), appears to be insufficient. Here we show that HIF activation in renal tubules through Pax8-rtTA-based inducible knockout of von Hippel-Lindau protein (VHL-KO) protects from rhabdomyolysis-induced AKI. In this model, histological observations indicate that injury mainly affects proximal convoluted tubules, with 5% necrosis at d1 and 40% necrosis at d2. HIF-1alpha up-regulation in distal tubules reflects renal hypoxia. However, lack of HIF in proximal tubules suggests insufficient adaptation by HIF. AKI in VHL-KO mice leads to prominent HIF activation in all nephron segments, as well as to reduced serum creatinine, serum urea, tubular necrosis, and apoptosis marker caspase-3 protein. At d1 after rhabdomyolysis, when tubular injury is potentially reversible, HIF mediated protection in AKI is associated with activated glycolysis, cellular glucose uptake and utilization, autophagy, vasodilation, and proton removal as demonstrated by qPCR, pathway enrichment analysis and immunohistochemistry. Together, our data provide evidence for a HIF-orchestrated multi-level shift towards glycolysis as a major mechanism for protection against acute tubular injury. All experiments were carried out in transgenic mice in which selective renal tubular VHL knockout (VHL-KO) was inducible by doxycycline (Reference: Mathia S, Paliege A, Koesters R, Peters H, Neumayer HH, Bachmann S, Rosenberger C. Action of hypoxia-inducible factor in liver and kidney from mice with Pax8-rtTA-based deletion of von Hippel-Lindau protein. Acta Physiol (Oxf). 2013; 207(3):565-76.). Four groups of animals were used: 1) controls: untreated mice; 2) VHL-KO: injected with doxycycline (0.1 mg per 10 g body weight SC), 4 days prior to sacrifice; 3) AKI: rhabdomyolysis; 4) VHL-KO/AKI: doxycycline plus rhabdomyolysis. To induce AKI, 50% glycerol (0.05 ml per 10 g body weight) was injected IM into the left hind limb under isoflurane narcosis. Drinking water was withdrawn between 20 h prior and 24 h after glycerol injection.

Project description:Background and objectivesHow to best medically manage patients who survived hospitalized AKI is unclear. Use of renin-angiotensin system blockers in this setting may increase risk of recurrent AKI.Design, setting, participants, & measurementsThis is a cohort study of 10,242 members of an integrated health care delivery system in Northern California who experienced AKI and survived a hospitalization between January 1, 2006 and December 31, 2013. All study participants did not have prior heart failure or use of angiotensin-converting enzyme inhibitors (ACE-Is) or angiotensin receptor blockers (ARBs) up to 5 years prior. New receipt and time-updated exposure of ACE-Is/ARBs was identified on the basis of dispensed prescriptions found in outpatient health plan pharmacy databases. The main outcome of interest was subsequent episode of hospitalized AKI after discharge from an initial index hospitalization complicated by AKI. Recurrent AKI episode was defined using acute changes in serum creatinine concentrations. Marginal structural models were used to adjust for baseline and potential time-dependent confounders.ResultsForty-seven percent of the study population had a documented eGFR<60 ml/min per 1.73 m2 or documented proteinuria before hospitalization. With a median of 3 (interquartile range, 1-5) years of follow-up, 1853 (18%) patients initiated use of ACE-Is/ARBs and 2124 (21%) patients experienced recurrent AKI. Crude rate of recurrent AKI was 6.1 (95% confidence interval [95% CI], 5.9 to 6.4) per 100 person-years off ACE-Is/ARBs and 5.7 (95% CI, 4.9 to 6.5) per 100 person-years on ACE-Is/ARBs. In marginal structural causal inference models that adjusted for baseline and potential time-dependent confounders, exposure to ACE-I/ARB use was not associated with higher incidence of recurrent AKI (adjusted odds ratio, 0.71; 95% CI, 0.45 to 1.12).ConclusionsIn this study of AKI survivors without heart failure, new use of ACE-I/ARB therapy was not independently associated with increased risk of recurrent hospitalized AKI.

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Acute Kidney Injury in the Era of the AKI E-Alert.

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Acute Kidney Injury in the Era of the AKI E-Alert.

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