Abstract
Acute kidney injury (AKI) in hospitalized patients is independently associated with increased morbidity and mortality in pediatric and adult populations. Continued reliance on serum creatinine and urine output to diagnose AKI has resulted in our inability to provide successful therapeutic and supportive interventions to prevent and mitigate AKI and its effects. Research efforts over the last decade have focused on the discovery and validation of novel urinary biomarkers to detect AKI prior to a change in kidney function and to aid in the differential diagnosis of AKI. The aim of this article is to review the AKI biomarker literature with a focus on the context in which they should serve to add to the clinical context facing physicians caring for patients with, or at-risk for, AKI. The optimal and appropriate utilization of AKI biomarkers will only be realized by understanding their characteristics and placing reasonable expectations on their performance in the clinical arena.
Highlights
Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function, which in its most severe form, acute renal failure, is manifested by changes in blood chemistry and decreased urine output [1]
Clinicians caring for patients with AKI have been hindered by the reliance on serum creatinine or decreased urine output, both kidney function markers, to make the AKI diagnosis
Seventy-one children were enrolled and AKI was defined as a serum creatinine rise of 50% over baseline
Summary
Acute kidney injury (AKI) is defined as an abrupt decrease in kidney function, which in its most severe form, acute renal failure, is manifested by changes in blood chemistry and decreased urine output [1]. Very recent data from the large US National Institutes of Health (NIH)-funded multi-center Translational Research Investigating Biomarker Endpoints in Acute Kidney Injury (TRIBE-AKI) consortium has demonstrated both urinary NGAL and IL-18 [26] in children [33] and adults [34] after CPB In both populations, NGAL and IL-18 demonstrated moderate predictive ability for AKI with a significant improvement above clinical risk factors alone. Validation in other populations Subsequent to the initial promising results observed for novel biomarker prediction of AKI development and severity after CPB, biomarkers (especially NGAL [36]) have been assessed in multiple other clinical AKI settings including contrast induced nephropathy [37,38], hemolytic uremic syndrome (HUS) [39], lupus nephritis [40], and renal [28,41,42] and orthotopic hepatic transplantation [43]. Renal angina presence only increases AKI development risk and biomarkers should add value to predict the AKI spectrum and help guide management
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