Abstract
Acute kidney injury (AKI) affects one in four neonates, children, and adults admitted to the intensive care unit (ICU). AKI-associated outcomes, including mortality, are significantly worsened. Several decades of research demonstrate evidence for a need to rethink the pathophysiology and drivers of injury as well as to reconsider the existing diagnostic framework. Novel urinary and serum biomarkers of injury have, however, not been readily integrated into practice—partially because of the limited scope to current testing. The predominant focus to date has been the adjudication of a single biomarker measured at a single point of time for the prediction of either AKI progression or disease-related mortality. This approach is pragmatically problematic. The imprecise, umbrella classification of AKI diagnosis coupled with the absence of a consistently effective set of therapies creates a difficult rubric for biomarkers to demonstrate value in the scope of practice. AKI is, however, not a binary process but more an ICU syndrome—with complex biology underpinning injury, interacting and disrupting other organ function, multidimensional in manifestation, and varying in severity over time. As such, a more appropriate diagnostic paradigm is needed. In this minireview, the status quo for AKI diagnosis and associated limitations will be discussed, and a novel, dynamic, and multidimensional paradigm will be presented. Appreciation of AKI as an ICU syndrome and creation of an appropriately matching and sophisticated diagnostic platform of injury assessment are possible and represent the next step in AKI management.
Highlights
Acute kidney injury (AKI) continues to be an epidemic in patients admitted to the intensive care unit (ICU) [1,2,3,4]
Significant academic effort has been placed into improved earlier recognition and prediction of disease, either through the tradition markers of serum creatinine (SCr) and/or urine output (UOP) or more novel biomarkers in the urine or serum
Correction of SCr for fluid balance and as the fluid balance changes may delineate the independent effects of AKI and fluid overload (FO), identifying unique AKI-FO phenotypes [42, 43]
Summary
Acute kidney injury (AKI) continues to be an epidemic in patients admitted to the intensive care unit (ICU) [1,2,3,4]. The 16th ADQI recommended study (including risk scores, functional markers, and use of biomarkers) to identify, predict, and further characterize patients with persistent AKI (i.e., ≥48 h of SCr elevation or oliguria) and to consider SCr elevation with return to baseline in the first 48 h to be considered separately from actual AKI [28]. Correction of SCr for fluid balance and as the fluid balance changes may delineate the independent effects of AKI and fluid overload (FO), identifying unique AKI-FO phenotypes [42, 43] Recent data from both adults and children demonstrate the importance of close monitoring of urine output early in ICU course [19, 20]. Following biomarkers in a multiplicative fashion and as they change over time will likely facilitate a deeper understanding of what injury is occurring under the umbrella diagnosis of AKI and potentially the trajectory of these injuries
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