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Management of acute kidney injury during critical illness - what is on the horizon?

DOI:10.1097/MCC.0000000000000780 Over the past decade, the pace of acute kidney injury (AKI) research and innovation has accelerated. Although much of the 2012 Kidney Disease: Improving Global Outcomes (KDIGO) AKIguideline remains state of the art [1], our understanding of the pathophysiology of AKI has improved and new tools to diagnose and manage AKI have been developed, in particular new biomarkers, improved imaging and monitoring techniques, new decision-support programs and the application of artificial intelligence. Furthermore, many promising drugs and compounds are entering clinical trials. As a result, new opportunities for prevention, early intervention and personalized management are on the horizon. AKI is a heterogeneous disease with multiple different subphenotypes and variable outcomes [2–4]. Patients who survive AKI face an increased risk of chronic kidney disease, premature long-term dialysis and increased mortality but not everyone with AKI has a poor outcome. To date, most clinical trials examining pharmacotherapy, novelbiologics and intensity of renal replacement therapy (RRT) have been negative. One postulated reason for this dearth of positive trials is the delay in diagnosing and monitoring AKI due to a reliance on serum creatinine and urine output [5]. Another contributing factor is our approach of treating AKI as a single entity without differentiating between different causes and subtypes. The discovery of new kidney biomarkers has not only improved our understanding of the pathophysiology of AKI and allowed an earlier diagnosis of AKI, biomarkers have also identified high-risk patients and AKI subtypes and provided opportunities for biomarker-guided management [6,7]. Current evidence supports the utilization of new biomarkers in routine clinical practice but substantial gaps in knowledge remain [8–11,30]. Determining the cause and sub-type of AKI is also essential for future clinical trials. As an example, Bhatraju et al. identified two molecularly distinct subphenotypes of AKI with different clinical outcomes and responses to vasopressin [2]. Not surprisingly, experts have called for a revision of the KDIGO AKI consensus definition and suggested to incorporate cause, pathophysiology and potentially new kidney biomarkers [12].