Changing Paradigms in Acute Kidney Injury: From Mechanisms to Management

cium (Ca 2+ )-permeable cation channel of the transient receptor potential melastatin 2, and iron in mediating oxidative stress in AKI were discussed. New targets for intervention were described including autophagy, sphingolipid signaling, macrophage, complement and tubular transport mechanisms [1–6]. A major theme was to explore the contributors to progression of AKI to chronic kidney disease, and speakers provided elegant overviews of the experimental evidence and molecular mechanisms that are in play [7, 8]. Although it has been difficult to translate findings from experimental models to human interventions, several topics focused on translational research applied to clinical care demonstrating that the field is promising for AKI. Advances in understanding the role of micro-RNA regulation of injury and repair pathways [4], organ crosstalk and lipid pathways were discussed. Knowledge obtained from pre-clinical models is now being applied to Recent advances in the field of acute kidney injury (AKI) have provided key insights into understanding the mechanisms and pathways of AKI and its effects on other organs. Biomarkers have been identified that have provided new tools and techniques to characterize this disorder and facilitate point-of-care testing. Multiple underlying mechanisms contribute to the pathophysiology of AKI including genetic and epigenetic modifications, environmental influences and, more importantly, inherent mechanisms within the kidney offer challenging perspectives for clinical and translational research. This issue summarizes proceedings from the 6th University of Alabama at Birmingham (UAB)-University of California San Diego (UCSD) O’Brien Core Center for AKI Research symposium held during the 21st Annual Continuous Renal Replacement Therapy meeting in San Diego, California, USA, on Tuesday, February 16, 2016. The overall goal of this symposium was to provide a review of the most recent developments in the field and describe emerging knowledge from basic and translational research. The meeting included 21 experts invited from around the world and over 100 participants were in attendance. Symposia sessions focused on defining key molecules and mechanisms involved in the pathogenesis and repair from AKI. The role of the non-selective, calReceived: May 27, 2016 Accepted: June 15, 2016 Published online: September 7, 2016