• Hernando Gomez, Can Ince, Daniel De Backer, Peter Pickkers, Didier Payen, John Hotchkiss, and John A Kellum.
• *The Center for Critical Care Nephrology and †The CRISMA Laboratory (Clinical Research, Investigation, and Systems Modeling of Acute Illness), Department of Critical Care Medicine, University of Pittsburgh, Pittsburgh, Pennsylvania; ‡Department of Intensive Care Adults, Erasmus MC University Medical Centre Rotterdam, Rotterdam, the Netherlands; §Department of Intensive Care, Erasme University Hospital, Universite Libre de Bruxelles, Brussels, Belgium; ∥Departments of Intensive Care Medicine and Nijmegen Institute for Infection, Inflammation, and Immunity (N4i), Radboud University Nijmegen Medical Centre, Nijmegen, the Netherlands; and ¶Department of Anesthesiology and Critical Care, Lariboisière Hospital, Assistance Publique-Hôpitaux de Paris, and University Paris 7 Denis Diderot, Sorbonne Paris Cité, Paris, France.
• Shock. 2014 Jan 1; 41 (1): 3113-11.

AbstractGiven that the leading clinical conditions associated with acute kidney injury (AKI), namely, sepsis, major surgery, heart failure, and hypovolemia, are all associated with shock, it is tempting to attribute all AKI to ischemia on the basis of macrohemodynamic changes. However, an increasing body of evidence has suggested that in many patients, AKI can occur in the absence of overt signs of global renal hypoperfusion. Indeed, sepsis-induced AKI can occur in the setting of normal or even increased renal blood flow. Accordingly, renal injury may not be entirely explained solely on the basis of the classic paradigm of hypoperfusion, and thus other mechanisms must come into play. Herein, we put forward a "unifying theory" to explain the interplay between inflammation and oxidative stress, microvascular dysfunction, and the adaptive response of the tubular epithelial cell to the septic insult. We propose that this response is mostly adaptive in origin, that it is driven by mitochondria, and that it ultimately results in and explains the clinical phenotype of sepsis-induced AKI.

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