• Ilaria Umbro, Giuseppe Gentile, Francesca Tinti, Paolo Muiesan, and Anna Paola Mitterhofer.
• The Liver Unit, Queen Elizabeth Hospital Birmingham, Mindelsohn Way, Edgbaston, B15 2GW Birmingham, United Kingdom; Department of Clinical Medicine, Nephrology and Dialysis B, Sapienza University of Rome, Viale dell'Università 37, 00185 Rome, Italy. Electronic address: ilaria.umbro@hotmail.it.
• J. Infect. 2016 Feb 1; 72 (2): 131-42.

AbstractSepsis is a complex clinical syndrome characterized by a systemic inflammatory response to an infective insult. This process often leads to widespread tissue injury and multiple organ dysfunction. In particular, the development of acute kidney injury (AKI) is one of the most frequent complications, which increases the complexity and cost of care, and is an independent risk factor for mortality. Previous suggestions highlighting systemic hypotension, renal vasoconstriction and ischaemia-reperfusion injury as the primary pathophysiological mechanisms involved in sepsis-induced AKI have been challenged. Recently it has been shown that sepsis-induced AKI occurs in the setting of microvascular dysfunction with release of microparticles, inflammation and energetic adaptation of highly metabolic organs to cellular stress. The intolerable high mortality rate associated with sepsis-induced AKI is partially explained by an incomplete understanding of its pathophysiology and a delay in diagnosis. The aim of this review is to focus on advances in understanding the sepsis pathophysiology, with particular attention to the fundamental mechanisms of sepsis-induced AKI and the potential diagnostic and prognostic markers involved. Copyright © 2015 The British Infection Association. Published by Elsevier Ltd. All rights reserved.

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