A Unified Theory of Sepsis-Induced Acute Kidney Injury: Inflammation, Microcirculatory Dysfunction, Bioenergetics, and the Tubular Cell Adaptation to Injury
Year: 2013
Type: review
Abstract: Given 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.
Source: Shock
Institutions: Université Libre de Bruxelles, Radboud University Nijmegen, University of Pittsburgh, Erasmus MC, Erasmus Hospital, Radboud University Medical Center, Assistance Publique – Hôpitaux de Paris, Université Paris Diderot, Erasmus University Rotterdam, Sorbonne Paris Cité, Hôpital Lariboisière
Language: English
Topic: Acute Kidney Injury Research
Subfield: Nephrology
Field: Medicine
Domain: Health Sciences
Open Access status: green
OpenAlex ID: W2000167232