A unified theory of sepsis-induced acute kidney injury: inflammation, microcirculatory dysfunction, bioenergetics, and the tubular cell adaptation to injury.
Identifieur interne : 000285 ( France/Analysis ); précédent : 000284; suivant : 000286A unified theory of sepsis-induced acute kidney injury: inflammation, microcirculatory dysfunction, bioenergetics, and the tubular cell adaptation to injury.
Auteurs : Hernando Gomez [France] ; Can Ince ; Daniel De Backer ; Peter Pickkers ; Didier Payen ; John Hotchkiss ; John A. KellumSource :
- Shock (Augusta, Ga.) [ 1540-0514 ] ; 2014.
Descripteurs français
- KwdFr :
- Adaptation physiologique (physiologie), Animaux, Atteinte rénale aigüe (physiopathologie), Atteinte rénale aigüe (étiologie), Circulation rénale (physiologie), Humains, Inflammation (), Microcirculation (physiologie), Métabolisme énergétique (physiologie), Sepsie (), Sepsie (physiopathologie), Taux de filtration glomérulaire (physiologie), Tubules rénaux (physiopathologie).
- MESH :
- physiologie : Adaptation physiologique, Circulation rénale, Microcirculation, Métabolisme énergétique, Taux de filtration glomérulaire.
- physiopathologie : Atteinte rénale aigüe, Sepsie, Tubules rénaux.
- étiologie : Atteinte rénale aigüe.
- Animaux, Humains, Inflammation, Sepsie.
English descriptors
- KwdEn :
- Acute Kidney Injury (etiology), Acute Kidney Injury (physiopathology), Adaptation, Physiological (physiology), Animals, Energy Metabolism (physiology), Glomerular Filtration Rate (physiology), Humans, Inflammation (complications), Kidney Tubules (physiopathology), Microcirculation (physiology), Renal Circulation (physiology), Sepsis (complications), Sepsis (physiopathology).
- MESH :
- complications : Inflammation, Sepsis.
- etiology : Acute Kidney Injury.
- physiology : Adaptation, Physiological, Energy Metabolism, Glomerular Filtration Rate, Microcirculation, Renal Circulation.
- physiopathology : Acute Kidney Injury, Kidney Tubules, Sepsis.
- Animals, Humans.
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.
DOI: 10.1097/SHK.0000000000000052
PubMed: 24346647
Affiliations:
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pubmed:24346647Le document en format XML
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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.</div></front></TEI><affiliations><list><country><li>France</li></country><region><li>Île-de-France</li></region><settlement><li>Paris</li><li>Pittsburgh</li></settlement><orgName><li>Université de Pittsburgh</li></orgName></list><tree><noCountry><name sortKey="De Backer, Daniel" sort="De Backer, Daniel" uniqKey="De Backer D" first="Daniel" last="De Backer">Daniel De Backer</name><name sortKey="Hotchkiss, John" sort="Hotchkiss, John" uniqKey="Hotchkiss J" first="John" last="Hotchkiss">John Hotchkiss</name><name sortKey="Ince, Can" sort="Ince, Can" uniqKey="Ince C" first="Can" last="Ince">Can Ince</name><name sortKey="Kellum, John A" sort="Kellum, John A" uniqKey="Kellum J" first="John A" last="Kellum">John A. Kellum</name><name sortKey="Payen, Didier" sort="Payen, Didier" uniqKey="Payen D" first="Didier" last="Payen">Didier Payen</name><name sortKey="Pickkers, Peter" sort="Pickkers, Peter" uniqKey="Pickkers P" first="Peter" last="Pickkers">Peter Pickkers</name></noCountry><country name="France"><region name="Île-de-France"><name sortKey="Gomez, Hernando" sort="Gomez, Hernando" uniqKey="Gomez H" first="Hernando" last="Gomez">Hernando Gomez</name></region></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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