A Unified Theory of Sepsis-Induced Acute Kidney Injury: Inflammation, microcirculatory dysfunction, bioenergetics and the tubular cell adaptation to injury
By H. Gómez, Can Ince, D. De Backer, P. Pickkers, D. Payen, J. Hotchkiss, John A. Kellum. Shock, 2014
729 citations recorded by the source corpus.
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.
Subfields: Critical Care and Intensive Care Medicine, Epidemiology, Nephrology
View Paper: https://www.semanticscholar.org/paper/5d1cff97728ec20390cf0750d0916b69369488f1
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In Critical Care and Intensive Care Medicine
In Epidemiology
Citations in the corpus
- Systemic inflammation in decompensated cirrhosis: Characterization and role in acute‐on‐chronic liver failure (2016, neutral): “TNFa (pg/mL) 9 (7-12) 20 (14-27) 29 (17-41) <0.”
- Cirrhosis-associated immune dysfunction: distinctive features and clinical relevance. (2014, background): “…the oxidative stress that results from the organized interaction between PAMPs/ DAMPs and the tubular epithelial cell can hurt tubular function and cause acute kidney injury in patients with severe bacterial infection or even sepsis in the absence of overt signs of renal hypoperfusion [132,133].”
- Sepsis: current dogma and new perspectives. (2014, background): “…comes at the expense of systemic homeostasis, because individual cells regress to function like unicellular organisms— maintaining intracellular homeostasis but no longer performing their specialized function that is critical for interorgan homeostatic stability (Buchman, 2002; Gomez et al., 2014).”