Abstract
Acute kidney injury (AKI) is a common complication in critically ill patients, and is associated with increased morbidity and mortality. Sepsis is the most common cause of AKI in the critically ill. Considerable evidence has shown that AKI can occur in the absence of overt clinical signs of shock, and in the setting of increased renal blood flow. This has challenged the traditional paradigm that renal dysfunction was solely on the basis of hypoperfusion and ischemia. Animal and human data have further shown that sepsis-induced AKI is characterized not by acute tubular necrosis, but by a paucity of apoptosis and necrosis in the context of a very bland histology, by inflammation, by microvascular dysfunction, and cellular bioenergetics adaptive responses. These novel findings suggest that other potential mechanisms centered in these three domains may help explain the pathophysiology of sepsis-induced AKI. Furthermore, the extreme functional changes seen in sepsis-induced AKI and the response of the tubular epithelial cells to inflammation and injury may be adaptive. This chapter focuses on the recent advances in this area and discusses possible therapeutic interventions that might derive from these new insights into the pathogenesis of sepsis-induced AKI.
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Acknowledgments
The authors declare no conflicts of interest. This work was funded by NIH/NHLBI grant number 1K12HL109068-02 awarded to H.G., and research grant from the German research foundation (ZA428/10-1) and Else-Kröner Fresenius Stiftung awarded to A.Z.
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Gomez, H., Zarbock, A., Murugan, R., Kellum, J.A. (2017). Sepsis-Induced AKI. In: Ward, N., Levy, M. (eds) Sepsis. Respiratory Medicine. Humana Press, Cham. https://doi.org/10.1007/978-3-319-48470-9_8
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