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HERO ID
2839411
Reference Type
Journal Article
Title
Sepsis-induced acute kidney injury revisited: pathophysiology, prevention and future therapies
Author(s)
Zarbock, A; Gomez, H; Kellum, JA
Year
2014
Is Peer Reviewed?
0
Journal
Current Opinion in Critical Care
ISSN:
1070-5295
EISSN:
1531-7072
Volume
20
Issue
6
Page Numbers
588-595
PMID
25320909
DOI
10.1097/MCC.0000000000000153
Web of Science Id
WOS:000344529000002
Abstract
Purpose of review
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. Considerable evidence now suggests that the pathogenic mechanisms of sepsis-induced AKI are different from those seen in other causes of AKI. This review 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.
Recent findings
The traditional paradigm that sepsis-induced AKI arises from ischemia has been challenged by recent evidence that total renal blood flow in is not universally impaired during sepsis, and AKI can develop in the presence of normal or even increased renal blood flow. Animal and human studies suggest that adaptive responses of tubular epithelial cells to injurious signals are responsible for renal dysfunction. Simultaneously occurring renal inflammation and microcirculatory dysfunction further amplify these mechanisms.
Summary
An understanding of the pathologic mechanisms of sepsis-induced AKI emphasizes the important role of maladaptive responses to the septic insult. Preventive and therapeutic measures should be based on counteracting these maladaptive responses of tubular epithelial cells, inflammation, and microvascular dysfunction.
Keywords
acute kidney injury; inflammation; microvascular dysfunction; sepsis; tubular epithelial cells
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