Abstract
Sepsis is a common and important cause of mortality in critically ill patients. Acute kidney injury (AKI) is one of the most important factors determining morbidity and mortality in this clinical picture. Recent studies have indicated that the pathogenetic mechanism in septic acute kidney injury (AKI) is totally different from that in non-septic AKI. Our understanding of sepsis-associated AKI pathophysiology is shifting from renal vasoconstriction, ischemia, and acute tubular necrosis to that of heterogeneous vasodilation, hyperemia, and acute tubular apoptosis.
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