Research status of pathophysiological mechanisms and biomarkers of sepsis-associated acute kidney injury
Abstract
Sepsis is a life-threatening condition triggered by infection. According to the 45th Critical Care Medicine Sepsis 3.0 criteria, sepsis is defined as a life-threatening organ dysfunction caused by a dysregulated immune response to infection. Renal injury is a common manifestation of organ dysfunction in this setting. Acute kidney injury (AKI) that develops within seven days of a sepsis diagnosis is classified as sepsis-associated acute kidney injury (SA-AKI). Earlier studies proposed that renal damage during sepsis was primarily attributed to insufficient renal blood flow. However, more recent experimental and clinical evidence suggests that renal blood flow often remains stable or even increases during sepsis. As a result, reduced renal blood flow is no longer considered the primary mechanism underlying AKI. Current research efforts are increasingly focused on elucidating the roles of immune dysregulation, inflammatory cascades, coagulation abnormalities, and metabolic reprogramming in the pathogenesis of sepsis. The identification of novel kidney stress and injury biomarkers has also advanced risk prediction and early diagnosis of acute kidney injury in the context of sepsis. This paper primarily reviews the pathophysiological mechanisms and early diagnostic biomarkers of sepsis-associated acute kidney injury from a cellular perspective, aiming to enhance clinicians’ understanding of this condition and improve patient outcomes.
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