Acute kidney injury (AKI) is a common complication of critical illness and is associated with significant morbidity, mortality, and financial cost. Sepsis is the leading association of acute kidney injury in the intensive care unit and is implicated in more than half the cases. Our understanding of the pathogenesis of sepsis-associated acute kidney injury continues to evolve. Current evidence suggests that pathways involving inflammatory injury to the renal tubules and microcirculation play a leading role in the development of the acute kidney injury syndrome, and these mechanisms may be dissociated from sepsis-induced changes in systemic hemodynamics.

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