Abstract

Development of acute renal failure during sepsis syndrome is common and portends a poor outcome. The interplay between systemic host responses, local insults in the kidney, vascular bed, and immune system, all play a role in the development of sepsis-induced acute renal failure. Despite advances in critical care, mortality rates have remained high for sepsis-associated acute renal failure. This may be, in part, a function of our poor understanding of the mechanisms of sepsis-induced acute renal failure, leading to misguided management strategies for acute renal failure. Improved understanding of various emerging mechanisms of sepsis-induced acute renal failure such as epithelial barrier dysfunction, apoptosis, and cytokine-mediated injury, should open newer avenues of therapeutic targets in this field. As has often been the case in the study of sepsis, simple universal mechanisms such as tissue perfusion, have failed to explain the diverse and complex clinical response, and therapeutic strategies aimed at single mechanisms have not been successful. The pathophysiologic mechanisms now understood to be operative in sepsis-induced acute renal failure overlap and interact at many levels. Therefore, therapeutic strategies to prevent acute renal failure or to facilitate recovery will likely need to be multifaceted.

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