• Adam Romanovsky, Catherine Morgan, and Sean M Bagshaw.
• Division of Critical Care Medicine, Faculty of Medicine and Dentistry, University of Alberta, 8440-122 Street, 3C1.12 Walter C. Mackenzie Centre, Edmonton, AB, T6G2B7, Canada.
• Pediatr. Nephrol. 2014 Jan 1;29(1):1-12.

AbstractAcute kidney injury (AKI) is a commonly encountered complication in critically ill children and portends a worse prognosis. Sepsis-induced AKI (SAKI) is a leading contributor to AKI in children and significantly modifies the risk for less favorable outcome. It has increasingly become clear that SAKI represents a unique and distinct cause of AKI. Studies focused on renal hemodynamics, bioenergetics, and immune-mediated injury have provided further insights into the pathobiology of SAKI; however, many of the nuanced mechanisms remain incompletely understood. Although there have been numerous strategies evaluated for the prevention and management of SAKI, no specific intervention has proven unequivocally efficacious. Currently, the mainstays for managing SAKI focus on alleviating ongoing kidney damage by optimizing systemic and kidney hemodynamic support, avoiding nephrotoxins, and mitigating the anticipated complications of kidney failure. The timely referral for renal support to manage azotemia, metabolic derangements, and fluid accumulation remains critical for this population. The extracorporeal removal of inflammatory mediators has shown some potential benefit in limiting systemic and kidney immune-mediated injury; however, the precise role of these technologies in the management of SAKI has yet to be defined.

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