The Pathogenesis of Acute Kidney Injury
نویسندگان
چکیده
Acute kidney injury (AKI) is common in critically ill patients affecting 20 60% of patients (Chertow, et al., 2005; de Mendonca, et al., 2000; Mehta, et al., 2005; Ostermann & Chang, 2008; Silvester, et al., 2001; Uchino, et al., 2005). The exact incidence varies depending on patient population, associated comorbid factors and criteria used to define AKI. Sepsis induced AKI accounts for approximately 50% of cases and AKI is commonly a manifestation of multiple organ dysfunction (Chertow, et al., 2005; de Mendonca, et al., 2000; Mehta, et al., 2005; Ostermann & Chang, 2008; Silvester, et al., 2001; Uchino, et al., 2005). Many patients with AKI have a mixed aetiology where the presence of sepsis, ischaemia and nephrotoxicity co-exist. Current management of AKI is supportive, ensuring adequate perfusion pressures, correction of fluid depletion, avoidance of nephrotoxins and when required institution of renal replacement therapy (RRT). Despite the widespread use of RRT in the intensive care unit (ICU), AKI is associated with an associated mortality risk of 40 – 90% depending on patient population (Chertow, et al., 2005; Ostermann & Chang, 2008; Silvester, et al., 2001). Furthermore, evidence has emerged that AKI survivors have an increased risk of chronic kidney disease, long-term dialysis, increased mortality and reduced quality of life (Johansen, et al., 2010; Lo, et al., 2009; Lopes, et al., 2010; Wald, et al., 2009). AKI is no longer viewed as a reversible bystander of critical illness but a significant contributor to short and long-term morbidity and mortality.
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