Abstract
Acute kidney injury (AKI) is a common complication in hospitalized patients, mainly during critical illness. Patients affected by AKI usually require admission to the intensive care unit (ICU) and are typically burdened by longer ICU and in-hospital lengths of stay as well as worse short- and long-term outcomes.
A more accurate understanding of the pathophysiology of AKI is essential to develop new clinical tools for earlier diagnosis, monitoring, treatment and follow up of this syndrome and thus to improve clinical practice and the outcome of AKI patients. The definition, diagnosis and staging of AKI is currently obtained through the application of indices based on the glomerular filtration rate (GFR), such as serum creatinine and/or urinary output. In 2004, the Acute Dialysis Quality Initiative (ADQI) attempted to standardize AKI definition, summarizing different stages of severity and outcome into the RIFLE (an acronym indicating different severity classes: Risk, Injury, Failure, Loss of Function and End Stage kidney Disease) classification. In 2007, the Acute Kidney Injury Network (AKIN) modified this classification, suggesting the use of smaller variation in serum creatinine in order to earlier identify AKI. These classifications were finally summarized in 2012 into the KDIGO (Kidney Disease Improving Global Outcomes) classification. All these clinical classifications are based on alteration of serum creatinine and/or urinary output in order to identify an acute reduction of the GFR [1].
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Ricci, Z., Villa, G., Ronco, C. (2015). Management of AKI: The Role of Biomarkers. In: Vincent, JL. (eds) Annual Update in Intensive Care and Emergency Medicine 2015. Annual Update in Intensive Care and Emergency Medicine 2015, vol 2015. Springer, Cham. https://doi.org/10.1007/978-3-319-13761-2_26
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DOI: https://doi.org/10.1007/978-3-319-13761-2_26
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