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Etiology and Pathophysiology of Acute Kidney Injury

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Abstract

Acute kidney injury (AKI) is estimated to complicate around 5 % of critical care admissions [1]. AKI frequently occurs in the context of multiple organ failure and entails mortality rates in excess of 40 % despite appropriate therapy [1]. Etiologies for AKI are varied and multiple factors often coexist in critically ill patients. While sepsis and nephrotoxin exposure are major risk factors for AKI in the ICU, direct ischemia/reperfusion (I/R) injury may also play a role, especially in hypovolemic and cardiogenic shock. It seems likely that most patients develop AKI as a result of multiple risk factors [2]. Despite these diverse causes, the ultimate presentation of established AKI is relatively uniform, with renal tubular injury mediating a decline in glomerular filtration rate and in the most severe cases oliguric renal failure. This chapter focuses on the causes and pathophysiology of AKI in critical illness. For clarity we separately discuss AKI etiologies, although it should be reemphasized that in the real world these mechanisms often coexist [3–5].

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de Pont, AC.J.M., Prowle, J.R., Legrand, M., Groeneveld, A.B.J. (2015). Etiology and Pathophysiology of Acute Kidney Injury. In: Oudemans-van Straaten, H., Forni, L., Groeneveld, A., Bagshaw, S., Joannidis, M. (eds) Acute Nephrology for the Critical Care Physician. Springer, Cham. https://doi.org/10.1007/978-3-319-17389-4_4

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