Understanding acute kidney injury in sepsis

Excerpt

Acute kidney injury (AKI) affects approximately 40 % of critically ill patients [1] using the latest clinical Kidney Diseases: Improving Global Outcomes (KDIGO) criteria based on both serum creatinine and urine output [2]. The impact of AKI on outcome is substantial. One-third of critically ill patients with AKI die before day 90 [1], and the attributable excess 90-day mortality is approximately 10 %. Septic AKI accounts for approximately half of all AKI cases in the critically ill patients [3]. Yet, the pathophysiology of septic AKI is still inadequately understood. Previous suggestions highlighting systemic hypotension, renal vasoconstriction, and ischemia–reperfusion injury as the major mechanisms for septic AKI have been challenged by reproducible experimental large animal models. Such models show that septic AKI occurs in the setting of renal vasodilatation and increased renal blood flow (RBF) [4]. Thus, pathophysiological mechanisms which differ from the traditional “ischemia paradigm” may instead be responsible for septic AKI. Recently proposed mechanisms for the loss of glomerular filtration rate (GFR) seen in septic AKI comprise dominant efferent arteriole dilatation (compared to afferent arteriole) and subsequent decrease in glomerular filtration pressure (“intraglomerular hypotension”), intra-renal hemodynamic alterations (periglomerular shunting), excessive inflammatory activation, or any combination of the above factors (Fig. 1).

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