Abstract
Both severe infection and acute kidney injury (AKI) have a high, and rising incidence in critically ill patients admitted to the intensive care unit (ICU), and are associated with increased in-hospital mortality. Septic AKI patients are more severely ill compared to non-septic AKI patients and have worse outcome. Severe infection is a major cause of AKI in ICU patients, while conversely, AKI patients are at increased risk for infection. The dogma from the past relates the development of AKI in sepsis patients to decreased renal blood flow. However, current data suggest that there is no impairment of renal blood flow in patients with sepsis. The pathogenesis of AKI in sepsis is probably related to cyto-toxic effects of inflammation, and impaired microcirculation. In addition, hyperglycaemia, and antimicrobial agent-induced drug nephrotoxicity may contribute to the development of AKI. On the other hand, AKI patients are at greater risk for infection as a result of volume overload, dialysis catheter insertion and secondary manipulation, inflammation of the kidneys leading to ‘organ cross talk’, and impaired host immunity.
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