• Mark D Okusa.
• Division of Nephrology and the Center for Immunity, Inflammation and Regenerative Medicine, University of Virginia, Charlottesville, VA 22908, USA. mdo7y@virginia.edu
• Contrib Nephrol. 2010 Jan 1;165:153-8.

AbstractAcute kidney injury (AKI) is frequently encountered in the intensive care unit, and from its inception, morbidity and mortality increase in these patients compared to those without AKI. Despite numerous clinical trials and newer pharmacological agents, very little progress has been made to reduce the deaths that occur in this population. An important emerging concept is that AKI does not occur in isolation and it frequently involves other organs. Clinical conditions such as shock, trauma, and sepsis lead to an increase in fluid volume, cytokines/chemokines, uremic toxins and other soluble mediators that are known to affect distant organs. This critical loss of balance of these mediators appears to be due both to a reduction in clearance and increase in production as demonstrated by experimental studies of bilateral nephrectomy and ischemia-reperfusion, respectively. The evidence and mechanisms for distant organ injury following AKI will be discussed.2010 S. Karger AG, Basel.

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