AKI assessment
Although AKI is defined in terms of changes in serum creatinine from baseline, as well as the less-frequently measured urine output, these measures, particularly serum creatinine, are inadequate in the acute situation. Much recent research has led to the quest for novel biomarkers as an acute assessment of renal function at the onset of AKI. Indeed, biomarkers are now available in some areas of clinical practice, which are able to better predict the severity of AKI, particularly when associated with sepsis.7 The most promising of these are plasma and urinary neutrophil gelatinase-associated lipocalin and urinary interleukin (IL)-18 and kidney injury molecule-1.8,9 These biomarkers are proteins that are upregulated in response to renal injury. Cystatin-C, a functional marker, was also a promising plasma marker, although one study of 327 patients demonstrated no signal for SA-AKI.10
Sepsis assessment
As with AKI, there is a uniform approach to the definition of sepsis. The American College of Chest Physicians and the Society of Critical Care Medicine joint statement defines sepsis and severe sepsis.11 This requires the presence of infection together with systemic manifestations, whilst severe sepsis is sepsis with sepsis-induced organ dysfunction and/or tissue hypoperfusion