الفهرس 
Acute Kidney InjuryOnly 14 pages are availabe for public view
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Abstract
In 2002, the Acute Dialysis Quality Initiative (ADQI)
group proposed a standard definition and classification system
for the syndrome of acute renal failure through a broad
consensus of experts across disciplines and international
boundaries. The classification system coins the acronym RIFLE
and has three levels: Risk, Injury, and Failure; and two
outcomes: persistent acute renal failure (termed Loss) and End
stage kidney disease (Uchino et al., 2006). Classically, the
causes of AKI have been subdivided into three groups: prerenal,
intrinsic, and post renal. While there is considerable overlap
between these, especially the first two, it remains a useful
clinical guide
Current diagnostic paradigms for AKI are limited by
reliance on serum creatinine, which is affected by age, gender
and muscle mass. In addition, elevations in serum creatinine
may occur several days after the actual injury. The search for
AKI biomarkers has focused on identifying alternatives to
serum creatinine. Urinary neutrophil gelatinase associated
lipocalin (NGAL) and interleukin-18 may provide insights into
the cause of AKI 9 (Nickolas et al., 2008). Similarly, urinary
and serum NGAL, serum cystatin C and urinary kidney injury
molecule-1 (KIM-1) may facilitate the early diagnosis of AKI.
KIM-1 also shows promise in predicting adverse events in
patients with established AKI (Liangos et al., 2007). Ongoing
studies are clarifying the role of these biomarkers in larger
patient cohorts. Ultimately, it will need to be shown that