الفهرس 
2. Definition and epidemiology of acute kidney injury in the critically illOnly 14 pages are availabe for public view
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Abstract
AKI is a clinical syndrome characterized by an abrupt decline in renal function resulting from inability to excrete metabolic wastes and maintain proper fluid and electrolyte balance.
In 2004, RIFLE definition of AKI was increase serum creatinine≥50% from baseline. Recommended to use MDRD with eGFR of 75-100 ml/min/1.73m² to estimate baseline creatinine when missing.
In 2006, AKIN definition offered a revised definition of AKI. Increase serum creatinine ≥0.3 mg/dl (26.4 umol/l) or ≥50% within 48 hours. No baseline needed, but two measures within 48 hours needed.
In 2012, the recent KDIGO definition is a combination of AKIN and RIFLE. It defined by a ≥ 0.3 mg/dl increase in creatinine within 48 hours, or ≥ 50% above baseline within 7 days.
The incidence of AKI in critically ill patients has risen during the past decade due to increased acuity as well as increased recognition. Following recent standards, overall incidence ranges from 20% to 50% but, current rates are dependent on the specific ICU population under study, with lower rates for scheduled surgery and higher rates in septic patients.
New biomarkers hold the promise of allowing clinicians to detect kidney injury earlier, to guide future therapy, and to better prognosticate of AKI, differential diagnosis of AKI.
The novel serum markers under investigation include cystatin C and neutrophil gelatinase associated lipocalin (NGAL), the urinary markers include cystatin C, NGAL, KIM-1, IL-18, N-acetyl-β-D-glucosaminidase (NAG), The sodium/hydrogen exchanger isoform 3 (NHE3) protein, Liver fatty acid binding protein (L-FABP).
Cystatin C is a nonglycosylated 13 kDa basic protein produced by all nucleated cells in the body, belonging to cysteine-proteinase inhibitors superfamily.
Cystatin C is a better predictor of true GFR than creatinine in diverse populations including patients of diabetics and kidney transplant patients which have fueled interest in using cystatin C as a biomarker of AKI.
plasma cystatin C levels increase 1–2 days before plasma creatinine in patients developing AKI in a variety of settings, including radiocontrast nephropathy and AKI in critically ill patients.
Cystatin C is excreted by glomerular filtration, then undergoes essentially complete tubular reabsorption (by proximal collecting tubule) and catabolism (without secretion), so that it is not normally found in urine in significant amounts, but urinary levels increase in the context of acute tubular injury.
Urinary cystatin C has better predictive ability for need of RRT than several other urinary biomarkers.
Reference range of cystatin C is 0.7 – 1.21 mg/L in adults 20 – 50 years of age.
This systematic review showed that cystatin C is a sensitive marker in predicting AKI in the critically ill as it preced the rise in serum creatinine concentration by 1-2 days, and the utility of NGAL may be limited by its lack of specificity.