**1. Introduction**

172 Basic Nephrology and Acute Kidney Injury

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Yuan HT, Libermann TA, Stillman IE, Roberts D, D'Amore PA, Epstein FH, Sellke FW, Romero R, Sukhatme VP, Letarte M, Karumanchi SA. (2006). "Soluble endoglin Acute kidney injury (AKI), impairment of kidney function requires special attention in intensive care unit's (ICU), because if multiorgan failure affect the kidney, it carries a greater risk for worse outcome and furthermore survivors have higher risk then normal population for chronic renal failure. It was reported that they also have higher mortality and morbidity rates compared to normal population (Kellum, 2008 & Shiffle, 2006).

Acute tubular necrosis (ATN) is the primary causes of AKI in hospital and ICU and sepsis, ischemic or toxic insults were reported as the most common reason for ATN. The rates of AKI have been reported in hospitalized patients to be between 3.2%-20% and in ICUs this rate rises up to 22% and even to 67% depending on the population studied and the definition used (Murugan 2011). Based on the administrative data, the incidence of severe AKI (defined requiring dialysis) from 1988 to2002 has increased from 4 to 27 per 100000 population. But fortunately in hospital mortality, has decreased from 41.3 to28 % (p<0.001) (Waikar, 2008). Likewise a progressive 2.8% annual increase in incidence of AKI and progressive 3.8% annual decrease in AKI associated mortality(95%CI:-4.7 to-2.12:p<0.001) was observed from 1996-2005 in a large database in Australia and New Zealand (Pisoni, 2008&Bagshaw, 2007). Despite the fact that mortality might be decreasing in ICU patients with AKI, it is still high and reported to be up to 43-88%. Mortality rate becomes even higher when patients require renal replacement therapy (Kellum, 2008).

Interestingly, it was reported that irreversible AKI requiring chronic dialysis therapy increased from 3.7% in 1984 to 18.2% in 1995 in surviving patients. Even higher number of patients (33-68%) at discharge whose kidney failed to recover and who needed long term dialysis. This changing renal outcome in the survivors of ICU acquired AKI cases might be related to increasing number of older patients, several co morbid conditions, more severe AKI cases than before and in addition, complication of the more aggressive renal replacement therapies currently used (Shiffle, 2006).

Since AKI in critical ill patients have high mortality rate and even if patients survive, they are at risk for End Stage Renal Disease (ESRD) and higher mortality than the normal population, it is important to recognize the clinical picture of AKI and to institute prevention as early as possible. Thus, physician should be alarmed and be ready for early intervention in this particular group of patients. With the introduction of the RIFLE

Evaluation of Acute Kidney Injury in Intensive Care Unit 175

1.5-fold OR GFR decrease >25% from baseline

2.0-fold OR GFR decrease >50% from baseline

3.0-fold OR GFR decrease >75% from baseline OR serum creatine ≥354µmol/l (≥4mg/dl)with an acute increase of at least 44µmol/l

26.5 µmol/l (0.3mg/dl) OR increase to 1.5-2.0-fold from

2.0-3.0 fold from baseline

>3.0-fold from baseline OR serum creatine ≥354µmol/l (≥4.0mg/dl) with an acute increase of at least 44µmol/l (0.5mg/dl) OR need for RRT

interval for the diagnosis of AKI was introduced to ensure that the process is acute. Unlike RIFLE, in AKIN criteria there has been an attempt to resolve some easily reversible causes of azotemia (for example, volume depletion and urinary obstruction). AKIN criteria declare that diagnosis based on the urine criterion alone will require exclusion of urinary tract

*Determination of baseline renal function:* Since AKI was defined as rapid decline in renal function from baseline levels, it is important how to measure baseline renal function. The baseline serum creatinine level has been recommended for use as a marker to reflect the renal function. The baseline serum creatinine value has been estimated in various ways, such as the serum creatinine level on hospital admission, the minimum creatinine level during the hospital stay, the serum creatinine value estimated from the MDRD calculation (assuming estimated GFR=75ml/min/1,73m2) or the lowest value among these (Ricci,

(0.5mg/dl)

baseline

obstructions and other easily reversible causes of decreased urine output.

**Risk** Serum creatine increase to

**Injury** Serum creatine increase to

**Failure** Serum creatine increase to

**1** Serum creatine increase ≥

**2** Serum creatine increase ≥

**3** Serum creatine increase

Table 1. Two definitions of AKI

*RIFLE class* 

*AKIN Stage* 

**Serum Creatine Criteria Urine output criteria** 

<0.5ml/kg/h for 6h

<0.5ml/kg/h for 12h

Anuria for 12h

<0.5ml/kg/h for 6h

<0.5ml/kg/h for 12h

RRT

<0.3ml/kg/h for 24h OR anuria for 12h OR need for

classification for the definition of AKI, the viewpoint of this subject has changed and now it is possible to be aware of patients with high risk for AKI(Bellomo 2004). Nevertheless recently several biomarkers have been introduced to diagnose AKI even before creatinine starts to increase(Waiker, 2008).

In this review, new perspective and favorable improvement of this subject will be discussed; furthermore definition, epidemiology, risk factors, biomarkers of AKI will be evaluated.
