Acute kidney injury (AKI) is a common and strong problem in the diagnosis of which based on measurement of BUN and serum creatinine. These traditional methods are not sensitive and specific for the diagnosis of AKI. AKI is associated with increased morbidity and mortality in critically ill patients and a quick detection is impossible with BUN and serum creatinine. A number of serum and urinary proteins have been identified that may messenger AKI prior to a rise in BUN and serum creatinine. New biomarkers of AKI, including NGAL, KIM-1, cystatin-C, IL-18, and L-FABP, are more favourable tests than creatinine which have been identified and studied in several experimental and clinical training. This paper will discuss some of these new biomarkers and their potential as useful signs of AKI. We searched the literature using PubMed and MEDLINE with acute kidney injury, urine, and serum new biomarkers and the articles were selected only from publication types in English. 1. Introduction Acute kidney injury (AKI) remains a common and significant problem in the last decade [1]. Between 5% and 20% of critically ill patients in the intensive care unit (ICU) have an episode of AKI, with acute tubular necrosis (ATN) accounting for about 75% of cases [1–3]. Despite significant advances in both critical care and nephrology, the mortality rate of hospitalized patients with AKI has remained relatively unchanged at around 50% over the past few decades [4]. The most common causes of AKI are septic shock, ischemia, and nephrotoxins. AKI has been defined conceptually as a rapid decline in glomerular filtration rate (GFR) that occurs over hours and days. It propels to a clinical syndrome characterized by a rapid decrease in renal excretory function, with the accumulation of products of nitrogen metabolism such as creatinine and urea clinically unmeasured waste products. The described notions have led to a consensus definitions of AKI by the Acute Dialysis Quality Initiative. These RIFLE (risk, injury, failure, loss, end stage) criteria have been broadly supported with minor modifications by the acute kidney injury network (AKIN) [5, 6], and both definitions have now been validated in thousands of patients [7]. The AKIN group attempted to increase the sensitivity of the RIFLE criteria by recommending that a smaller change in serum creatinine (0.3？mg/dL) be used as a threshold to define the presence of AKI and identify patients with stage 1 AKI (RIFLE-Risk) [8]. In the AKIN classifications of AKI, a time of 48？h over which AKI occurs was proposed. However, there still remains
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