Traditional diagnosis of acute kidney injury (AKI) depends on detection of oliguria and rise of serum creatinine level, which is an unreliable and delayed marker of kidney damage. Delayed diagnosis of AKI in the critically ill patient is related to increased morbidity and mortality, prolonged length of stay, and cost escalation. The discovery of a reliable biomarker for early diagnosis of AKI would be very helpful in facilitating early intervention, evaluating the effectiveness of therapy, and eventually reducing cost and improving outcome. Innovative technologies such as genomics and proteomics have contributed to the discovery of new biomarkers, such as neutrophil gelatinase-associated lipocalin (NGAL), cystatin C (Cys C), kidney injury molecule-1 (KIM-1), interleukin-18 (IL-18), and liver-type fatty acid binding protein (L-FABP). The current status of the most promising of these novel AKI biomarkers, including NGAL, Cys C, KIM-1, L-FABP, and IL-18, is reviewed. 1. Introduction Acute kidney injury is a heterogeneous process, defined by the Acute Kidney Injury Network (AKIN) as “functional and structural disorder or signs of renal damage including any defect from blood and urine test, or tissue imaging that is less than 3 months”. AKI is usually classified into three broad categories as follows: (a) prerenal—an adaptive response to severe volume depletion and/or hypotension, with structurally intact nephrons—it is a functional damage that represents the most common form of kidney injury but can lead to intrinsic AKI if it is not promptly corrected; (b) intrinsic—structural injury in the kidney, which is the hallmark of intrinsic AKI—the most common form of intrinsic injury is acute tubular necrosis (ATN), either due to ischemic, inflammatory, or cytotoxic insults; and (c) postrenal—from mechanical obstruction of the urinary collecting system, including the renal pelvis, ureters, bladder, or urethra [1]. “RIFLE” (Risk, Injury, Failure, Loss, and End-Stage Kidney Disease) and AKIN criteria are the most frequently used scoring systems [1, 2]. Therapeutic interventions have failed to reduce morbidity and mortality, largely due to the heterogeneity of the process, the incomplete understanding of AKI pathogenesis, and therefore the delayed diagnosis and implementation of the various procedures. The reliance on conventional biomarkers such as urea and creatinine explains the time frame between the occurrence and detection of the disease process [3]. AKI biomarkers can be components of serum or urine. The term biomarker (acronym for biological marker) was
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