The incidence of acute kidney injury (AKI), previously referred to as acute renal failure, has reached epidemic proportions world-wide, affecting about 7% of hospitalised patients. In the critical care setting, the prevalence of AKI requiring dialysis is about 6%, with a mortality rate exceeding 60% [1, 2]. A significant increase in morbidity and mortality associated with AKI has been demonstrated in a wide variety of clinical situations, including exposure to radiocontrast dye, cardiopulmonary bypass, mechanical ventilation and sepsis. Once established, the treatment is largely supportive, at an annual cost surpassing $10 billion in the US alone.

The early diagnosis of AKI currently depends on detection of reduced kidney function by the rise in serum creatinine concentration, which is a delayed and unreliable measure in the acute setting. In general, there are several non-renal factors influencing the serum creatinine concentration such as body weight, muscle mass, race, age, gender, total body volume, drugs, muscle metabolism and protein intake.

In the face of AKI, serum creatinine is an even poorer reflection of kidney function, because the subjects are not in steady state, and serum creatinine therefore lags far behind renal injury. Furthermore, significant chronic kidney disease can exist with minimal or no change in creatinine because of renal reserve and enhanced tubular secretion of creatinine. Ironically, experimental studies have identified interventions that may prevent or treat AKI if instituted early in the disease process, well before the serum creatinine rises [2, 3]. The lack of predictive biomarkers has impaired our ability to translate these promising findings to human AKI. A troponinlike biomarker of AKI that is easily measured, unaffected by other biobiological variables and capable of both early detection and risk stratification would represent a tremendous advance in clinical medicine [4].

The search for AKI biomarkers is an area of intense contemporary research. Conventional urinary biomarkers such as casts and fractional excretion of sodium are insensitive and non-specific for the early recognition of AKI. Other traditional urinary biomarkers such as filtered high molecular weight proteins and tubular proteins or enzymes have also suffered from lack of specificity and dearth of standardised assays. Fortunately, the application of innovative technologies such as functional genomics and proteomics to human and animal models of AKI has uncovered several novel genes and gene products that are emerging as biomarkers. The most promising of these are listed in Table 1, and detailed in this article (Please, download the .pdf version of the article on the right hand side)