Biomarkers of acute kidney injury: Can we replace serum creatinine?

Acute kidney injury (AKI) is frequent in hospitalized critically ill patients and mortality associated with AKI is largely unchanged over many decades. The new nomenclature, AKI, reflects the entire spectrum of acute renal failure, recognizing that an acute decline in kidney function can be secondary to an injury that causes functional or structural changes in the kidneys [Mehta et al. 2007]. An abrupt change in serum creatinine level has been the primary method for diagnosing AKI for nearly 60 years despite its well recognized limitations [Addis et al. 1947, Barrett and Addis 1947, Fisher and Wilhelmi 1937, Star 1998]. These limitations are mainly related to the delayed diagnosis of AKI associated with delayed rise in serum creatinine and the lack of specificity and sensitivity associated with small changes in serum creatinine. It is believed that these limitations associated with diagnosis of AKI have prevented progress by interfering with the design of clinical trials for newer therapies. It is now widely believed that the availability of accurate and objective early biomarkers of AKI will stimulate progress in the development of early interventions in AKI. Recognition of this concept has led to a surge in preclinical, translational and clinical research for discovery and validation of biomarkers in AKI. In this review we will discuss the role of biomarkers in AKI and the promising biomarkers on the horizons.