At present, various biomarkers of acute renal failure are established. These biomarkers can be detected in urine or blood and signify structural damage to the kidney. Clinically, they are proposing as adjunct diagnostics to serum creatinine and urinary output to improve the early detection, differential diagnosis and prognostic assessment of AKI. The most obvious requirements for a biomarker include its reflection of the underlying pathophysiology of the disease. Unfortunately, established functional biomarkers of glomerular filtration rate such as serum creatinine, urea delay AKI diagnosis by 24 to 48 hours. Novel renal biomarkers indicating tubular injury are emerging and may have wide implications. Here, we provide an overview of the basic pathophysiology, the cellular sources, the clinical performance, the functional significance. This review focuses on several novel renal biomarkers with the most promising biologic characteristics and clinical evidence for their AKI predictive ability: neutrophil gelatinase-associated lipocalin, kidney injury molecule-1, nterleukin 18, cystatin C, creatinine and urea. These markers might extend the therapeutic window during which timely and individualized patient management might be possible. The use of these biomarkers in clinical practice helps to detect acute renal failure in a timely manner, which in turn helps to reduce the frequency of serious complications.
Authors declare lack of the possible conflicts of interests