Biomarkers in acute kidney injury – pathophysiological basis and clinical performance

<jats:title>Abstract</jats:title><jats:p>Various biomarkers of acute kidney injury (<jats:styled-content style="fixed-case">AKI</jats:styled-content>) have been discovered and characterized in the recent past. These molecules can be detected in urine or blood and signify structural damage to the kidney. Clinically, they are proposed as adjunct diagnostics to serum creatinine and urinary output to improve the early detection, differential diagnosis and prognostic assessment of <jats:styled-content style="fixed-case">AKI</jats:styled-content>. The most obvious requirements for a biomarker include its reflection of the underlying pathophysiology of the disease. Hence, a biomarker of <jats:styled-content style="fixed-case">AKI</jats:styled-content> should derive from the injured kidney and reflect a molecular process intimately connected with tissue injury. Here, we provide an overview of the basic pathophysiology, the cellular sources and the clinical performance of the most important currently proposed biomarkers of <jats:styled-content style="fixed-case">AKI</jats:styled-content>: neutrophil gelatinase‐associated lipocalin (<jats:styled-content style="fixed-case">NGAL</jats:styled-content>), kidney injury molecule‐1 (<jats:styled-content style="fixed-case">KIM</jats:styled-content>‐1), liver‐type fatty acid‐binding protein (L‐<jats:styled-content style="fixed-case">FABP</jats:styled-content>), interleukin‐18 (<jats:styled-content style="fixed-case">IL</jats:styled-content>‐18), insulin‐like growth factor‐binding protein 7 (<jats:styled-content style="fixed-case">IGFBP</jats:styled-content>7), tissue inhibitor of metalloproteinase 2 (<jats:styled-content style="fixed-case">TIMP</jats:styled-content>‐2) and calprotectin (S100A8/9). We also acknowledge each biomarker's advantages and disadvantages as well as important knowledge gaps and perspectives for future studies.</jats:p>