Biomarkers reliable to detect subclinical AKI could be the key to identify such patients at risk and initiate nephroprotective treatments during this “golden hour of AKI prevention.” Therefore, damage biomarkers like neutrophil gelatinase­associated lipocalin (NGAL) and tissue stress biomarkers like tissue inhibitor of metalloproteinases-2 and insulin-like growth factor-binding protein ([TIMP2]* [IGFPB7]) are in the focus of recent studies (see below parag of patients at high risk for postoperative AKI”). But even when detected early, concrete treatment options to prevent the progression of AKI are limited. Addressing this issue, studies are investigating the implementation of a nephroprotective care bundle. Other biomarkers have been investigated for their performance to predict progress or persistence of AKI: for example, high levels of urinary C-C motif chemokine ligand-14 (CCL14) have been i AKI stage 3 in ICU patients with severe AKI [ furosemide stress test, this marker has also shown a high predictive value for developing an indication for RRT and could therefore be helpful to find the optimal time for initiation of RRT in the future [15]. Furthermore, the optimal timing for cessation of RRT remains unknown [16, 17]. Concerning this issue, Proenkephalin A 119–159 might be a suitable biomarker. Recent studies evaluated whether plasma Proenkephalin A 199–159 predicts successful and early liberation from RRT in critically ill patients with RRT-dependent AKI (see below paragraph “Biomarkers for other indications”).