New and better biomarkers of acute kidney injury

Abstract

Acute kidney injury (AKI) affects 50% of critically ill patients and has a high mortality rate. Diagnosis with plasma creatinine leads to 48–72 hour delays in treatments. Future treatment modalities may follow the paradigm of early intervention following triage with an injury biomarker or biomarker panel. 1 We compared six potential urinary biomarker candidates for early detection of AKI measured on entry to an intensive care unit in 528 patients: gammaglutamyl transpeptidase (GGT), alkaline phosphatase (AP), cystatin C (CysC), neutrophil gelatinase associated lipocalin (NGAL), kidney injury molecule-1 (KIM-1) and interleukin-18 (IL-18). The composite biomarker (GGTxAP) was used to triage a higher at risk group to a randomised control trial of erythropoietin within 6.3 ± 4.2 hours of admission. The prognostic performance of GGTxAP in predicting AKI (in patients not treated with EPO and without AKI on admission) depended on the time from insult to first sample. The maximum area under the receiver operator characteristic curve (AUC) was at 6–12 hours post-insult, AUC=0.69 (95%CI 0.55–0.82). The prognostic performance of the other biomarkers depended similarly on timing in relation to injury.