INTRODUCTION: Conventional markers of acute kidney injury (AKI) lack diagnostic 
accuracy and are expressed only late after cardiac surgery with cardiopulmonary 
bypass (CPB). Recently, interest has focused on hepcidin, a regulator of iron 
homeostasis, as a unique renal biomarker.
METHODS: We studied 100 adult patients in the control arm of a randomized, 
controlled trial http://www.clinicaltrials.gov/NCT00672334 who were identified 
as being at increased risk of AKI after cardiac surgery with CPB. AKI was 
defined according to the Risk, Injury, Failure, Loss, End-stage renal disease 
classification of AKI classification stage. Samples of plasma and urine were 
obtained simultaneously (1) before CPB (2) six hours after the start of CPB and 
(3) twenty-four hours after CPB. Plasma and urine hepcidin 25-isoforms were 
quantified by competitive enzyme-linked immunoassay.
RESULTS: In AKI-free patients (N = 91), urine hepcidin concentrations had 
largely increased at six and twenty-four hours after CPB, and they were three to 
seven times higher compared to patients with subsequent AKI (N = 9) in whom 
postoperative urine hepcidin remained at preoperative levels (P = 0.004, P = 
0.002). Furthermore, higher urine hepcidin and, even more so, urine hepcidin 
adjusted to urine creatinine at six hours after CPB discriminated patients who 
did not develop AKI (area under the curve (AUC) receiver operating 
characteristic curve 0.80 [95% confidence interval (95% CI) 0.71 to 0.87] and 
0.88 [95% CI 0.78 to 0.97]) or did not need renal replacement therapy initiation 
(AUC 0.81 [95% CI 0.72 to 0.88] 0.88 [95% CI 0.70 to 0.99]) from those who did. 
At six hours, urine hepcidin adjusted to urine creatinine was an independent 
predictor of ruling out AKI (P = 0.011). Plasma hepcidin did not predict no 
development of AKI. The study findings remained essentially unchanged after 
excluding patients with preoperative chronic kidney disease.
CONCLUSIONS: Our findings suggest that urine hepcidin is an early predictive 
biomarker of ruling out AKI after CPB, thereby contributing to early patient 
risk stratification.