Plasma and urine neutrophil gelatinase-associated lipocalin in septic versus non-septic acute kidney injury in critical illness.
OBJECTIVE
Sepsis is the most common trigger for acute kidney injury (AKI) in critically ill patients. We sought to determine whether there are unique patterns to plasma and urine neutrophil gelatinase-associated lipocalin (NGAL) in septic compared with non-septic AKI.


METHODS
Prospective observational study.


METHODS
Two adult ICUs in Melbourne, Australia.


METHODS
Critically ill patients with septic and non-septic AKI.


METHODS
None.


RESULTS
Blood and urine specimens collected at enrollment, 12, 24 and 48 h to measure plasma and urine NGAL. Eighty-three patients were enrolled (septic n = 43). Septic AKI patients had more co-morbid disease (p = 0.005), emergency surgical admissions (p < 0.001), higher illness severity (p = 0.008), more organ dysfunction (p = 0.008) and higher white blood cell counts (p = 0.01). There were no differences at enrollment between groups in AKI severity. Septic AKI was associated with significantly higher plasma (293 vs. 166 ng/ml) and urine (204 vs. 39 ng/mg creatinine) NGAL at enrollment compared with non-septic AKI (p < 0.001). Urine NGAL remained higher in septic compared with non-septic AKI at 12 h (p < 0.001) and 24 h (p < 0.001). Plasma NGAL showed fair discrimination for AKI progression (area under receiver-operator characteristic curve 0.71) and renal replacement therapy (AuROC 0.78). Although urine NGAL performed less well (AuROC 0.70, 0.70), peak urine NGAL predicted AKI progression better in non-septic AKI (AuROC 0.82).


CONCLUSIONS
Septic AKI patients have higher detectable plasma and urine NGAL compared with non-septic AKI patients. These differences in NGAL values in septic AKI may have diagnostic and clinical relevance as well as pathogenetic implications.
Bagshaw
Sean M
SM
Division of Critical Care Medicine, University of Alberta Hospital, University of Alberta, 3C1.16 Walter C Mackenzie Centre, 8440-122 Street, Edmonton, AB T6G2B7, Canada. bagshaw@ualberta.ca
Bennett
Michael
M
Haase
Michael
M
Haase-Fielitz
Anja
A
Egi
Moritoki
M
Morimatsu
Hiroshi
H
D'amico
Giuseppe
G
Goldsmith
Donna
D
Devarajan
Prasad
P
Bellomo
Rinaldo
R
D058186:Acute Kidney Injury / Q000209:etiology / Q000503:physiopathology* / Q000628:therapy; D000209:Acute-Phase Proteins / Q000652:urine*; D000368:Aged; D000369:Aged, 80 and over; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016022:Case-Control Studies; D016638:Critical Illness; D005260:Female; D006801:Humans; D007362:Intensive Care Units; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood* / Q000652:urine*; D008297:Male; D008875:Middle Aged; D019370:Observation; D011446:Prospective Studies; D011518:Proto-Oncogene Proteins / Q000097:blood* / Q000652:urine*; D018805:Sepsis / Q000150:complications* / Q000503:physiopathology; D014739:Victoria
D000209:Acute-Phase Proteins; D015415:Biomarkers; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins