title: Increased Neutrophil Gelatinase-Associated Lipocalin is Associated with Mortality and Multiple Organ Dysfunction Syndrome in Severe Sepsis and Septic Shock.
abstract: BACKGROUND
  This study examines the clinical utility of increased neutrophil gelatinase-associated lipocalin (NGAL) as an indicator of mortality and multiple organ dysfunction syndrome (MODS) in severe sepsis and septic shock.
  
  
  METHODS
  We designed a prospective cohort study in an intensive care unit, and 123 patients with severe sepsis or septic shock were included. Data were used to determine a relationship between NGAL and the development of MODS and mortality. These associations were determined by the Mann-Whitney U test, log-rank test, Cox proportional hazards regression analyses, and plotting the receiver operating characteristic curve.
  
  
  RESULTS
  Patients with high NGAL (75th percentile) had increased risk of mortality and MODS compared with patients with low NGAL (log-rank test, P < 0.05). There were 39 patients (32%) with mortality during follow-up at 12 months, 10 patients (8%) with MODS on day 1, and 37 patients (30%) on day 7. The area under the receiver operating characteristic curve showed that high NGAL could predict mortality (0.6385) during intensive care unit stay. After adjustment for confounding risk factors chosen by backward elimination by Cox regression analysis, high NGAL remained an independent predictor of mortality and MODS (hazard ratios, 2.128 [95% confidence interval, 1.078-4.203; P = 0.030] and 1.896 [95% confidence interval, 1.012-3.552; P = 0.046], respectively).
  
  
  CONCLUSIONS
  High plasma NGAL independently predicts mortality and MODS in severe sepsis and septic shock.
authors.affiliation: Department of Critical Care Medicine, The Affiliated Suzhou Municipal Hospital, Nanjing Medical University, Suzhou, Jiangsu, People's Republic of China.
authors.forename: Biao
authors.initials: B
authors.lastname: Wang
authors.forename: Gang
authors.initials: G
authors.lastname: Chen
authors.forename: Jun
authors.initials: J
authors.lastname: Zhang
authors.forename: Jiping
authors.initials: J
authors.lastname: Xue
authors.forename: Yifei
authors.initials: Y
authors.lastname: Cao
authors.forename: Yunfu
authors.initials: Y
authors.lastname: Wu
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood; D000209:Acute-Phase Proteins; D000368:Aged; D015415:Biomarkers / Q000097:blood; D002097:C-Reactive Protein / Q000378:metabolism; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D007362:Intensive Care Units; D053208:Kaplan-Meier Estimate; D007668:Kidney / Q000503:physiopathology; D000071068:Lipocalin-2; D054834:Lipocalins / Q000097:blood*; D008297:Male; D008875:Middle Aged; D009102:Multiple Organ Failure / Q000097:blood / Q000175:diagnosis* / Q000209:etiology / Q000503:physiopathology; D011379:Prognosis; D011446:Prospective Studies; D011518:Proto-Oncogene Proteins / Q000097:blood*; D018805:Sepsis / Q000097:blood* / Q000150:complications / Q000503:physiopathology; D012772:Shock, Septic / Q000097:blood / Q000150:complications / Q000503:physiopathology
chemical_list: D000209:Acute-Phase Proteins; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; C489506:LCN2 protein, human; D000071068:Lipocalin-2; D054834:Lipocalins; D011518:Proto-Oncogene Proteins; C036309:fibrin fragment D; D002097:C-Reactive Protein