title: Prognostic significance of acute kidney injury after reperfused ST-elevation myocardial infarction: synergistic acceleration of renal dysfunction and left ventricular remodeling.
abstract: BACKGROUND
  Acute kidney injury (AKI) after myocardial infarction is associated with poor clinical outcome. However, mechanisms of the adverse effect of AKI on clinical outcome after reperfused ST-elevation myocardial infarction (STEMI) have not been fully elucidated.
  
  
  RESULTS
  We examined 141 consecutive patients with reperfused first anterior STEMI. AKI was defined as an increase in serum creatinine of >or=0.3mg/dL within 48hours after admission. Patients with AKI had higher incidence of in-hospital cardiac death (P=.0004) and major adverse cardiac events (MACE, P=.020) during a mean of 39+/-40 (range, 1 to 96) months than those without, in association with adverse left ventricular (LV) remodeling. White blood cell count on admission and peak C-reactive protein were higher in patients with than those without AKI. Plasma norepinephrine on admission, interleukin-6, brain natriuretic peptide, and malondialdehyde-modified low-density lipoprotein 2 weeks after STEMI were higher in patients with AKI than those without AKI. Cox proportional hazards model analysis revealed AKI was an independent predictor of MACE (hazard ratio=2.38, P=.019).
  
  
  CONCLUSIONS
  AKI was a strong predictor of MACE in association with adverse LV remodeling. Enhanced inflammatory response, oxidative stress, and neurohormonal activation may synergistically accelerate renal dysfunction and LV remodeling after STEMI.
authors.affiliation: Division of Cardiology, Department of Medicine, Keio University School of Medicine, Tokyo, Japan.
authors.forename: Atsushi
authors.initials: A
authors.lastname: Anzai
authors.forename: Toshihisa
authors.initials: T
authors.lastname: Anzai
authors.forename: Kotaro
authors.initials: K
authors.lastname: Naito
authors.forename: Hidehiro
authors.initials: H
authors.lastname: Kaneko
authors.forename: Yoshinori
authors.initials: Y
authors.lastname: Mano
authors.forename: Yusuke
authors.initials: Y
authors.lastname: Jo
authors.forename: Yuji
authors.initials: Y
authors.lastname: Nagatomo
authors.forename: Yuichiro
authors.initials: Y
authors.lastname: Maekawa
authors.forename: Akio
authors.initials: A
authors.lastname: Kawamura
authors.forename: Tsutomu
authors.initials: T
authors.lastname: Yoshikawa
authors.forename: Satoshi
authors.initials: S
authors.lastname: Ogawa
mesh_terms: D058186:Acute Kidney Injury / Q000209:etiology* / Q000401:mortality / Q000473:pathology; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D002097:C-Reactive Protein; D008078:Cholesterol, LDL; D003404:Creatinine / Q000097:blood; D005260:Female; D006333:Heart Failure / Q000473:pathology; D006352:Heart Ventricles / Q000473:pathology; D006801:Humans; D015994:Incidence; D007249:Inflammation / Q000097:blood; D015850:Interleukin-6 / Q000097:blood; D007564:Japan; D016015:Logistic Models; D008297:Male; D008315:Malondialdehyde / Q000097:blood; D008875:Middle Aged; D009203:Myocardial Infarction / Q000150:complications / Q000628:therapy*; D015428:Myocardial Reperfusion Injury / Q000150:complications*; D020097:Natriuretic Peptide, Brain / Q000097:blood; D009638:Norepinephrine / Q000097:blood; D018384:Oxidative Stress; D011379:Prognosis; D016016:Proportional Hazards Models; D012307:Risk Factors; D018487:Ventricular Dysfunction, Left / Q000209:etiology* / Q000473:pathology; D020257:Ventricular Remodeling
chemical_list: D008078:Cholesterol, LDL; D015850:Interleukin-6; D020097:Natriuretic Peptide, Brain; D008315:Malondialdehyde; D002097:C-Reactive Protein; D003404:Creatinine; D009638:Norepinephrine