title: CD147/basigin reflects renal dysfunction in patients with acute kidney injury.
abstract: BACKGROUND
  Acute tubular necrosis (ATN) describes a form of intrinsic acute kidney injury (AKI) that results from persistent hypoperfusion and subsequent activation of the immune system. A glycosylated transmembrane protein, CD147/basigin, is involved in the pathogenesis of renal ischemia and fibrosis. The present study investigated whether CD147 can reflect pathological features and renal dysfunction in patients with AKI.
  
  
  METHODS
  Plasma and spot urine samples were collected from 24 patients (12 controls and 12 with ATN) who underwent renal biopsy between 2008 and 2012. In another study, patients undergoing open surgery to treat abdominal aortic aneurysms (AAAs) were enrolled in 2004. We collected urine and plasma samples from seven patients with AKI and 33 patients without AKI, respectively. In these experiments, plasma and urinary CD147, and urinary L-fatty acid-binding protein (L-FABP) levels were measured, and the former expression in kidneys was examined by immunostaining.
  
  
  RESULTS
  In biopsy tissues of ATN with severe histological features, CD147 induction was strikingly present in inflammatory cells such as macrophages and lymphocytes in the injured interstitium, but not in damaged tubules representing atrophy. Both plasma and urinary CD147 levels were strikingly increased in ATN patients; both values showed greater correlations with renal dysfunction compared to urinary L-FABP. In patients who had undergone open AAA surgery, urinary and plasma CD147 values in AKI patients were significantly higher than in non-AKI patients at post-operative day 1, similar to the profile of urinary L-FABP.
  
  
  CONCLUSIONS
  CD147 was prominent in its ability to detect AKI and may allow the start of preemptive medication.
authors.affiliation: Department of Nephrology, Nagoya University Graduate School of Medicine, 65 Tsurumai-cho, Showa-ku, Nagoya, 466-8550, Japan.
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Nagaya
authors.forename: Tomoki
authors.initials: T
authors.lastname: Kosugi
authors.forename: Mayuko
authors.initials: M
authors.lastname: Maeda-Hori
authors.forename: Kayaho
authors.initials: K
authors.lastname: Maeda
authors.forename: Yuka
authors.initials: Y
authors.lastname: Sato
authors.forename: Hiroshi
authors.initials: H
authors.lastname: Kojima
authors.forename: Hiroki
authors.initials: H
authors.lastname: Hayashi
authors.forename: Noritoshi
authors.initials: N
authors.lastname: Kato
authors.forename: Takuji
authors.initials: T
authors.lastname: Ishimoto
authors.forename: Waichi
authors.initials: W
authors.lastname: Sato
authors.forename: Yukio
authors.initials: Y
authors.lastname: Yuzawa
authors.forename: Seiichi
authors.initials: S
authors.lastname: Matsuo
authors.forename: Kenji
authors.initials: K
authors.lastname: Kadomatsu
authors.forename: Shoichi
authors.initials: S
authors.lastname: Maruyama
mesh_terms: D058186:Acute Kidney Injury / Q000097:blood* / Q000652:urine; D000293:Adolescent; D000328:Adult; D000368:Aged; D051926:Basigin / Q000097:blood* / Q000652:urine; D015415:Biomarkers / Q000097:blood / Q000652:urine; D016022:Case-Control Studies; D003404:Creatinine / Q000097:blood; D050556:Fatty Acid-Binding Proteins / Q000097:blood; D005260:Female; D006801:Humans; D007511:Ischemia / Q000097:blood / Q000652:urine; D007668:Kidney / Q000098:blood supply / Q000378:metabolism / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009336:Necrosis / Q000097:blood / Q000652:urine; D055815:Young Adult
chemical_list: C497886:BSG protein, human; D015415:Biomarkers; C493319:FABP1 protein, human; D050556:Fatty Acid-Binding Proteins; D051926:Basigin; D003404:Creatinine