title: Increase in urinary markers during the acute phase reflects the degree of chronic tubulointerstitial injury after ischemia-reperfusion renal injury.
abstract: BACKGROUND
  Acute kidney injury (AKI) could lead to progressive chronic kidney disease (CKD).
  
  
  OBJECTIVE
  To demonstrate that urinary markers in AKI are associated with the degree of persistent renal injury.
  
  
  METHODS
  Human L-FABP chromosomal transgenic (Tg) mice were subjected to ischemia-reperfusion (I/R) clamping renal pedicle for 20 min or 30 min. Kidneys were obtained at one and 40 days after I/R.
  
  
  RESULTS
  Urinary L-FABP, NGAL, Kim-1 and albumin levels increased during the acute phase and were significantly correlated with the degree of tubulointerstitial fibrosis during the chronic phase.
  
  
  CONCLUSIONS
  These markers could detect higher risk of progression to CKD.
authors.affiliation: a Department of Internal Medicine, From the Division of Nephrology and Hypertension , St. Marianna University School of Medicine , Kanagawa , Japan.
authors.forename: Mikako
authors.initials: M
authors.lastname: Hisamichi
authors.affiliation: a Department of Internal Medicine, From the Division of Nephrology and Hypertension , St. Marianna University School of Medicine , Kanagawa , Japan.|b Department of Anatomy , St. Marianna University School of Medicine , Kanagawa , Japan.
authors.forename: Atsuko
authors.initials: A
authors.lastname: Kamijo-Ikemori
authors.affiliation: a Department of Internal Medicine, From the Division of Nephrology and Hypertension , St. Marianna University School of Medicine , Kanagawa , Japan.
authors.forename: Takeshi
authors.initials: T
authors.lastname: Sugaya
authors.affiliation: a Department of Internal Medicine, From the Division of Nephrology and Hypertension , St. Marianna University School of Medicine , Kanagawa , Japan.
authors.forename: Daisuke
authors.initials: D
authors.lastname: Ichikawa
authors.affiliation: b Department of Anatomy , St. Marianna University School of Medicine , Kanagawa , Japan.
authors.forename: Seiko
authors.initials: S
authors.lastname: Hoshino
authors.affiliation: b Department of Anatomy , St. Marianna University School of Medicine , Kanagawa , Japan.
authors.forename: Kazuaki
authors.initials: K
authors.lastname: Hirata
authors.affiliation: c JCHO Tokyo Takanawa Hospital , Tokyo , Japan.
authors.forename: Kenjiro
authors.initials: K
authors.lastname: Kimura
authors.affiliation: a Department of Internal Medicine, From the Division of Nephrology and Hypertension , St. Marianna University School of Medicine , Kanagawa , Japan.
authors.forename: Yugo
authors.initials: Y
authors.lastname: Shibagaki
mesh_terms: D058186:Acute Kidney Injury / Q000652:urine*; D000418:Albumins / Q000032:analysis; D000818:Animals; D015415:Biomarkers / Q000652:urine; D050556:Fatty Acid-Binding Proteins / Q000652:urine; D005355:Fibrosis; D000072596:Hepatitis A Virus Cellular Receptor 1 / Q000032:analysis; D006801:Humans; D000071068:Lipocalin-2 / Q000652:urine; D051379:Mice; D008822:Mice, Transgenic; D009395:Nephritis, Interstitial / Q000175:diagnosis / Q000473:pathology*; D051436:Renal Insufficiency, Chronic / Q000175:diagnosis*; D015427:Reperfusion Injury / Q000150:complications*
chemical_list: D000418:Albumins; D015415:Biomarkers; C493319:FABP1 protein, human; D050556:Fatty Acid-Binding Proteins; C442240:Havcr1 protein, mouse; D000072596:Hepatitis A Virus Cellular Receptor 1; D000071068:Lipocalin-2; C071332:Lcn2 protein, mouse
keywords: AKI to CKD transition; Acute kidney injury; chronic kidney disease; renal damage