title: Changes in urinary angiotensinogen posttreatment in pediatric IgA nephropathy patients.
abstract: BACKGROUND
  Recently, we demonstrated that urinary angiotensinogen (AGT) levels are increased and reflect intrarenal renin-angiotensin system (RAS) status in pediatric patients with chronic glomerulonephritis. Therefore, this study was performed to test the hypothesis that urinary AGT (UAGT) levels provide a specific index of intrarenal RAS status associated with RAS blockade treatment in pediatric IgA nephropathy (IgAN) patients.
  
  
  METHODS
  We measured plasma and UAGT levels and urinary transforming growth factor beta (TGF-β) levels, after which we performed immunohistochemical analysis of AGT, angiotensin II (Ang II), and TGF-β in 24 pediatric IgAN patients treated with RAS blockades for 2 years. Paired tests were used to analyze the changes from baseline to study end.
  
  
  RESULTS
  Although there was no change in plasma AGT levels, UAGT and TGF-β levels were significantly decreased after RAS blockade, which was accompanied by the expression levels of AGT, Ang II, and TGF-β, as well as the magnitude of glomerular injury. Baseline UAGT levels positively correlated with diastolic blood pressure, urinary protein levels, scores for mesangial hypercellularity, and the expression levels of AGT, Ang II, and TGF-β in renal tissues.
  
  
  CONCLUSIONS
  These data indicate that UAGT is a useful biomarker of intrarenal RAS activation, which is associated with glomerular injury during RAS blockade in pediatric IgAN patients.
authors.affiliation: Department of Pediatrics, Institute of Health Biosciences, University of Tokushima Graduate School, Kuramoto-cho 3-18-15, Tokushima, 770-8503, Japan, urushihara@tokushima-u.ac.jp.
authors.forename: Maki
authors.initials: M
authors.lastname: Urushihara
authors.forename: Takashi
authors.initials: T
authors.lastname: Nagai
authors.forename: Yukiko
authors.initials: Y
authors.lastname: Kinoshita
authors.forename: Sato
authors.initials: S
authors.lastname: Nishiyama
authors.forename: Kenichi
authors.initials: K
authors.lastname: Suga
authors.forename: Natsuko
authors.initials: N
authors.lastname: Ozaki
authors.forename: Ariunbold
authors.initials: A
authors.lastname: Jamba
authors.forename: Shuji
authors.initials: S
authors.lastname: Kondo
authors.forename: Hiroyuki
authors.initials: H
authors.lastname: Kobori
authors.forename: Shoji
authors.initials: S
authors.lastname: Kagami
mesh_terms: D000293:Adolescent; D000804:Angiotensin II / Q000097:blood / Q000652:urine; D047228:Angiotensin II Type 1 Receptor Blockers / Q000627:therapeutic use*; D000806:Angiotensin-Converting Enzyme Inhibitors / Q000627:therapeutic use*; D000808:Angiotensinogen / Q000097:blood / Q000652:urine*; D015415:Biomarkers / Q000097:blood / Q000652:urine; D001706:Biopsy; D002648:Child; D004797:Enzyme-Linked Immunosorbent Assay; D005260:Female; D005922:Glomerulonephritis, IGA / Q000175:diagnosis / Q000188:drug therapy* / Q000503:physiopathology / Q000652:urine; D006801:Humans; D007150:Immunohistochemistry; D007668:Kidney / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D008297:Male; D011237:Predictive Value of Tests; D012084:Renin-Angiotensin System / Q000187:drug effects*; D013997:Time Factors; D016212:Transforming Growth Factor beta / Q000097:blood / Q000652:urine; D016896:Treatment Outcome; D016482:Urinalysis
chemical_list: C534931:AGT protein, human; D047228:Angiotensin II Type 1 Receptor Blockers; D000806:Angiotensin-Converting Enzyme Inhibitors; D015415:Biomarkers; D016212:Transforming Growth Factor beta; D000808:Angiotensinogen; D000804:Angiotensin II