title: KIM-1 expression predicts renal outcomes in IgA nephropathy.
abstract: BACKGROUND
  Kidney injury molecule-1 (KIM-1) is a sensitive biomarker for proximal tubular injury. Recently, a few studies have shown that urinary KIM-1 has clinical implications in IgA nephropathy (IgAN). We performed this study to determine whether tissue KIM-1 has clinical implications for predicting long-term outcome and whether urinary KIM-1 is correlated with tissue KIM-1 and kidney injury in IgAN patients.
  
  
  METHODS
  We assessed the prognostic prediction capability of tissue KIM-1 expression in 69 adult patients with IgAN retrospectively. Renal biopsies from all patients were scored by a pathologist who was blinded to the clinical data for the pathologic variables. The primary outcome was the composite of a 50 % reduction in eGFR or end-stage renal disease. Tissue KIM-1 expression was assessed semiquantitatively by counting the stained tubules per 100× power field; 0 tubule indicates grade 0; 1-5 tubules, grade 1; 6-10 tubules, grade 2; and more than 10 tubules, grade 3. Comparing urinary KIM-1 and tissue KIM-1 expression, 50 consecutive IgAN patients were prospectively enrolled to measure urinary KIM-1 levels and examine their biopsy specimens by KIM-1 immunohistochemistry.
  
  
  RESULTS
  Univariate analysis showed that tissue KIM-1 expression was associated with the renal outcome in IgAN. Multivariate regression analysis, as the relationship of tissue KIM-1 with prognosis, was consistent. Proteinuria at biopsy and tissue KIM-1 grade 3 were shown to have a prognostic value. The concentration of urinary KIM-1/Cr in patients with IgAN was significantly higher than that in the normal controls.
  
  
  CONCLUSIONS
  Tissue KIM-1 expression is an independent predictor of adverse renal outcomes in IgA nephropathy patients.
authors.affiliation: Hyonam Kidney Laboratory, Dae Sa Gwan Ro 59, Hannam-dong Yongsan-gu, Seoul, Korea.
authors.forename: Soon Hyo
authors.initials: SH
authors.lastname: Kwon
authors.forename: Moo Yong
authors.initials: MY
authors.lastname: Park
authors.forename: Jin Seok
authors.initials: JS
authors.lastname: Jeon
authors.forename: Hyunjin
authors.initials: H
authors.lastname: Noh
authors.forename: Soo Jeong
authors.initials: SJ
authors.lastname: Choi
authors.forename: Jin Kuk
authors.initials: JK
authors.lastname: Kim
authors.forename: Seung Duk
authors.initials: SD
authors.lastname: Hwang
authors.forename: So Young
authors.initials: SY
authors.lastname: Jin
authors.forename: Dong Cheol
authors.initials: DC
authors.lastname: Han
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000652:urine*; D005260:Female; D005922:Glomerulonephritis, IGA / Q000150:complications* / Q000473:pathology; D000072596:Hepatitis A Virus Cellular Receptor 1; D006801:Humans; D007150:Immunohistochemistry; D007668:Kidney / Q000473:pathology*; D008297:Male; D008562:Membrane Glycoproteins / Q000378:metabolism* / Q000652:urine; D008875:Middle Aged; D011379:Prognosis; D011446:Prospective Studies; D011991:Receptors, Virus / Q000378:metabolism*; D012189:Retrospective Studies
chemical_list: D015415:Biomarkers; C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1; D008562:Membrane Glycoproteins; D011991:Receptors, Virus