title: Urinary kidney injury molecule-1 is related to pathologic involvement in IgA nephropathy with normotension, normal renal function and mild proteinuria.
abstract: BACKGROUND
  IgA nephropathy (IgAN) may progress to renal failure for some patients without any clinical risk factors and it is not unusual to find severe pathologic damage in clinically mild IgAN. We therefore investigated whether urinary kidney injury molecule-1 (KIM-1) was related to pathologic involvement in clinically mild IgAN.
  
  
  METHODS
  Urinary KIM-1/creatinine of 51 IgAN patients with normotension, normal renal function and proteinuria < 1.0 g/24 h were tested. Relationships between urinary KIM-1 and pathologic features were analyzed.
  
  
  RESULTS
  Eighteen of the 51 patients had elevated urinary KIM-1. The tubular atrophy/interstitial fibrosis was more severe in patients with elevated urinary KIM-1 than that in patients with normal urinary KIM-1 (T0/T1/T2, 13/5/0 vs. 33/0/0, P = 0.004). Proportion of glomeruli containing cresecents was higher in patients with elevated urinary KIM-1 than that in patients with normal urinary KIM-1 (50% vs. 18%, P = 0.026). Urinary KIM-1 correlated with the proportion of total crescents (R = 0.303, p = 0.031) and fibrous crescents (R = 0.456, p = 0.001), but did not correlate with the proportion of cellular crescents or fibrocellular crescents. Although the proportion of vascular lesions was higher in patients with elevated urinary KIM-1 (44.4%) than that in patients with normal urinary KIM-1 (18.1%), the difference was not significant (p = 0.057). There was no difference of the response to treatment between patients with and without elevated urinary KIM-1 during a short-term follow-up.
  
  
  CONCLUSIONS
  Urinary KIM-1 is a reflection of tubularinstitial injury. For patients with clinically mild IgAN, high urinary KIM-1 is related to relatively severe pathologic involvement on renal biopsy.
authors.forename: Peng-cheng
authors.initials: PC
authors.lastname: Xu
authors.forename: Li
authors.initials: L
authors.lastname: Wei
authors.forename: Wen-ya
authors.initials: WY
authors.lastname: Shang
authors.forename: Shun-li
authors.initials: SL
authors.lastname: Tian
authors.forename: Dong-mei
authors.initials: DM
authors.lastname: Gu
authors.forename: Tie-kun
authors.initials: TK
authors.lastname: Yan
authors.affiliation: Department of Nephrology, General Hospital of Tianjin Medical University, Tianjin 300052, China. shanlin_55@163.com.
authors.forename: Shan
authors.initials: S
authors.lastname: Lin
mesh_terms: D000328:Adult; D015415:Biomarkers / Q000652:urine; D005260:Female; D005500:Follow-Up Studies; D005922:Glomerulonephritis, IGA / Q000175:diagnosis* / Q000453:epidemiology / Q000652:urine*; D000072596:Hepatitis A Virus Cellular Receptor 1; D006801:Humans; D007668:Kidney / Q000502:physiology*; D008297:Male; D008562:Membrane Glycoproteins / Q000652:urine*; D011507:Proteinuria / Q000175:diagnosis* / Q000453:epidemiology / Q000652:urine*; D011991:Receptors, Virus; D055815:Young Adult
chemical_list: D015415:Biomarkers; C491143:HAVCR1 protein, human; D000072596:Hepatitis A Virus Cellular Receptor 1; D008562:Membrane Glycoproteins; D011991:Receptors, Virus