title: Hepatitis C virus-associated tubulointerstitial injury.
abstract: BACKGROUND
  Tubulointerstitial damage is recognized as a determinant of the prognosis of kidney disease. Various types of viral infection have been reported to induce tubulointerstitial lesions; however, that caused by hepatitis C virus (HCV) remains unclear, although glomerular lesions caused by this viral infection have been well documented.
  
  
  METHODS
  To identify any association, we retrospectively investigated 320 patients who underwent renal biopsy and did not have extrarenal diseases causing tubulointerstitial nephritis.
  
  
  RESULTS
  Of these patients, 13 patients had HCV infection and 307 patients did not. In a case-control study, HCV infection showed a significant association with the prevalence of tubulointerstitial injury. To offset the secondary tubulointerstitial change caused by advanced glomerulopathy, we performed a glomerular stage-matched comparison of patients with membranous nephropathy (MN). Nine patients with MN among the 13 HCV-infected patients and 18 HCV-negative patients with electron microscopic glomerular stage-matched MN were randomly selected from the overall pool of patients. Comparing areas of interstitial fibrosis and inflammatory cell infiltration, both were greater in HCV-infected than HCV-negative patients. In biopsy tissues from HCV-infected patients, positive signal for HCV was observed in the perinuclear area of tubular epithelial cells and infiltrating cells on immunohistochemistry and in situ hybridization. By a strand-specific reverse-transcription polymerase chain reaction for HCV, both genomic- and replicative-strand RNA were detected in renal tissues.
  
  
  CONCLUSIONS
  These results suggest that HCV infection is a potent pathogenic factor of tubulointerstitial injury.
authors.affiliation: Department of Biological Responses, Laboratory of Infection and Prevention, Institute for Virus Research, Japan.
authors.forename: Kenji
authors.initials: K
authors.lastname: Kasuno
authors.forename: Takahiko
authors.initials: T
authors.lastname: Ono
authors.forename: Akira
authors.initials: A
authors.lastname: Matsumori
authors.forename: Fumiaki
authors.initials: F
authors.lastname: Nogaki
authors.forename: Hitoshi
authors.initials: H
authors.lastname: Kusano
authors.forename: Hitomi
authors.initials: H
authors.lastname: Watanabe
authors.forename: Junji
authors.initials: J
authors.lastname: Yodoi
authors.forename: Eri
authors.initials: E
authors.lastname: Muso
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D001706:Biopsy; D016022:Case-Control Studies; D005260:Female; D005921:Glomerulonephritis / Q000453:epidemiology / Q000473:pathology; D015433:Glomerulonephritis, Membranous / Q000453:epidemiology / Q000473:pathology; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology / Q000302:isolation & purification; D006526:Hepatitis C / Q000150:complications* / Q000453:epidemiology / Q000821:virology; D018937:Hepatitis C Antibodies / Q000097:blood; D018936:Hepatitis C Antigens / Q000032:analysis; D006801:Humans; D007564:Japan / Q000453:epidemiology; D007678:Kidney Glomerulus / Q000473:pathology; D008297:Male; D008875:Middle Aged; D009395:Nephritis, Interstitial / Q000453:epidemiology / Q000209:etiology* / Q000473:pathology / Q000821:virology; D015995:Prevalence; D012367:RNA, Viral / Q000032:analysis; D012189:Retrospective Studies
chemical_list: D018937:Hepatitis C Antibodies; D018936:Hepatitis C Antigens; D012367:RNA, Viral