Hepatitis C virus-associated tubulointerstitial injury.
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.
Kasuno
Kenji
K
Department of Biological Responses, Laboratory of Infection and Prevention, Institute for Virus Research, Japan.
Ono
Takahiko
T
Matsumori
Akira
A
Nogaki
Fumiaki
F
Kusano
Hitoshi
H
Watanabe
Hitomi
H
Yodoi
Junji
J
Muso
Eri
E
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
D018937:Hepatitis C Antibodies; D018936:Hepatitis C Antigens; D012367:RNA, Viral