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Article: Hepatitis C virus infection in patients on renal replacement therapy

TitleHepatitis C virus infection in patients on renal replacement therapy
Authors
KeywordsChronic hepatitis
Dialysis
Hepatitis C virus
Interferon
Transplantation
Issue Date1996
PublisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEP
Citation
Nephrology, 1996, v. 2 SUPPL. 1, p. S85-S87 How to Cite?
AbstractThe hepatitis C virus (HCV) is a major cause of chronic liver disease in patients on renal replacement therapy. Spontaneous clearance of HCV is unusual. Second generation assays for anti-HCV, which have high sensitivity and specificity, are used conventionally for diagnosis. They are supplemented by the polymerase chain reaction (PCR) assay for HCV RNA. Quantitative HCV RNA assays, although expensive, may he useful in patients receiving anti-viral therapy. Preliminary data also suggest that the clinical course and response to treatment may vary according to the HCV genotypes. The higher prevalence of HCV infection among haemodialysed patients (approximately 30%), as compared to patients on continuous ambulatory peritoneal dialysis (CAPD; <5%), is largely attributable to their higher transfusion requirement. Yet there is accumulating evidence to incriminate nosocomial transmission. Organ transplantation is another mode of infection, but the incidence remains controversial. Chronic liver disease is demonstrable in around 60% of HCV-positive patients on renal replacement therapy. Patients can present with prominent elevations in ductal enzyme levels, in addition to abnormalities in parenchymal enzymes. Histologic examination is mandatory to assess the activity and chronicity of liver disease. Liver pathology due to chronic HCV in renal allograft recipients correlates with the dialysis duration and the profile of abnormal liver biochemistry. Although HCV infection does not appear to adversely affect the short-term graft or patient survival, patients can develop potentially fatal exacerbations of liver disease after renal transplantation. Interferon therapy results in sustained virologie remission in ≤20% of HCV-positive dialysis patients, but is associated with a high incidence of symptomatic side effects. In renal allograft recipients, the risk of allograft dysfunction is too high to justify the routine use of interferon, which should be considered only in patients with rapidly deteriorating liver pathology.
Persistent Identifierhttp://hdl.handle.net/10722/77692
ISSN
2023 Impact Factor: 2.4
2023 SCImago Journal Rankings: 0.641
ISI Accession Number ID
References

 

DC FieldValueLanguage
dc.contributor.authorChan, TMen_HK
dc.date.accessioned2010-09-06T07:34:40Z-
dc.date.available2010-09-06T07:34:40Z-
dc.date.issued1996en_HK
dc.identifier.citationNephrology, 1996, v. 2 SUPPL. 1, p. S85-S87en_HK
dc.identifier.issn1320-5358en_HK
dc.identifier.urihttp://hdl.handle.net/10722/77692-
dc.description.abstractThe hepatitis C virus (HCV) is a major cause of chronic liver disease in patients on renal replacement therapy. Spontaneous clearance of HCV is unusual. Second generation assays for anti-HCV, which have high sensitivity and specificity, are used conventionally for diagnosis. They are supplemented by the polymerase chain reaction (PCR) assay for HCV RNA. Quantitative HCV RNA assays, although expensive, may he useful in patients receiving anti-viral therapy. Preliminary data also suggest that the clinical course and response to treatment may vary according to the HCV genotypes. The higher prevalence of HCV infection among haemodialysed patients (approximately 30%), as compared to patients on continuous ambulatory peritoneal dialysis (CAPD; <5%), is largely attributable to their higher transfusion requirement. Yet there is accumulating evidence to incriminate nosocomial transmission. Organ transplantation is another mode of infection, but the incidence remains controversial. Chronic liver disease is demonstrable in around 60% of HCV-positive patients on renal replacement therapy. Patients can present with prominent elevations in ductal enzyme levels, in addition to abnormalities in parenchymal enzymes. Histologic examination is mandatory to assess the activity and chronicity of liver disease. Liver pathology due to chronic HCV in renal allograft recipients correlates with the dialysis duration and the profile of abnormal liver biochemistry. Although HCV infection does not appear to adversely affect the short-term graft or patient survival, patients can develop potentially fatal exacerbations of liver disease after renal transplantation. Interferon therapy results in sustained virologie remission in ≤20% of HCV-positive dialysis patients, but is associated with a high incidence of symptomatic side effects. In renal allograft recipients, the risk of allograft dysfunction is too high to justify the routine use of interferon, which should be considered only in patients with rapidly deteriorating liver pathology.en_HK
dc.languageengen_HK
dc.publisherBlackwell Publishing Asia. The Journal's web site is located at http://www.blackwellpublishing.com/journals/NEPen_HK
dc.relation.ispartofNephrologyen_HK
dc.subjectChronic hepatitisen_HK
dc.subjectDialysisen_HK
dc.subjectHepatitis C virusen_HK
dc.subjectInterferonen_HK
dc.subjectTransplantationen_HK
dc.titleHepatitis C virus infection in patients on renal replacement therapyen_HK
dc.typeArticleen_HK
dc.identifier.openurlhttp://library.hku.hk:4550/resserv?sid=HKU:IR&issn=1320-5358&volume=2&issue=suppl 1&spage=85&epage=87&date=1996&atitle=Hepatitis+C+virus+infection+in+patients+on+renal+replacement+therapyen_HK
dc.identifier.emailChan, TM:dtmchan@hku.hken_HK
dc.identifier.authorityChan, TM=rp00394en_HK
dc.description.naturelink_to_subscribed_fulltext-
dc.identifier.scopuseid_2-s2.0-1842432120en_HK
dc.identifier.hkuros23600en_HK
dc.relation.referenceshttp://www.scopus.com/mlt/select.url?eid=2-s2.0-1842432120&selection=ref&src=s&origin=recordpageen_HK
dc.identifier.volume2en_HK
dc.identifier.issueSUPPL. 1en_HK
dc.identifier.spageS85en_HK
dc.identifier.epageS87en_HK
dc.identifier.isiWOS:A1996WC44900019-
dc.publisher.placeAustraliaen_HK
dc.identifier.scopusauthoridChan, TM=7402687700en_HK
dc.identifier.issnl1320-5358-

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