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Hepatitis C virus infection in kidney transplant recipients
To determine the prevalence and significance of hepatitis C virus infection in kidney transplant recipients, paired serum samples collected from 100 renal allograft recipients on admission for kidney transplantation and 1 yr after transplantation were tested for antibody to hepatitis C virus with se...
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| Published in: | Hepatology (Baltimore, Md.) Md.), 1993-11, Vol.18 (5), p.1027-1031 |
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| container_end_page | 1031 |
| container_issue | 5 |
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| container_title | Hepatology (Baltimore, Md.) |
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| creator | Lau, Johnson Y. N. Davis, Gary L. Brunson, Mathew E. Qian, Ke‐Ping Lin, Hsiang‐Ju Quan, Stella Dinello, Robert Polito, Alan J. Scornik, Juan C. |
| description | To determine the prevalence and significance of hepatitis C virus infection in kidney transplant recipients, paired serum samples collected from 100 renal allograft recipients on admission for kidney transplantation and 1 yr after transplantation were tested for antibody to hepatitis C virus with second‐generation enzyme immunoassay and recombinant immunoblot assay and for hepatitis C virus RNA with reverse transcription–polymerase chain reaction. Before kidney transplantation, hepatitis C virus antibody was detected with second‐generation enzyme immunoassay in 18 patients (12 second‐generation recombinant immunoblot assay–positive, 6 second‐generation recombinant immunoblot assay–indeterminate). Nine of 12 second‐generation recombinant immunoblot assay–positive and 2 of 6 second‐generation recombinant immunoblot assay–indeterminate samples were hepatitis C virus RNA positive. In addition, 7 of 82 patients who had no detectable antibody on second‐generation enzyme immunoassay or second‐generation recombinant immunoblot assay were hepatitis C virus RNA positive. After kidney transplantation, hepatitis C virus antibody was detected in 19 patients (12 second‐generation recombinant immunoblot assay–positive, 7 second‐generation recombinant immunoblot assay–indeterminate, 14 seropositive for hepatitis C virus antibody). Eleven of 12 patients with second‐generation recombinant immunoblot assay–positive results and 4 of 7 with second‐generation recombinant immunoblot assay–indeterminate results were positive for hepatitis C virus RNA. Hepatitis C virus RNA was present in 28 patients 1 yr after kidney transplantation. Six patients appeared to have acquired active hepatitis C virus infection 1 yr after kidney transplantation (seroconverted to hepatitis C virus RNA positivity). We found no correlation between the presence of hepatitis C virus markers in the pretransplant and posttransplant sera and clinical/biochemical parameters or clinical outcome. Hepatitis C virus infection was clinically silent in most patients. Semiquantitation of serum hepatitis C virus RNA in 25 patients with hepatitis C virus infection showed that the hepatitis C virus RNA titer remained the same (n = 12) or increased at least 10‐fold (n = 12), and only 1 patient had a decrease in serum hepatitis C virus RNA level. These data suggest that (a) the prevalence of hepatitis C virus infection is high in kidney transplant recipients, (b) active hepatitis C virus replication may be present in the |
| doi_str_mv | 10.1002/hep.1840180502 |
| format | article |
| fullrecord | <record><control><sourceid>wiley_cross</sourceid><recordid>TN_cdi_crossref_primary_10_1002_hep_1840180502</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>HEP1840180502</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3782-6f426613023d2f71b96bbcd54e0bf8a199b5e3284e9eec00e27a0791cbe2d3053</originalsourceid><addsrcrecordid>eNqFkDFPwzAQhS0EKqWwsiFlYE0523FsiwlVhSJVggHmyHbOwpCmkR1A_fekalXYmO6k-97dvUfIJYUpBWA3b9hNqSqAKhDAjsiYCiZzzgUckzEwCbmmXJ-Ss5TeAUAXTI3ISJaai1KOye0CO9OHPqRsln2F-Jmy0Hp0fVi3Q5d9hLrFTdZH06auMW2fRXShC9j26ZyceNMkvNjXCXm9n7_MFvny6eFxdrfMHZeK5aUvWFlSDozXzEtqdWmtq0WBYL0yVGsrkDNVoEZ0AMikAamps8hqDoJPyHS318V1ShF91cWwMnFTUai2IVRDCNVvCIPgaifoPu0K6wO-dz3Mr_dzk5xp_GDOhXTAuKKU0S2md9h3aHDzz9FqMX_-88IPim90xA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Hepatitis C virus infection in kidney transplant recipients</title><source>Alma/SFX Local Collection</source><creator>Lau, Johnson Y. N. ; Davis, Gary L. ; Brunson, Mathew E. ; Qian, Ke‐Ping ; Lin, Hsiang‐Ju ; Quan, Stella ; Dinello, Robert ; Polito, Alan J. ; Scornik, Juan C.</creator><creatorcontrib>Lau, Johnson Y. N. ; Davis, Gary L. ; Brunson, Mathew E. ; Qian, Ke‐Ping ; Lin, Hsiang‐Ju ; Quan, Stella ; Dinello, Robert ; Polito, Alan J. ; Scornik, Juan C.</creatorcontrib><description>To determine the prevalence and significance of hepatitis C virus infection in kidney transplant recipients, paired serum samples collected from 100 renal allograft recipients on admission for kidney transplantation and 1 yr after transplantation were tested for antibody to hepatitis C virus with second‐generation enzyme immunoassay and recombinant immunoblot assay and for hepatitis C virus RNA with reverse transcription–polymerase chain reaction. Before kidney transplantation, hepatitis C virus antibody was detected with second‐generation enzyme immunoassay in 18 patients (12 second‐generation recombinant immunoblot assay–positive, 6 second‐generation recombinant immunoblot assay–indeterminate). Nine of 12 second‐generation recombinant immunoblot assay–positive and 2 of 6 second‐generation recombinant immunoblot assay–indeterminate samples were hepatitis C virus RNA positive. In addition, 7 of 82 patients who had no detectable antibody on second‐generation enzyme immunoassay or second‐generation recombinant immunoblot assay were hepatitis C virus RNA positive. After kidney transplantation, hepatitis C virus antibody was detected in 19 patients (12 second‐generation recombinant immunoblot assay–positive, 7 second‐generation recombinant immunoblot assay–indeterminate, 14 seropositive for hepatitis C virus antibody). Eleven of 12 patients with second‐generation recombinant immunoblot assay–positive results and 4 of 7 with second‐generation recombinant immunoblot assay–indeterminate results were positive for hepatitis C virus RNA. Hepatitis C virus RNA was present in 28 patients 1 yr after kidney transplantation. Six patients appeared to have acquired active hepatitis C virus infection 1 yr after kidney transplantation (seroconverted to hepatitis C virus RNA positivity). We found no correlation between the presence of hepatitis C virus markers in the pretransplant and posttransplant sera and clinical/biochemical parameters or clinical outcome. Hepatitis C virus infection was clinically silent in most patients. Semiquantitation of serum hepatitis C virus RNA in 25 patients with hepatitis C virus infection showed that the hepatitis C virus RNA titer remained the same (n = 12) or increased at least 10‐fold (n = 12), and only 1 patient had a decrease in serum hepatitis C virus RNA level. These data suggest that (a) the prevalence of hepatitis C virus infection is high in kidney transplant recipients, (b) active hepatitis C virus replication may be present in the absence of hepatitis C virus antibody, (c) many of these patients who are second‐generation enzyme immunoassay–positive but second‐generation recombinant immunoblot assay–indeterminate are hepatitis C virus RNA positive, (d) hepatitis C virus infection is usually clinically silent during the initial follow‐up period and (e) antirejection immunosuppression may enhance hepatitis C virus replication. (HEPATOLOGY 1993;18:1027‐1031).</description><identifier>ISSN: 0270-9139</identifier><identifier>EISSN: 1527-3350</identifier><identifier>DOI: 10.1002/hep.1840180502</identifier><identifier>PMID: 7693567</identifier><identifier>CODEN: HPTLD9</identifier><language>eng</language><publisher>Philadelphia, PA: W.B. Saunders</publisher><subject>Adult ; Aged ; Biological and medical sciences ; Female ; Hepacivirus - genetics ; Hepacivirus - immunology ; Hepatitis Antibodies - analysis ; Hepatitis C - diagnosis ; Hepatitis C - epidemiology ; Hepatitis C - immunology ; Hepatitis C Antibodies ; Humans ; Immunoblotting ; Immunoenzyme Techniques ; Kidney Failure, Chronic - surgery ; Kidney Transplantation ; Male ; Medical sciences ; Middle Aged ; Polymerase Chain Reaction ; Prevalence ; Prognosis ; RNA, Viral - analysis ; Seroepidemiologic Studies ; Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases ; Surgery of the urinary system</subject><ispartof>Hepatology (Baltimore, Md.), 1993-11, Vol.18 (5), p.1027-1031</ispartof><rights>Copyright © 1993 American Association for the Study of Liver Diseases</rights><rights>1994 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3782-6f426613023d2f71b96bbcd54e0bf8a199b5e3284e9eec00e27a0791cbe2d3053</citedby><cites>FETCH-LOGICAL-c3782-6f426613023d2f71b96bbcd54e0bf8a199b5e3284e9eec00e27a0791cbe2d3053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=3811217$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/7693567$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lau, Johnson Y. N.</creatorcontrib><creatorcontrib>Davis, Gary L.</creatorcontrib><creatorcontrib>Brunson, Mathew E.</creatorcontrib><creatorcontrib>Qian, Ke‐Ping</creatorcontrib><creatorcontrib>Lin, Hsiang‐Ju</creatorcontrib><creatorcontrib>Quan, Stella</creatorcontrib><creatorcontrib>Dinello, Robert</creatorcontrib><creatorcontrib>Polito, Alan J.</creatorcontrib><creatorcontrib>Scornik, Juan C.</creatorcontrib><title>Hepatitis C virus infection in kidney transplant recipients</title><title>Hepatology (Baltimore, Md.)</title><addtitle>Hepatology</addtitle><description>To determine the prevalence and significance of hepatitis C virus infection in kidney transplant recipients, paired serum samples collected from 100 renal allograft recipients on admission for kidney transplantation and 1 yr after transplantation were tested for antibody to hepatitis C virus with second‐generation enzyme immunoassay and recombinant immunoblot assay and for hepatitis C virus RNA with reverse transcription–polymerase chain reaction. Before kidney transplantation, hepatitis C virus antibody was detected with second‐generation enzyme immunoassay in 18 patients (12 second‐generation recombinant immunoblot assay–positive, 6 second‐generation recombinant immunoblot assay–indeterminate). Nine of 12 second‐generation recombinant immunoblot assay–positive and 2 of 6 second‐generation recombinant immunoblot assay–indeterminate samples were hepatitis C virus RNA positive. In addition, 7 of 82 patients who had no detectable antibody on second‐generation enzyme immunoassay or second‐generation recombinant immunoblot assay were hepatitis C virus RNA positive. After kidney transplantation, hepatitis C virus antibody was detected in 19 patients (12 second‐generation recombinant immunoblot assay–positive, 7 second‐generation recombinant immunoblot assay–indeterminate, 14 seropositive for hepatitis C virus antibody). Eleven of 12 patients with second‐generation recombinant immunoblot assay–positive results and 4 of 7 with second‐generation recombinant immunoblot assay–indeterminate results were positive for hepatitis C virus RNA. Hepatitis C virus RNA was present in 28 patients 1 yr after kidney transplantation. Six patients appeared to have acquired active hepatitis C virus infection 1 yr after kidney transplantation (seroconverted to hepatitis C virus RNA positivity). We found no correlation between the presence of hepatitis C virus markers in the pretransplant and posttransplant sera and clinical/biochemical parameters or clinical outcome. Hepatitis C virus infection was clinically silent in most patients. Semiquantitation of serum hepatitis C virus RNA in 25 patients with hepatitis C virus infection showed that the hepatitis C virus RNA titer remained the same (n = 12) or increased at least 10‐fold (n = 12), and only 1 patient had a decrease in serum hepatitis C virus RNA level. These data suggest that (a) the prevalence of hepatitis C virus infection is high in kidney transplant recipients, (b) active hepatitis C virus replication may be present in the absence of hepatitis C virus antibody, (c) many of these patients who are second‐generation enzyme immunoassay–positive but second‐generation recombinant immunoblot assay–indeterminate are hepatitis C virus RNA positive, (d) hepatitis C virus infection is usually clinically silent during the initial follow‐up period and (e) antirejection immunosuppression may enhance hepatitis C virus replication. (HEPATOLOGY 1993;18:1027‐1031).</description><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Hepacivirus - genetics</subject><subject>Hepacivirus - immunology</subject><subject>Hepatitis Antibodies - analysis</subject><subject>Hepatitis C - diagnosis</subject><subject>Hepatitis C - epidemiology</subject><subject>Hepatitis C - immunology</subject><subject>Hepatitis C Antibodies</subject><subject>Humans</subject><subject>Immunoblotting</subject><subject>Immunoenzyme Techniques</subject><subject>Kidney Failure, Chronic - surgery</subject><subject>Kidney Transplantation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Polymerase Chain Reaction</subject><subject>Prevalence</subject><subject>Prognosis</subject><subject>RNA, Viral - analysis</subject><subject>Seroepidemiologic Studies</subject><subject>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</subject><subject>Surgery of the urinary system</subject><issn>0270-9139</issn><issn>1527-3350</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><recordid>eNqFkDFPwzAQhS0EKqWwsiFlYE0523FsiwlVhSJVggHmyHbOwpCmkR1A_fekalXYmO6k-97dvUfIJYUpBWA3b9hNqSqAKhDAjsiYCiZzzgUckzEwCbmmXJ-Ss5TeAUAXTI3ISJaai1KOye0CO9OHPqRsln2F-Jmy0Hp0fVi3Q5d9hLrFTdZH06auMW2fRXShC9j26ZyceNMkvNjXCXm9n7_MFvny6eFxdrfMHZeK5aUvWFlSDozXzEtqdWmtq0WBYL0yVGsrkDNVoEZ0AMikAamps8hqDoJPyHS318V1ShF91cWwMnFTUai2IVRDCNVvCIPgaifoPu0K6wO-dz3Mr_dzk5xp_GDOhXTAuKKU0S2md9h3aHDzz9FqMX_-88IPim90xA</recordid><startdate>199311</startdate><enddate>199311</enddate><creator>Lau, Johnson Y. N.</creator><creator>Davis, Gary L.</creator><creator>Brunson, Mathew E.</creator><creator>Qian, Ke‐Ping</creator><creator>Lin, Hsiang‐Ju</creator><creator>Quan, Stella</creator><creator>Dinello, Robert</creator><creator>Polito, Alan J.</creator><creator>Scornik, Juan C.</creator><general>W.B. Saunders</general><general>Wiley</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope></search><sort><creationdate>199311</creationdate><title>Hepatitis C virus infection in kidney transplant recipients</title><author>Lau, Johnson Y. N. ; Davis, Gary L. ; Brunson, Mathew E. ; Qian, Ke‐Ping ; Lin, Hsiang‐Ju ; Quan, Stella ; Dinello, Robert ; Polito, Alan J. ; Scornik, Juan C.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3782-6f426613023d2f71b96bbcd54e0bf8a199b5e3284e9eec00e27a0791cbe2d3053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Female</topic><topic>Hepacivirus - genetics</topic><topic>Hepacivirus - immunology</topic><topic>Hepatitis Antibodies - analysis</topic><topic>Hepatitis C - diagnosis</topic><topic>Hepatitis C - epidemiology</topic><topic>Hepatitis C - immunology</topic><topic>Hepatitis C Antibodies</topic><topic>Humans</topic><topic>Immunoblotting</topic><topic>Immunoenzyme Techniques</topic><topic>Kidney Failure, Chronic - surgery</topic><topic>Kidney Transplantation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Polymerase Chain Reaction</topic><topic>Prevalence</topic><topic>Prognosis</topic><topic>RNA, Viral - analysis</topic><topic>Seroepidemiologic Studies</topic><topic>Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases</topic><topic>Surgery of the urinary system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lau, Johnson Y. N.</creatorcontrib><creatorcontrib>Davis, Gary L.</creatorcontrib><creatorcontrib>Brunson, Mathew E.</creatorcontrib><creatorcontrib>Qian, Ke‐Ping</creatorcontrib><creatorcontrib>Lin, Hsiang‐Ju</creatorcontrib><creatorcontrib>Quan, Stella</creatorcontrib><creatorcontrib>Dinello, Robert</creatorcontrib><creatorcontrib>Polito, Alan J.</creatorcontrib><creatorcontrib>Scornik, Juan C.</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><jtitle>Hepatology (Baltimore, Md.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lau, Johnson Y. N.</au><au>Davis, Gary L.</au><au>Brunson, Mathew E.</au><au>Qian, Ke‐Ping</au><au>Lin, Hsiang‐Ju</au><au>Quan, Stella</au><au>Dinello, Robert</au><au>Polito, Alan J.</au><au>Scornik, Juan C.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hepatitis C virus infection in kidney transplant recipients</atitle><jtitle>Hepatology (Baltimore, Md.)</jtitle><addtitle>Hepatology</addtitle><date>1993-11</date><risdate>1993</risdate><volume>18</volume><issue>5</issue><spage>1027</spage><epage>1031</epage><pages>1027-1031</pages><issn>0270-9139</issn><eissn>1527-3350</eissn><coden>HPTLD9</coden><abstract>To determine the prevalence and significance of hepatitis C virus infection in kidney transplant recipients, paired serum samples collected from 100 renal allograft recipients on admission for kidney transplantation and 1 yr after transplantation were tested for antibody to hepatitis C virus with second‐generation enzyme immunoassay and recombinant immunoblot assay and for hepatitis C virus RNA with reverse transcription–polymerase chain reaction. Before kidney transplantation, hepatitis C virus antibody was detected with second‐generation enzyme immunoassay in 18 patients (12 second‐generation recombinant immunoblot assay–positive, 6 second‐generation recombinant immunoblot assay–indeterminate). Nine of 12 second‐generation recombinant immunoblot assay–positive and 2 of 6 second‐generation recombinant immunoblot assay–indeterminate samples were hepatitis C virus RNA positive. In addition, 7 of 82 patients who had no detectable antibody on second‐generation enzyme immunoassay or second‐generation recombinant immunoblot assay were hepatitis C virus RNA positive. After kidney transplantation, hepatitis C virus antibody was detected in 19 patients (12 second‐generation recombinant immunoblot assay–positive, 7 second‐generation recombinant immunoblot assay–indeterminate, 14 seropositive for hepatitis C virus antibody). Eleven of 12 patients with second‐generation recombinant immunoblot assay–positive results and 4 of 7 with second‐generation recombinant immunoblot assay–indeterminate results were positive for hepatitis C virus RNA. Hepatitis C virus RNA was present in 28 patients 1 yr after kidney transplantation. Six patients appeared to have acquired active hepatitis C virus infection 1 yr after kidney transplantation (seroconverted to hepatitis C virus RNA positivity). We found no correlation between the presence of hepatitis C virus markers in the pretransplant and posttransplant sera and clinical/biochemical parameters or clinical outcome. Hepatitis C virus infection was clinically silent in most patients. Semiquantitation of serum hepatitis C virus RNA in 25 patients with hepatitis C virus infection showed that the hepatitis C virus RNA titer remained the same (n = 12) or increased at least 10‐fold (n = 12), and only 1 patient had a decrease in serum hepatitis C virus RNA level. These data suggest that (a) the prevalence of hepatitis C virus infection is high in kidney transplant recipients, (b) active hepatitis C virus replication may be present in the absence of hepatitis C virus antibody, (c) many of these patients who are second‐generation enzyme immunoassay–positive but second‐generation recombinant immunoblot assay–indeterminate are hepatitis C virus RNA positive, (d) hepatitis C virus infection is usually clinically silent during the initial follow‐up period and (e) antirejection immunosuppression may enhance hepatitis C virus replication. (HEPATOLOGY 1993;18:1027‐1031).</abstract><cop>Philadelphia, PA</cop><pub>W.B. Saunders</pub><pmid>7693567</pmid><doi>10.1002/hep.1840180502</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 0270-9139 |
| ispartof | Hepatology (Baltimore, Md.), 1993-11, Vol.18 (5), p.1027-1031 |
| issn | 0270-9139 1527-3350 |
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| source | Alma/SFX Local Collection |
| subjects | Adult Aged Biological and medical sciences Female Hepacivirus - genetics Hepacivirus - immunology Hepatitis Antibodies - analysis Hepatitis C - diagnosis Hepatitis C - epidemiology Hepatitis C - immunology Hepatitis C Antibodies Humans Immunoblotting Immunoenzyme Techniques Kidney Failure, Chronic - surgery Kidney Transplantation Male Medical sciences Middle Aged Polymerase Chain Reaction Prevalence Prognosis RNA, Viral - analysis Seroepidemiologic Studies Surgery (general aspects). Transplantations, organ and tissue grafts. Graft diseases Surgery of the urinary system |
| title | Hepatitis C virus infection in kidney transplant recipients |
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