Effect of impaired hepatic and renal function on [131]bence jones protein catabolism in human subjects
Identifieur interne : 001807 ( Istex/Corpus ); précédent : 001806; suivant : 001808Effect of impaired hepatic and renal function on [131]bence jones protein catabolism in human subjects
Auteurs : Tatu A. Miettinen ; Matti KekkiSource :
- Clinica Chimica Acta [ 0009-8981 ] ; 1967.
Abstract
The role of the kidneys and the liver in the catabolism of Bence Jones protein was investigated by studying the kinetics of [131]Bence Jones protein in normal subjects and in patients with hepatic and renal insufficiency. Bence Jones protein was isolated from urine of a myeloma patient who had earlier suffered from polycythemia vera. After radioiodination, [131]Bence Jones protein was infused to recipients, and both the protein-bound 131I and free 131I were determined serially from serum and urine. The kinetic analysis was carried out with an analogy computer.Results showed that the Bence Jones protein half-time was normally only about 4 h. The rapid disappearance of the protein from the circulation was mainly due to extensive catabolism because only 3 to 4% of the total removal was caused by proteinuria. The half-time of Bence Jones protein was longer in patients with renal insufficiency, ranging from 8 to 32 h. 30 to 50% of the urinary radioactivity was present in protein-bound form, indicating that the endogenous catabolism of Bence Jones protein is markedly reduced in uremia. Furthermore, gel filtration of the urine of the uremic myeloma patient suggested that a part of the bound radioactivity was in peptide form. That the liver apparently plays a minor role in the catabolism of Bence Jones protein was shown by finding that the half-time of [131]Bence Jones protein was within normal range in two patients with moderate liver damage. One patient with severe liver insufficiency and with signs of renal tubular dysfunction had, however, a markedly reduced Bence Jones protein catabolism.
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DOI: 10.1016/0009-8981(67)90036-8
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Miettinen</name><affiliation><mods:affiliation>Third and Second Departments of Medicine and Department of Medical Chemistry, University of Helsinki Finland</mods:affiliation></affiliation></author><author><name sortKey="Kekki, Matti" sort="Kekki, Matti" uniqKey="Kekki M" first="Matti" last="Kekki">Matti Kekki</name><affiliation><mods:affiliation>Third and Second Departments of Medicine and Department of Medical Chemistry, University of Helsinki Finland</mods:affiliation></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">ISTEX</idno><idno type="RBID">ISTEX:A4581596494DDD855263BA568C4B3A17D0FEF6EE</idno><date when="1967" year="1967">1967</date><idno type="doi">10.1016/0009-8981(67)90036-8</idno><idno type="url">https://api.istex.fr/document/A4581596494DDD855263BA568C4B3A17D0FEF6EE/fulltext/pdf</idno><idno type="wicri:Area/Istex/Corpus">001807</idno></publicationStmt><sourceDesc><biblStruct><analytic><title level="a">Effect of impaired hepatic and renal function on [131]bence jones protein catabolism in human subjects</title><author><name sortKey="Miettinen, Tatu A" sort="Miettinen, Tatu A" uniqKey="Miettinen T" first="Tatu A." last="Miettinen">Tatu A. Miettinen</name><affiliation><mods:affiliation>Third and Second Departments of Medicine and Department of Medical Chemistry, University of Helsinki Finland</mods:affiliation></affiliation></author><author><name sortKey="Kekki, Matti" sort="Kekki, Matti" uniqKey="Kekki M" first="Matti" last="Kekki">Matti Kekki</name><affiliation><mods:affiliation>Third and Second Departments of Medicine and Department of Medical Chemistry, University of Helsinki Finland</mods:affiliation></affiliation></author></analytic><monogr></monogr><series><title level="j">Clinica Chimica Acta</title><title level="j" type="abbrev">CCA</title><idno type="ISSN">0009-8981</idno><imprint><publisher>ELSEVIER</publisher><date type="published" when="1967">1967</date><biblScope unit="volume">18</biblScope><biblScope unit="issue">3</biblScope><biblScope unit="page" from="395">395</biblScope><biblScope unit="page" to="407">407</biblScope></imprint><idno type="ISSN">0009-8981</idno></series><idno type="istex">A4581596494DDD855263BA568C4B3A17D0FEF6EE</idno><idno type="DOI">10.1016/0009-8981(67)90036-8</idno><idno type="PII">0009-8981(67)90036-8</idno></biblStruct></sourceDesc><seriesStmt><idno type="ISSN">0009-8981</idno></seriesStmt></fileDesc><profileDesc><textClass></textClass><langUsage><language ident="en">en</language></langUsage></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">The role of the kidneys and the liver in the catabolism of Bence Jones protein was investigated by studying the kinetics of [131]Bence Jones protein in normal subjects and in patients with hepatic and renal insufficiency. Bence Jones protein was isolated from urine of a myeloma patient who had earlier suffered from polycythemia vera. After radioiodination, [131]Bence Jones protein was infused to recipients, and both the protein-bound 131I and free 131I were determined serially from serum and urine. The kinetic analysis was carried out with an analogy computer.Results showed that the Bence Jones protein half-time was normally only about 4 h. The rapid disappearance of the protein from the circulation was mainly due to extensive catabolism because only 3 to 4% of the total removal was caused by proteinuria. The half-time of Bence Jones protein was longer in patients with renal insufficiency, ranging from 8 to 32 h. 30 to 50% of the urinary radioactivity was present in protein-bound form, indicating that the endogenous catabolism of Bence Jones protein is markedly reduced in uremia. Furthermore, gel filtration of the urine of the uremic myeloma patient suggested that a part of the bound radioactivity was in peptide form. That the liver apparently plays a minor role in the catabolism of Bence Jones protein was shown by finding that the half-time of [131]Bence Jones protein was within normal range in two patients with moderate liver damage. One patient with severe liver insufficiency and with signs of renal tubular dysfunction had, however, a markedly reduced Bence Jones protein catabolism.</div></front></TEI><istex><corpusName>elsevier</corpusName><author><json:item><name>Tatu A. 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The kinetic analysis was carried out with an analogy computer.Results showed that the Bence Jones protein half-time was normally only about 4 h. The rapid disappearance of the protein from the circulation was mainly due to extensive catabolism because only 3 to 4% of the total removal was caused by proteinuria. The half-time of Bence Jones protein was longer in patients with renal insufficiency, ranging from 8 to 32 h. 30 to 50% of the urinary radioactivity was present in protein-bound form, indicating that the endogenous catabolism of Bence Jones protein is markedly reduced in uremia. Furthermore, gel filtration of the urine of the uremic myeloma patient suggested that a part of the bound radioactivity was in peptide form. That the liver apparently plays a minor role in the catabolism of Bence Jones protein was shown by finding that the half-time of [131]Bence Jones protein was within normal range in two patients with moderate liver damage. 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Bence Jones protein was isolated from urine of a myeloma patient who had earlier suffered from polycythemia vera. After radioiodination, [131]Bence Jones protein was infused to recipients, and both the protein-bound 131I and free 131I were determined serially from serum and urine. The kinetic analysis was carried out with an analogy computer.Results showed that the Bence Jones protein half-time was normally only about 4 h. The rapid disappearance of the protein from the circulation was mainly due to extensive catabolism because only 3 to 4% of the total removal was caused by proteinuria. The half-time of Bence Jones protein was longer in patients with renal insufficiency, ranging from 8 to 32 h. 30 to 50% of the urinary radioactivity was present in protein-bound form, indicating that the endogenous catabolism of Bence Jones protein is markedly reduced in uremia. Furthermore, gel filtration of the urine of the uremic myeloma patient suggested that a part of the bound radioactivity was in peptide form. That the liver apparently plays a minor role in the catabolism of Bence Jones protein was shown by finding that the half-time of [131]Bence Jones protein was within normal range in two patients with moderate liver damage. One patient with severe liver insufficiency and with signs of renal tubular dysfunction had, however, a markedly reduced Bence Jones protein catabolism.</p></abstract></profileDesc><revisionDesc><change when="1967-07-18">Received</change><change when="1967">Published</change></revisionDesc></teiHeader></istex:fulltextTEI></fulltext><metadata><istex:metadataXml wicri:clean="Elsevier, elements deleted: tail"><istex:xmlDeclaration>version="1.0" encoding="utf-8"</istex:xmlDeclaration><istex:docType PUBLIC="-//ES//DTD journal article DTD version 4.5.2//EN//XML" URI="art452.dtd" name="istex:docType"></istex:docType><istex:document><converted-article version="4.5.2" docsubtype="fla"><item-info><jid>CCA</jid><aid>67900368</aid><ce:pii>0009-8981(67)90036-8</ce:pii><ce:doi>10.1016/0009-8981(67)90036-8</ce:doi><ce:copyright type="unknown" year="1967"></ce:copyright></item-info><head><ce:title>Effect of impaired hepatic and renal function on [<ce:sup loc="pre">131</ce:sup>]bence jones protein catabolism in human subjects</ce:title><ce:author-group><ce:author><ce:given-name>Tatu A.</ce:given-name><ce:surname>Miettinen</ce:surname></ce:author><ce:author><ce:given-name>Matti</ce:given-name><ce:surname>Kekki</ce:surname></ce:author><ce:affiliation><ce:textfn>Third and Second Departments of Medicine and Department of Medical Chemistry, University of Helsinki Finland</ce:textfn></ce:affiliation></ce:author-group><ce:date-received day="18" month="7" year="1967"></ce:date-received><ce:abstract><ce:section-title>Abstract</ce:section-title><ce:abstract-sec><ce:simple-para>The role of the kidneys and the liver in the catabolism of Bence Jones protein was investigated by studying the kinetics of [<ce:sup loc="pre">131</ce:sup>]Bence Jones protein in normal subjects and in patients with hepatic and renal insufficiency. Bence Jones protein was isolated from urine of a myeloma patient who had earlier suffered from polycythemia vera. After radioiodination, [<ce:sup loc="pre">131</ce:sup>]Bence Jones protein was infused to recipients, and both the protein-bound <ce:sup loc="pre">131</ce:sup>I and free <ce:sup loc="pre">131</ce:sup>I were determined serially from serum and urine. The kinetic analysis was carried out with an analogy computer.</ce:simple-para><ce:simple-para>Results showed that the Bence Jones protein half-time was normally only about 4 h. The rapid disappearance of the protein from the circulation was mainly due to extensive catabolism because only 3 to 4% of the total removal was caused by proteinuria. The half-time of Bence Jones protein was longer in patients with renal insufficiency, ranging from 8 to 32 h. 30 to 50% of the urinary radioactivity was present in protein-bound form, indicating that the endogenous catabolism of Bence Jones protein is markedly reduced in uremia. Furthermore, gel filtration of the urine of the uremic myeloma patient suggested that a part of the bound radioactivity was in peptide form. That the liver apparently plays a minor role in the catabolism of Bence Jones protein was shown by finding that the half-time of [<ce:sup loc="pre">131</ce:sup>]Bence Jones protein was within normal range in two patients with moderate liver damage. One patient with severe liver insufficiency and with signs of renal tubular dysfunction had, however, a markedly reduced Bence Jones protein catabolism.</ce:simple-para></ce:abstract-sec></ce:abstract></head></converted-article></istex:document></istex:metadataXml><mods version="3.6"><titleInfo><title>Effect of impaired hepatic and renal function on [131]bence jones protein catabolism in human subjects</title></titleInfo><titleInfo type="alternative" contentType="CDATA"><title>Effect of impaired hepatic and renal function on [</title></titleInfo><name type="personal"><namePart type="given">Tatu A.</namePart><namePart type="family">Miettinen</namePart><affiliation>Third and Second Departments of Medicine and Department of Medical Chemistry, University of Helsinki Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><name type="personal"><namePart type="given">Matti</namePart><namePart type="family">Kekki</namePart><affiliation>Third and Second Departments of Medicine and Department of Medical Chemistry, University of Helsinki Finland</affiliation><role><roleTerm type="text">author</roleTerm></role></name><typeOfResource>text</typeOfResource><genre type="research-article" displayLabel="Full-length article"></genre><originInfo><publisher>ELSEVIER</publisher><dateIssued encoding="w3cdtf">1967</dateIssued><dateCaptured encoding="w3cdtf">1967-07-18</dateCaptured><copyrightDate encoding="w3cdtf">1967</copyrightDate></originInfo><language><languageTerm type="code" authority="iso639-2b">eng</languageTerm><languageTerm type="code" authority="rfc3066">en</languageTerm></language><physicalDescription><internetMediaType>text/html</internetMediaType></physicalDescription><abstract lang="en">The role of the kidneys and the liver in the catabolism of Bence Jones protein was investigated by studying the kinetics of [131]Bence Jones protein in normal subjects and in patients with hepatic and renal insufficiency. Bence Jones protein was isolated from urine of a myeloma patient who had earlier suffered from polycythemia vera. After radioiodination, [131]Bence Jones protein was infused to recipients, and both the protein-bound 131I and free 131I were determined serially from serum and urine. The kinetic analysis was carried out with an analogy computer.Results showed that the Bence Jones protein half-time was normally only about 4 h. The rapid disappearance of the protein from the circulation was mainly due to extensive catabolism because only 3 to 4% of the total removal was caused by proteinuria. The half-time of Bence Jones protein was longer in patients with renal insufficiency, ranging from 8 to 32 h. 30 to 50% of the urinary radioactivity was present in protein-bound form, indicating that the endogenous catabolism of Bence Jones protein is markedly reduced in uremia. Furthermore, gel filtration of the urine of the uremic myeloma patient suggested that a part of the bound radioactivity was in peptide form. That the liver apparently plays a minor role in the catabolism of Bence Jones protein was shown by finding that the half-time of [131]Bence Jones protein was within normal range in two patients with moderate liver damage. One patient with severe liver insufficiency and with signs of renal tubular dysfunction had, however, a markedly reduced Bence Jones protein catabolism.</abstract><relatedItem type="host"><titleInfo><title>Clinica Chimica Acta</title></titleInfo><titleInfo type="abbreviated"><title>CCA</title></titleInfo><genre type="Journal">journal</genre><originInfo><dateIssued encoding="w3cdtf">196712</dateIssued></originInfo><identifier type="ISSN">0009-8981</identifier><identifier type="PII">S0009-8981(00)X0791-7</identifier><part><date>196712</date><detail type="volume"><number>18</number><caption>vol.</caption></detail><detail type="issue"><number>3</number><caption>no.</caption></detail><extent unit="issue pages"><start>325</start><end>499</end></extent><extent unit="pages"><start>395</start><end>407</end></extent></part></relatedItem><identifier type="istex">A4581596494DDD855263BA568C4B3A17D0FEF6EE</identifier><identifier type="DOI">10.1016/0009-8981(67)90036-8</identifier><identifier type="PII">0009-8981(67)90036-8</identifier><recordInfo><recordContentSource>ELSEVIER</recordContentSource></recordInfo></mods></metadata><enrichments><istex:catWosTEI uri="https://api.istex.fr/document/A4581596494DDD855263BA568C4B3A17D0FEF6EE/enrichments/catWos"><teiHeader><profileDesc><textClass><classCode scheme="WOS">MEDICINE, GENERAL & INTERNAL</classCode><classCode scheme="WOS">BIOCHEMISTRY & MOLECULAR BIOLOGY</classCode><classCode scheme="WOS">MEDICAL LABORATORY TECHNOLOGY</classCode></textClass></profileDesc></teiHeader></istex:catWosTEI></enrichments><serie></serie></istex></record>Pour manipuler ce document sous Unix (Dilib)
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