Effect of impaired hepatic and renal function on [131]bence jones protein catabolism in human subjects
Identifieur interne : 004F84 ( Main/Exploration ); précédent : 004F83; suivant : 004F85Effect 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.
Url:
DOI: 10.1016/0009-8981(67)90036-8
Affiliations:
Links toward previous steps (curation, corpus...)
- to stream Istex, to step Corpus: 001807
- to stream Istex, to step Curation: 001807
- to stream Istex, to step Checkpoint: 004D21
- to stream Main, to step Merge: 005034
- to stream Main, to step Curation: 004F84
Le document en format XML
<record><TEI wicri:istexFullTextTei="biblStruct"><teiHeader><fileDesc><titleStmt><title>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></author><author><name sortKey="Kekki, Matti" sort="Kekki, Matti" uniqKey="Kekki M" first="Matti" last="Kekki">Matti Kekki</name></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><idno type="wicri:Area/Istex/Curation">001807</idno><idno type="wicri:Area/Istex/Checkpoint">004D21</idno><idno type="wicri:doubleKey">0009-8981:1967:Miettinen T:effect:of:impaired</idno><idno type="wicri:Area/Main/Merge">005034</idno><idno type="wicri:Area/Main/Curation">004F84</idno><idno type="wicri:Area/Main/Exploration">004F84</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><wicri:noCountry code="subField">University of Helsinki Finland</wicri:noCountry></affiliation></author><author><name sortKey="Kekki, Matti" sort="Kekki, Matti" uniqKey="Kekki M" first="Matti" last="Kekki">Matti Kekki</name><affiliation><wicri:noCountry code="subField">University of Helsinki Finland</wicri:noCountry></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><affiliations><list></list><tree><noCountry><name sortKey="Kekki, Matti" sort="Kekki, Matti" uniqKey="Kekki M" first="Matti" last="Kekki">Matti Kekki</name><name sortKey="Miettinen, Tatu A" sort="Miettinen, Tatu A" uniqKey="Miettinen T" first="Tatu A." last="Miettinen">Tatu A. Miettinen</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
EXPLOR_STEP=$WICRI_ROOT/Wicri/Informatique/explor/ScrumV1/Data/Main/Exploration
HfdSelect -h $EXPLOR_STEP/biblio.hfd -nk 004F84 | SxmlIndent | more
Ou
HfdSelect -h $EXPLOR_AREA/Data/Main/Exploration/biblio.hfd -nk 004F84 | SxmlIndent | more
Pour mettre un lien sur cette page dans le réseau Wicri
{{Explor lien
|wiki= Wicri/Informatique
|area= ScrumV1
|flux= Main
|étape= Exploration
|type= RBID
|clé= ISTEX:A4581596494DDD855263BA568C4B3A17D0FEF6EE
|texte= Effect of impaired hepatic and renal function on [131]bence jones protein catabolism in human subjects
}}
| This area was generated with Dilib version V0.6.39. |  |