Effect of impaired hepatic and renal function on [131]bence jones protein catabolism in human subjects
Identifieur interne : 004F84 ( Main/Curation ); 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.
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DOI: 10.1016/0009-8981(67)90036-8
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Tatu A. Miettinen<affiliation><wicri:noCountry code="subField">University of Helsinki Finland</wicri:noCountry>
</affiliation>
<affiliation><wicri:noCountry code="subField">University of Helsinki Finland</wicri:noCountry>
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<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>
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