Idiopathic hypoalbuminemia explained by reduced synthesis rate and an increased catabolic rate

Berthil H C M T Prinsen, George Kaysen, Leo W J Klomp, Jose De Boer, P. Hugh R Barrett, Paul J. Thornalley, Sinan Battah, Ruud Berger, Ton J. Rabelink, Monique G M De Sain-van der Velden

Research output: Contribution to journalArticle

7 Citations (Scopus)

Abstract

Objective: To determine the contribution of albumin synthetic and catabolic rates to steady state levels in a patient with idiopathic hypoalbuminemia. Methods: Using L-[1-13C] valine, both FSR (fractional synthesis rate) as well as FCR (fractional catabolic rate) were studied. Human albumin cDNA analysis and determination of the exact albumin mass by electrospray mass spectrometry were performed. Results: Compared with controls, plasma albumin concentration in the patient was reduced (6.7 vs. 37.0 ± 2.6 g/L). Albumin FSR (= FCR in steady state) was increased compared to controls. The ASR (absolute synthesis rate) of albumin was decreased based on the enrichment in plasma valine and KIV, but estimated to be normal based on VLDL apoB100 at plateau compared to controls. Direct estimation of albumin FCR rejected the latter. No mutation was found in the transcribed region of albumin gene. The exact mass of albumin (66.493 Da) was not different from controls. Conclusion: The hypoalbuminemia was a result of accelerated clearance of albumin from plasma in addition to defective albumin synthesis. This study also shows that the chosen method of the precursor pool could lead to misinterpretation of data in hepatic protein synthesis.

Original languageEnglish (US)
Pages (from-to)545-553
Number of pages9
JournalClinical Biochemistry
Volume35
Issue number7
DOIs
StatePublished - Oct 2002

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Hypoalbuminemia
Albumins
Valine
Serum Albumin
Mass spectrometry
Mass Spectrometry
Complementary DNA
Genes
Plasmas
Mutation

Keywords

  • Albumin
  • Idiopathic hypoalbuminemia
  • Mass spectrometry
  • Precursor pool
  • Stable isotopes

ASJC Scopus subject areas

  • Clinical Biochemistry

Cite this

Prinsen, B. H. C. M. T., Kaysen, G., Klomp, L. W. J., De Boer, J., Barrett, P. H. R., Thornalley, P. J., ... De Sain-van der Velden, M. G. M. (2002). Idiopathic hypoalbuminemia explained by reduced synthesis rate and an increased catabolic rate. Clinical Biochemistry, 35(7), 545-553. https://doi.org/10.1016/S0009-9120(02)00357-0

Idiopathic hypoalbuminemia explained by reduced synthesis rate and an increased catabolic rate. / Prinsen, Berthil H C M T; Kaysen, George; Klomp, Leo W J; De Boer, Jose; Barrett, P. Hugh R; Thornalley, Paul J.; Battah, Sinan; Berger, Ruud; Rabelink, Ton J.; De Sain-van der Velden, Monique G M.

In: Clinical Biochemistry, Vol. 35, No. 7, 10.2002, p. 545-553.

Research output: Contribution to journalArticle

Prinsen, BHCMT, Kaysen, G, Klomp, LWJ, De Boer, J, Barrett, PHR, Thornalley, PJ, Battah, S, Berger, R, Rabelink, TJ & De Sain-van der Velden, MGM 2002, 'Idiopathic hypoalbuminemia explained by reduced synthesis rate and an increased catabolic rate', Clinical Biochemistry, vol. 35, no. 7, pp. 545-553. https://doi.org/10.1016/S0009-9120(02)00357-0
Prinsen, Berthil H C M T ; Kaysen, George ; Klomp, Leo W J ; De Boer, Jose ; Barrett, P. Hugh R ; Thornalley, Paul J. ; Battah, Sinan ; Berger, Ruud ; Rabelink, Ton J. ; De Sain-van der Velden, Monique G M. / Idiopathic hypoalbuminemia explained by reduced synthesis rate and an increased catabolic rate. In: Clinical Biochemistry. 2002 ; Vol. 35, No. 7. pp. 545-553.
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