Brain metabolism of amino acids and ammonia in patients with chronic renal insufficiency

G. Deferrari, G. Garibotto, C. Robaudo, G. M. Ghiggeri, A. Tizianello

Research output: Contribution to journalArticle

Abstract

The cerebral metabolism of amino acids (AA) and ammonia in the postabsorptive state was evaluated in 8 subjects with normal renal function and in 6 patients with chronic renal insufficiency (CRI) by measuring the differences between the arterial and the internal jugular venous concentrations of free AA and ammonia. In normal conditions, the brain extracts serine, glutamine, proline, glycine, valine, 1/2 cystine, isoleucine, leucine, and lysine. In CRI, cerebral glycine and 1/2 cystine uptake increases, valine and isoleucine extraction decreases, glutamine uptake disappears, and ammonia extraction becomes evident. The cerebral extraction of glycine is correlated with the arterial concentration of glycine, serine, and branched-chain AA. The extraction of 1/2 cystine is correlated with the arterial concentration of 1/2 cystine and tyrosine. Finally, the extractions of valine and ammonia are correlated with the arterial concentration of valine and ammonia, respectively. It follows that alterations of blood AA and ammonia concentrations observed in CRI markedly affect the cerebral uptake of some AA and ammonia. The lack of cerebral glutamine extraction might be due to an enhanced production and/or, more likely, to an impaired utilization of this AA by the brain. Data reported here suggest that in CRI cerebral nitrogen metabolism is altered; such alterations may play a pathogenic role in uremic encephalopathy.

Original languageEnglish
Pages (from-to)505-510
Number of pages6
JournalKidney International
Volume20
Issue number4
Publication statusPublished - 1981

Fingerprint

Chronic Renal Insufficiency
Ammonia
Cystine
Amino Acids
Valine
Brain
Glycine
Glutamine
Isoleucine
Serine
Branched Chain Amino Acids
Brain Diseases
Proline
Leucine
Lysine
Neck
Nitrogen
Kidney

ASJC Scopus subject areas

  • Nephrology

Cite this

Deferrari, G., Garibotto, G., Robaudo, C., Ghiggeri, G. M., & Tizianello, A. (1981). Brain metabolism of amino acids and ammonia in patients with chronic renal insufficiency. Kidney International, 20(4), 505-510.

Brain metabolism of amino acids and ammonia in patients with chronic renal insufficiency. / Deferrari, G.; Garibotto, G.; Robaudo, C.; Ghiggeri, G. M.; Tizianello, A.

In: Kidney International, Vol. 20, No. 4, 1981, p. 505-510.

Research output: Contribution to journalArticle

Deferrari, G, Garibotto, G, Robaudo, C, Ghiggeri, GM & Tizianello, A 1981, 'Brain metabolism of amino acids and ammonia in patients with chronic renal insufficiency', Kidney International, vol. 20, no. 4, pp. 505-510.
Deferrari, G. ; Garibotto, G. ; Robaudo, C. ; Ghiggeri, G. M. ; Tizianello, A. / Brain metabolism of amino acids and ammonia in patients with chronic renal insufficiency. In: Kidney International. 1981 ; Vol. 20, No. 4. pp. 505-510.
@article{e65870e5a2f645eeb9ec6a1a7f9e7bae,
title = "Brain metabolism of amino acids and ammonia in patients with chronic renal insufficiency",
abstract = "The cerebral metabolism of amino acids (AA) and ammonia in the postabsorptive state was evaluated in 8 subjects with normal renal function and in 6 patients with chronic renal insufficiency (CRI) by measuring the differences between the arterial and the internal jugular venous concentrations of free AA and ammonia. In normal conditions, the brain extracts serine, glutamine, proline, glycine, valine, 1/2 cystine, isoleucine, leucine, and lysine. In CRI, cerebral glycine and 1/2 cystine uptake increases, valine and isoleucine extraction decreases, glutamine uptake disappears, and ammonia extraction becomes evident. The cerebral extraction of glycine is correlated with the arterial concentration of glycine, serine, and branched-chain AA. The extraction of 1/2 cystine is correlated with the arterial concentration of 1/2 cystine and tyrosine. Finally, the extractions of valine and ammonia are correlated with the arterial concentration of valine and ammonia, respectively. It follows that alterations of blood AA and ammonia concentrations observed in CRI markedly affect the cerebral uptake of some AA and ammonia. The lack of cerebral glutamine extraction might be due to an enhanced production and/or, more likely, to an impaired utilization of this AA by the brain. Data reported here suggest that in CRI cerebral nitrogen metabolism is altered; such alterations may play a pathogenic role in uremic encephalopathy.",
author = "G. Deferrari and G. Garibotto and C. Robaudo and Ghiggeri, {G. M.} and A. Tizianello",
year = "1981",
language = "English",
volume = "20",
pages = "505--510",
journal = "Kidney International",
issn = "0085-2538",
publisher = "Nature Publishing Group",
number = "4",

}

TY - JOUR

T1 - Brain metabolism of amino acids and ammonia in patients with chronic renal insufficiency

AU - Deferrari, G.

AU - Garibotto, G.

AU - Robaudo, C.

AU - Ghiggeri, G. M.

AU - Tizianello, A.

PY - 1981

Y1 - 1981

N2 - The cerebral metabolism of amino acids (AA) and ammonia in the postabsorptive state was evaluated in 8 subjects with normal renal function and in 6 patients with chronic renal insufficiency (CRI) by measuring the differences between the arterial and the internal jugular venous concentrations of free AA and ammonia. In normal conditions, the brain extracts serine, glutamine, proline, glycine, valine, 1/2 cystine, isoleucine, leucine, and lysine. In CRI, cerebral glycine and 1/2 cystine uptake increases, valine and isoleucine extraction decreases, glutamine uptake disappears, and ammonia extraction becomes evident. The cerebral extraction of glycine is correlated with the arterial concentration of glycine, serine, and branched-chain AA. The extraction of 1/2 cystine is correlated with the arterial concentration of 1/2 cystine and tyrosine. Finally, the extractions of valine and ammonia are correlated with the arterial concentration of valine and ammonia, respectively. It follows that alterations of blood AA and ammonia concentrations observed in CRI markedly affect the cerebral uptake of some AA and ammonia. The lack of cerebral glutamine extraction might be due to an enhanced production and/or, more likely, to an impaired utilization of this AA by the brain. Data reported here suggest that in CRI cerebral nitrogen metabolism is altered; such alterations may play a pathogenic role in uremic encephalopathy.

AB - The cerebral metabolism of amino acids (AA) and ammonia in the postabsorptive state was evaluated in 8 subjects with normal renal function and in 6 patients with chronic renal insufficiency (CRI) by measuring the differences between the arterial and the internal jugular venous concentrations of free AA and ammonia. In normal conditions, the brain extracts serine, glutamine, proline, glycine, valine, 1/2 cystine, isoleucine, leucine, and lysine. In CRI, cerebral glycine and 1/2 cystine uptake increases, valine and isoleucine extraction decreases, glutamine uptake disappears, and ammonia extraction becomes evident. The cerebral extraction of glycine is correlated with the arterial concentration of glycine, serine, and branched-chain AA. The extraction of 1/2 cystine is correlated with the arterial concentration of 1/2 cystine and tyrosine. Finally, the extractions of valine and ammonia are correlated with the arterial concentration of valine and ammonia, respectively. It follows that alterations of blood AA and ammonia concentrations observed in CRI markedly affect the cerebral uptake of some AA and ammonia. The lack of cerebral glutamine extraction might be due to an enhanced production and/or, more likely, to an impaired utilization of this AA by the brain. Data reported here suggest that in CRI cerebral nitrogen metabolism is altered; such alterations may play a pathogenic role in uremic encephalopathy.

UR - http://www.scopus.com/inward/record.url?scp=0019446189&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0019446189&partnerID=8YFLogxK

M3 - Article

C2 - 7311310

AN - SCOPUS:0019446189

VL - 20

SP - 505

EP - 510

JO - Kidney International

JF - Kidney International

SN - 0085-2538

IS - 4

ER -