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Renal ammonia and glutamine metabolism during liver insufficiency-induced hyperammonemia in the rat.
J Clin Invest. 1993 Dec; 92(6):2834-40.JCI

Abstract

Renal glutamine uptake and subsequent urinary ammonia excretion could be an important alternative pathway of ammonia disposal from the body during liver failure (diminished urea synthesis), but this pathway has received little attention. Therefore, we investigated renal glutamine and ammonia metabolism in midly hyperammonemic, portacaval shunted rats and severely hyperammonemic rats with acute liver ischemia compared to their respective controls, to investigate whether renal ammonia disposal from the body is enhanced during hyperammonemia and to explore the limits of the pathway. Renal fluxes, urinary excretion, and renal tissue concentrations of amino acids and ammonia were measured 24 h after portacaval shunting, and 2, 4, and 6 h after liver ischemia induction and in the appropriate controls. Arterial ammonia increased to 247 +/- 22 microM after portacaval shunting compared to controls (51 +/- 8 microM) (P < 0.001) and increased to 934 +/- 54 microM during liver ischemia (P < 0.001). Arterial glutamine increased to 697 +/- 93 microM after portacaval shunting compared to controls (513 +/- 40 microM) (P < 0.01) and further increased to 3781 +/- 248 microM during liver ischemia (P < 0.001). In contrast to controls, in portacaval shunted rats the kidney net disposed ammonia from the body by diminishing renal venous ammonia release (from 267 +/- 33 to -49 +/- 59 nmol/100 g body wt per min) and enhancing urinary ammonia excretion from 113 +/- 24 to 305 +/- 52 nmol/100 g body wt per min (both P < 0.01). Renal glutamine uptake diminished in portacaval shunted rats compared to controls (-107 +/- 33 vs. -322 +/- 41 nmol/100 g body wt per min) (P < 0.01). However, during liver ischemia, net renal ammonia disposal from the body did not further increase (294 +/- 88 vs. 144 +/- 101 nmol/100 g body wt per min during portacaval shunting versus liver ischemia). Renal glutamine uptake was comparable in both hyperammonemic models. These results indicate that the rat kidney plays an important role in ammonia disposal during mild hyperammonemia. However, during severe liver insufficiency induced-hyperammonemia, ammonia disposal capacity appears to be exceeded.

Authors+Show Affiliations

Department of Surgery, University of Limburg, Maastricht, The Netherlands.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article

Language

eng

PubMed ID

7902848

Citation

Dejong, C H., et al. "Renal Ammonia and Glutamine Metabolism During Liver Insufficiency-induced Hyperammonemia in the Rat." The Journal of Clinical Investigation, vol. 92, no. 6, 1993, pp. 2834-40.
Dejong CH, Deutz NE, Soeters PB. Renal ammonia and glutamine metabolism during liver insufficiency-induced hyperammonemia in the rat. J Clin Invest. 1993;92(6):2834-40.
Dejong, C. H., Deutz, N. E., & Soeters, P. B. (1993). Renal ammonia and glutamine metabolism during liver insufficiency-induced hyperammonemia in the rat. The Journal of Clinical Investigation, 92(6), 2834-40.
Dejong CH, Deutz NE, Soeters PB. Renal Ammonia and Glutamine Metabolism During Liver Insufficiency-induced Hyperammonemia in the Rat. J Clin Invest. 1993;92(6):2834-40. PubMed PMID: 7902848.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Renal ammonia and glutamine metabolism during liver insufficiency-induced hyperammonemia in the rat. AU - Dejong,C H, AU - Deutz,N E, AU - Soeters,P B, PY - 1993/12/1/pubmed PY - 1993/12/1/medline PY - 1993/12/1/entrez SP - 2834 EP - 40 JF - The Journal of clinical investigation JO - J Clin Invest VL - 92 IS - 6 N2 - Renal glutamine uptake and subsequent urinary ammonia excretion could be an important alternative pathway of ammonia disposal from the body during liver failure (diminished urea synthesis), but this pathway has received little attention. Therefore, we investigated renal glutamine and ammonia metabolism in midly hyperammonemic, portacaval shunted rats and severely hyperammonemic rats with acute liver ischemia compared to their respective controls, to investigate whether renal ammonia disposal from the body is enhanced during hyperammonemia and to explore the limits of the pathway. Renal fluxes, urinary excretion, and renal tissue concentrations of amino acids and ammonia were measured 24 h after portacaval shunting, and 2, 4, and 6 h after liver ischemia induction and in the appropriate controls. Arterial ammonia increased to 247 +/- 22 microM after portacaval shunting compared to controls (51 +/- 8 microM) (P < 0.001) and increased to 934 +/- 54 microM during liver ischemia (P < 0.001). Arterial glutamine increased to 697 +/- 93 microM after portacaval shunting compared to controls (513 +/- 40 microM) (P < 0.01) and further increased to 3781 +/- 248 microM during liver ischemia (P < 0.001). In contrast to controls, in portacaval shunted rats the kidney net disposed ammonia from the body by diminishing renal venous ammonia release (from 267 +/- 33 to -49 +/- 59 nmol/100 g body wt per min) and enhancing urinary ammonia excretion from 113 +/- 24 to 305 +/- 52 nmol/100 g body wt per min (both P < 0.01). Renal glutamine uptake diminished in portacaval shunted rats compared to controls (-107 +/- 33 vs. -322 +/- 41 nmol/100 g body wt per min) (P < 0.01). However, during liver ischemia, net renal ammonia disposal from the body did not further increase (294 +/- 88 vs. 144 +/- 101 nmol/100 g body wt per min during portacaval shunting versus liver ischemia). Renal glutamine uptake was comparable in both hyperammonemic models. These results indicate that the rat kidney plays an important role in ammonia disposal during mild hyperammonemia. However, during severe liver insufficiency induced-hyperammonemia, ammonia disposal capacity appears to be exceeded. SN - 0021-9738 UR - https://www.unboundmedicine.com/medline/citation/7902848/Renal_ammonia_and_glutamine_metabolism_during_liver_insufficiency_induced_hyperammonemia_in_the_rat_ L2 - https://doi.org/10.1172/JCI116903 DB - PRIME DP - Unbound Medicine ER -