Renal Clearance of Amino Acids in Patients with Severe Chronic Renal Failure

Nádvorníková, H; Schück, O; Malý, Jan; Pechar, J; Dobersky, P; Tomková, D

doi:10.1159/000181199

Cited by 14 publications

(1 citation statement)

References 11 publications

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“…Data presented in this study suggest that the renal metabolic alterations induced by chronic disease may be responsible for changes of arterial levels of some AA, that were observed in patients with CRI considered here, and previously outlined (5,(36)(37)(38)(39)). Thus, the lower level of tyrosine in arterial blood in patients with CRI may be accounted for by decreased renal production, as suggested by the relationship between renal tyrosine release and arterial level of this AA (Fig.…”

Section: Discussionsupporting

confidence: 81%

Renal metabolism of amino acids and ammonia in subjects with normal renal function and in patients with chronic renal insufficiency.

Tizianello¹,

Ferrari²,

Garibotto³

et al. 1980

J. Clin. Invest.

331

147

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A B S T R A C T The net renal metabolism of amino acids and ammonia in the post absorptive state was evaluated in subjects with normal renal functioin and in patients with chronic renal insufficiency by measuring renal uptake and release, and urinary excretion of free amino acids and ammonia. In normial subjects the kidney extracts glutamine, proline, citrulline, and phenylalanine and releases serine, arginine, taurine, threonine, tyrosine, ornithine, lysine, and perhaps alanine. The renal uptake of amino acids from arterial blood occurs by way of plasma only, whereas approximately a half of amino acid release takes place by way of blood cells. Glycine is taken up from arterial plasma, while similar amounts of this amino acid are released by way of blood cells. In the same subjects total renal ammonia production can be largely accounted for by glutamine extracted.In patients with chronic renal insufficiency (a) the renal uptake ofphenylalanine and the release oftaurine and ornithine disappear; (b) the uptake of glutamine and proline, and the release of serine and threonine are reduced by 80-90%; (c) the uptake of citrulline and the release of alanine, arginine, tyrosine, and lysine are reduced by 60-70%; (d) no exchange of glycine is detectable either by way of plasma or by way of blood cells; (e) exchange of any other amino acid via blood cells disappears, and (f) total renal ammonia production is reduced and not more than 35% of such production can be accounted for by glutamine extracted, so that alternative precursors must be used. A 140% excess of nitrogen release found in the same patients suggests an intrarenal protein and peptide breakdown, which eventually provides free amino acids for ammonia production.

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Section: Discussionsupporting

confidence: 81%

Renal metabolism of amino acids and ammonia in subjects with normal renal function and in patients with chronic renal insufficiency.

Tizianello¹,

Ferrari²,

Garibotto³

et al. 1980

J. Clin. Invest.

331

147

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Tubular Transport of Amino Acids and Small Peptides

Silbernagl

1992

Comprehensive Physiology

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The sections in this article are: The Intact Kidney Plasma Concentrations of Amino Acids Normal Excretion of Amino Acids Variability of Aminoaciduria Interorgan Transport and Renal Metabolism of Amino Acids The Tubule Level Sites of Reabsorption Internephron Heterogeneity Reabsorption Kinetics Transport Steps at the Membrane Level Brush Border Basolateral Membrane: Exit and Uptake Carrier, Pore, or Enzymatic Cycle? Secretion of Amino Acids Specificity of The Reabsorption Mechanisms Stereospecificity Specificities of the Different Reabsorption Systems Hyperaminoaciduria Renal Handling of Oligopeptides Prereabsorptive Hydrolysis in the Tubule Lumen Glutathione and Other γ‐Glutamyl Peptides Reabsorption of Intact Peptides

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Nutritional status and nitrogen metabolism in patients treated with short dialysis

Arisi¹

1987

Short Dialysis

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Renal Clearance of Amino Acids in Patients with Severe Chronic Renal Failure

Cited by 14 publications

References 11 publications

Renal metabolism of amino acids and ammonia in subjects with normal renal function and in patients with chronic renal insufficiency.

Renal metabolism of amino acids and ammonia in subjects with normal renal function and in patients with chronic renal insufficiency.

Tubular Transport of Amino Acids and Small Peptides

Nutritional status and nitrogen metabolism in patients treated with short dialysis

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