title: Alterations of protein metabolism by metabolic acidosis in children with chronic renal failure.
abstract: BACKGROUND
  Several reports suggest that metabolic acidosis may induce significant alterations in protein metabolism and that its outbreak may even result in growth retardation in children with chronic renal failure (CRF). However, the effects of metabolic acidosis on protein metabolism kinetics have never been investigated in these settings.
  
  
  METHODS
  Postabsorptive leucine metabolism, a marker of whole-body protein metabolism, was measured by using a primed, continuous intravenous infusion of L-[1-13C]leucine in 10 CRF children who were one to four years old.
  
  
  RESULTS
  Interindividual values of whole-body protein turnover exhibited a very large range, which was mainly accounted for by acidotic status (plasma HCO3-) and body composition [fat-free mass (FFM)]. After correction for differences in FFM, plasma HCO3- was highly correlated with protein breakdown (R2 = 0.65, P < 0.001), so that CRF children were divided in two groups according to their acid-base status: Group A had a mean plasma HCO3- level of 15.8 +/- 1.5 mmol. L-1 (mean +/- SD, N = 5), whereas group B had near-normal values (HCO3-, 22.6 +/- 3.0 mmol. L-1, N = 5). The leucine rate of appearance from protein breakdown was markedly higher in group A than in group B (4.15 +/- 1.43 vs. 2.46 +/- 0.47 micromol. kg-1. min-1, respectively, P < 0.05), and the net leucine balance tended to be more negative in group A (-0.73 +/- 0.34 vs. -0.44 +/- 0.26 micromol. kg-1. min-1, respectively).
  
  
  CONCLUSIONS
  Metabolic acidosis in children with CRF results in an excessive catabolic state, suggesting that acidosis-related protein wasting could contribute to growth retardation.
authors.affiliation: Laboratoire de Nutrition Humaine, Université d'Auvergne, Clermont-Ferrand, Paris, France. yves.boirie@clermont.inra.fr
authors.forename: Y
authors.initials: Y
authors.lastname: Boirie
authors.forename: M
authors.initials: M
authors.lastname: Broyer
authors.forename: M F
authors.initials: MF
authors.lastname: Gagnadoux
authors.forename: P
authors.initials: P
authors.lastname: Niaudet
authors.forename: J L
authors.initials: JL
authors.lastname: Bresson
mesh_terms: D000138:Acidosis / Q000150:complications / Q000378:metabolism*; D001639:Bicarbonates / Q000378:metabolism; D002247:Carbon Isotopes; D002675:Child, Preschool; D004044:Dietary Proteins / Q000493:pharmacokinetics*; D004734:Energy Metabolism / Q000502:physiology*; D005215:Fasting / Q000502:physiology; D005260:Female; D006801:Humans; D007223:Infant; D007676:Kidney Failure, Chronic / Q000150:complications / Q000378:metabolism*; D007930:Leucine / Q000493:pharmacokinetics; D008297:Male; D009748:Nutrition Disorders / Q000209:etiology / Q000378:metabolism; D011502:Protein-Energy Malnutrition / Q000378:metabolism
chemical_list: D001639:Bicarbonates; D002247:Carbon Isotopes; D004044:Dietary Proteins; D007930:Leucine