Original Article
Kidney International (2000) 58, 236–241; doi:10.1046/j.1523-1755.2000.00158.x
Alterations of protein metabolism by metabolic acidosis in children with chronic renal failure
Yves Boirie, Michel Broyer, Marie France Gagnadoux, Patrick Niaudet and Jean-Louis Bresson
Laboratoire de Nutrition Humaine, Université d'Auvergne, Clermont-Ferrand; Service de Néphrologie Pédiatrique; and Centre d'Investigation Clinique, Hôpital Necker-Enfants Malades, Paris, France
Correspondence: Dr. Yves Boirie, Laboratoire de Nutrition Humaine, B.P. 321-58, rue Montalembert, 63009 Clermont-Ferrand Cedex 1, France. E-mail: yves.boirie@clermont.inra.fr
Received 27 July 1999; Revised 11 January 2000; Accepted 11 February 2000.
Abstract
Alterations of protein metabolism by metabolic acidosis in children with chronic renal failure.
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 
mol 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 mol 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.
Keywords:
amino acids, kidney metabolism, muscle wasting, growth retardation, malnutrition
