Alterations of protein metabolism by metabolic acidosis in children with chronic renal failure

Background. Several reports suggest that metabolic acidosis may induce sign ificant alterations in protein metabolism and that its outbreak may even re sult in growth retardation in children with chronic renal failure (CRF). Ho wever, the effects of metabolic acidosis on protein metabolism kinetics hav e 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-C-13]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 di fferences in FFM, plasma HCO3- was highly correlated with protein breakdown (R-2 = 0.65, P < 0.001), so that CRF children were divided in two groups a ccording to their acid-base status: Group A had a mean plasma HCO3- level o f 15.8 +/- 1.5 mmol.L-1 (mean +/- SD, N = 5), whereas group B had near-norm al values (HCO3-, 22.6 +/- 3.0 mmol.L-1, N = 5). The leucine rate of appear ance from protein breakdown was markedly higher in group A than in group B (4.15 +/-. 1.43 vs. 2.46 +/- 0.47 mu 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 mu mol.kg(-1).min(-1), respectively). Conclusions. Metabolic acidosis in children with CRF results in an excessiv e catabolic state, suggesting that acidosis-related protein wasting could c ontribute to growth retardation.