To study protein metabolism in uremia, whole body leucine flux was measured by a primed constant infusion of L(1-33C) leucine in 9 chronic renal failure (CRF) patients on three occasions; twice before and once following the initiation of dialysis treatment. Before dialysis, one leucine flux was measured when the patients were acidotic, and the other, when acidosis was corrected with bicarbonate supplement. All subjects consumed a constant diet for 6 days during each study period. Plasma L(1-33C)leucine and L(1-33C) KIC were measured by gas chromatography/mass spectrometry and expired 13CO2.by isotope mass spectrometry. Leucine kinetics were calculated using standard equations and statistical analyses derived using one-way repeated measures Anova. The pH and PCO2 were [data presented as means+SD] 7.29+0.05, 7.39+0.04 and 7.43+0.05, and plasma total CO2 were 19+3, 26+2, and 31+3 nmol/L, respectively in A, NA and D, corresponding to acidotic, non-acidotic and dialysis period [p=0.87x10-5 and 0.24x10-6]. 33CO2 production rates were 0.48+0.15, 0.31+0.15 and 0.31+0.06 umol/kg/hr, and leucine oxidation were 16+5, 94, and 12+3 umol/kg/hr, respectively, during A, NA and D periods (p=.0002 and 0.005]. Leucine release from protein degradation were 101+12, 95+9 and 113+22, and leucine protein incorporation rate were 85+10, 85+8 and 101+20 umol/kg/hr, respectively, in the A, NA and D periods [p=0.004 and 0.001]. The observations indicate that acidosis led to accelerated leucine oxidation. Uremia per se did not increase protein degradation. Six to 10 weeks following the initiation of dialysis, protein anabolism occurred as evident by a rise in leucine flux and an increase in protein synthesis. These findings underscore the importance of alkali therapy and dialysis in maintaining nutritional status in CRF patients.
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