Some of the cellular abnormalities of severe protein-calorie malnutrition in children (PCM), e.g., reduced energy-related enzyme activities, energy and protein synthesis levels and intracellular amino acid deficits, are also thought to occur in chronic uremics. Improvement of these abnormal cell bioactivities, characterizing cellular malnutrition, should stabilize and possibly retard progressive cellular deterioration in uremics. We have used the circulating granulocyte as a cell model to study energy-related enzyme activities (pyruvate kinase (PK), phospho-fructokinase (PFK), adenylate kinase (AK), energy charge (Ech=ATP+0.5ADP/(ATP + ADP + AMP)), protein synthesis (3 H-leucine incorp.) and amino acid pools in 52 adult uremics (9 not dialyzed (ND), 40 hemodialyzed (HD) and 13 peritoneally dialyzed (CAPD)) and 61 normal control (C) subjects. Gross clinical estimators of chronic malnutrition (Wt/Ht ratio, skinfolds, arm muscle area, plasma albumin and total lymphocyte count) were within normal limits for the dialyzed uremics. In the ND uremics, all clinical and cell measures were abnormal. In the HD uremics, cell PK, AK, ATP, Ech and PS were significantly (p < .05) better than ND but less than C. A significant reduction in branched-chain amino acids (BCAA=valine, leucine, isoleucine) and methionine (MET) were noted in both ND and HD patients. In the CAPD patients, after 18 ±9 (SD) months of dialysis PK, PS, BCAAs and MET levels were normalized. Ech was 90% of normal and >HD, but ATP and AK were not improved. We conclude that cellular malnutrition occurs in apparently stabilized adult uremics without clinical signs of malnutrition. CAPD seems to improve many cell bioactivities, and therefore, cellular malnutrition in uremics.
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