Metabolic acidosis and nutrition in dialysis patients

The renal elimination of nonvolatile acids, mainly formed by oxidation of sulfuric amino acids, is about 70 mmol/day. In hemodialysis (HD) patients who cannot eliminate an excess of H+ via the kidneys, the accumulation of H+ in the interdialytic period results in progressive depletion of the bicarbonate buffer stores, which are repleted by the dialysis procedure. Metabolic acidosis is common In HD patients, since dialytic repletion of the bicarbonate stores is often far from complete; acidosis seems to be less common in CAPD patients, who are continuously provided with lactate from the dialysis fluid as a buffer source. Experimental and clinical studies have shown that metabolic acidosis induces negative nitrogen balance, increased muscle protein degradation and increased oxidation of the branched-chain amino acids (valine, leucine, isoleucine). Acidosis is the only uremic toxic factor identified which stimulates protein catabolism. Correction of metabolic acidosis in HD patients normalizes low muscle intracellular concentrations of the branched-chain amino acids and reduces signs of renal osteodystrophy. The long-term influence of correction of acidosis on nutritional status, morbidity and mortality needs to be assessed in prospective studies.