Abstract
A high prevalence of malnutrition has been reported in dialysis patients. Anorexia and vomiting associated with the uraemic state and increased protein breakdown induced by acidosis are some of the factors suggested to contribute to the development of malnutrition in these patients. There is evidence that the haemodialysis procedure per se promotes increased net protein catabolism. In healthy subjects, the passage of blood through a cuprophane dialyser without circulating dialysate leads to increased efflux of amino acids from muscle tissues, indicating that accelerated protein breakdown may be caused by the interaction between blood and regenerated cellulose membranes. The use of more biocompatible membranes, such as polysulfone and polyacrylonitrile, does not result in increased muscle protein catabolism. Loss of nutrients to the dialysate during clinical haemodialysis has been considered as an additional catabolic factor. Some recent reports indicate that, compared to low flux dialysers, the use of high flux membranes results in greater disturbances of plasma amino acid caused by increased loss to the dialysate. Thus, not only bioincompatibility but also the physical properties of the dialysis membrane seem to be involved in haemodialysis-related protein catabolism.

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