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In order to explain the pathogenesis of protein depletion in chronic uraemia, 13 measurements of albumin catabolism were performed in uraemic patients undergoing haemo‐or peritoneal dialysis treatment, during either the early phase or steady uraemic state. Catabolism was determined during a single haemo‐or peritoneal dialysis by a double tracer technique (Human Serum Albumin and sodium iodide labelled with two different isotopes of iodine). The output from both albumin and iodine systems was measured in the dialysis solution flowing out from the peritoneum or artificial kidney. The radioactive iodide arising in dialysate from albumin breakdown was concentrated by the use of an anion exchange resin. Catabolic rate was three times the normal in 3 patients showing clinical features of hypercatabolism (true rapid loss of body weight) in the early phase of uraemia, or during relapse of it; albumin turnover rate returned to normal in 2 of these patients, when measured during clinical steady state conditions. This behaviour suggests highly increased catabolism, not counterbalanced by a correspondingly increased synthesis, as the cause of albumin depletion in chronic uraemia.
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Mariani et al. (1974) studied this question.
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