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ALBUMIN METABOLISM AND GASTROINTESTINAL PROTEIN LOSS IN CHILDREN WITH NEPHROTIC SYNDROME
Author(s) -
YSSING MINNA,
JENSEN HERLUF,
JARNUM STIG
Publication year - 1969
Publication title -
acta pædiatrica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.772
H-Index - 115
eISSN - 1651-2227
pISSN - 0803-5253
DOI - 10.1111/j.1651-2227.1969.tb04692.x
Subject(s) - nephrotic syndrome , albumin , medicine , serum albumin , catabolism , endocrinology , protein catabolism , hypoalbuminemia , blood proteins , gastroenterology , metabolism , biochemistry , amino acid , chemistry
Summary In order to assess the significance of gastrointestinal protein loss as a cause of plasma protein hypercatabolism in patients with nephrotic syndrome, seven nephrotic children were studied simultaneously with radioiodine labelled albumin and a test substance, 51, Fe‐labelled iron dextran, for evaluation of gastrointestinal protein loss. All the patients displayed a pronounced hypercatabolism of albumin, which could not be accounted for by urinary protein loss. A slightly increased gastrointestinal protein loss was demonstrated in 4 patients, whereas, in 3 patients, the faecal loss of macromolecules was within normal limits. The relation between protein catabolism and faecal loss of macromolecules was compared in the nephrotic children and in 20 patients with protein‐losing enteropathies. It is concluded that gastrointestinal protein loss is insignificant in the nephrotic syndrome, and unable to account for the marked endogenous hypercatabolism of albumin. Albumin synthesis was normal or somewhat increased. An abnormally high fraction of the total albumin mass was present in the intravascular space in 4 of the 7 children.