Competition between low- and high-molecular-weight proteins for renal tubular uptake.
To explain the occurrence of tubular and glomerular proteinuria in patients with primarily tubular or glomerular dysfunction, it is usually assumed that the mechanisms responsible for the renal tubular transport of small and large proteins are different. The present in vivo study does not support this hypothesis since it clearly shows that small and large proteins (e.g., beta 2-microglobulin and albumin) can compete for renal uptake. Our results lead us to postulate the existence of common tubular reabsorption sites for which proteins exhibit different affinities depending on their charge, size and conformation.
D000818:Animals; D001798:Blood Proteins / Q000378:metabolism*; D003574:Cytochrome c Group / Q000378:metabolism; D005260:Female; D007684:Kidney Tubules / Q000378:metabolism*; D008970:Molecular Weight; D011487:Protein Conformation; D011507:Proteinuria / Q000378:metabolism*; D051381:Rats; D011919:Rats, Inbred Strains; D012709:Serum Albumin / Q000378:metabolism; D012710:Serum Albumin, Bovine / Q000378:metabolism; D001613:beta 2-Microglobulin / Q000378:metabolism
D001798:Blood Proteins; D003574:Cytochrome c Group; D012709:Serum Albumin; D001613:beta 2-Microglobulin; D012710:Serum Albumin, Bovine