The role of the kidney in the metabolism of plasma proteins can be defined by metabolic turnover techniques using representative radioiodinated, purified proteins. Low molecular weight (MW) proteins ( < 50,000 MW) readily transverse the glomerular filter and are largely taken up and catabolized by tubular cells; for this class of proteins the kidney is a primary organ of catabolism. Intermediate and high M W proteins ( > 60,000 M W) are generally retained by the glomerular filter and, therefore, do not normally have a significant exposure to tubular catabolic sites; for this class of proteins the kidney is not normally a primary organ of catabolism. Intermediate and even high M W proteins do pass through an abnormal glomerular filter, and are thereby lost to the body as intact proteins or are taken up and catabolized within tubular cells. In tubular diseases low MW proteins enter the tubular lumen in normal fashion, but are not taken up and catabolized within tubular cells. Thus, their loss pathway changes reciprocably from one of endogenous catabolism to excretion; this is the origin of tubular proteinuria. In nephron-loss disease, both excretion and endogenous catabolism of low MW proteins are diminished. Thus, these proteins accumulate in the blood.

Keywords:
Renal catabolism, Plasma protein metabolism, Tubular cell protein uptake, Glomerular permeability, Tubular proteinuria, Glomerular proteinuria, Nephron-loss disease
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© 1974 S. Karger AG, Basel
1974
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