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Abstract
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.