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From the Department of Biochemistry and Molecular
Biology,*
Monash University, and the Department of
Nephrology and Monash University Department of
Medicine,
Monash Medical Centre, Clayton,
Victoria, Australia; and the Laboratory of
Immunopathology,
School of Medical Sciences,
State University of Rio de Janeiro, Rio de Janeiro, Brazil
The increased fractional clearance of albumin in nephrotic
states has long been attributed to glomerular permselectivity
dysfunction. Using radiolabeled rat serum albumin,
transferrin, IgG, and polydisperse Ficoll, this
study investigated the changes in their in vivo
fractional clearance in puromycin aminonucleoside nephrosis and
anti-glomerular basement membrane glomerulonephritis. In control rats
the lack of charge selectivity was confirmed by the demonstration that
carboxymethyl Ficoll (valence 
-39) had the same fractional
clearance as uncharged Ficoll. Both diseases exhibited similar effects
on fractional clearance measurements suggesting an underlying common
mechanism. In disease, there was good agreement between the
fractional clearance of proteins determined by radioactivity as
compared to those determined by radioimmunoassay. A small increase in
the fractional clearance for IgG was evident in disease as compared to
controls, which mirrored the change in the equivalent size
Ficoll, suggesting that the increase is because of the
development of a small proportion of large pores in the glomerular
capillary wall. There was no increase, however, in the
fractional clearance of Ficoll of equivalent size to albumin in either
disease, yet the fractional clearance of the albumin increased
by 12 to 14 times as determined by radioactivity and 4500 to 6600 times
as determined by radioimmunoassay. This study demonstrates that
glomerulonephritis is not a disease associated with changes in
glomerular permeability to albumin but is because of alterations in
albumin processing by cells distal to the glomerular basement membrane.
It is also apparent that approaches to glomerular pathology and
proteinuria as risk factors in renal disease must be
reassessed.
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