In the present study in Munich-Wistar rats during the initial stages of autologous
immune complex nephritis (
protein excretion 3 to 50 mg/24 hours) we examined the sequential changes in binding of
cationized ferritin to anionic sites, as well as alterations in staining with colloidal
iron of podocyte membrane
sialoglycoprotein and correlated these with changes in glomerular basement membrane permeability to native
ferritin. The results are compared with those obtained from rats with advanced autologous
immune complex nephritis (
protein excretion 100 to 350 mg/24 hours) and with normal control rats. The formation of the smallest detectable
immune complex deposits was associated with a concomitant decrease in binding of
cationized ferritin to anionic sites in the lamina rara externa in the area of the deposits. This was accompanied by a diminution in staining by colloidal
iron of the epithelial cell coat overlying the deposits. The staining of the remainder of the epithelial cell glycocalyx, however, remained unaltered even in the presence of severe
proteinuria. Alterations in the permeability of the glomerular basement membrane to native
ferritin could not be documented until
protein excretion exceeded 10 mg/24 hours. The gradual loss of staining of the epithelial cell glycocalyx adjacent to
immune complexes supports the concept that, as
immune complexes are formed in situ by the interaction of
antibodies with a
glycoprotein present on the epithelial cell surface, they are shed and gradually accumulate in the lamina rara externa. Furthermore, as the
immune complex deposits enlarge they destroy and/or mask the
heparan sulfate anionic sites in the lamina rara externa resulting in a decreased number of anionic binding sites for
cationized ferritin.