The effect of increased capillary permeability on glomerular
immune complex localization was studied in rats immunized with proximal tubular
antigen (Fx1A) to induce autologous
immune complex nephropathy (AICN). AICN rats were made proteinuric by injection or unilateral renal perfusion with
aminonucleoside of
puromycin (PA) before developing subepithelial complex deposits. Control AICN kidneys developed diffuse granular deposits of
IgG and Fx1A on the subepithelial surface of the glomerular basement membrane (GBM) at 3 wk by immunofluorescence and electron microscopy, and deposits increased in subsequent weekly biopsies. In contrast, PA-nephrotic AICN kidneys developed few or no GBM deposits and a significant increase in mesangial localization of
IgG and Fx1A during the period of PA-induced
proteinuria. These alterations in complex localization were documented both in rats with PA
nephrosis and in unilaterally PA-nephrotic kidneys compared with contralateral controls in the same animals, thus excluding any effect of PA on the immunopathogenetic mechanism in AICN as an explanation for these findings. The absence of GBM deposits closely correlated with reduced staining for polyanionic
glomerular sialoprotein in proteinuric kidneys, since PA-perfused kidneys studied 2 wk after resolution of
proteinuria demonstrated return of normal staining for
sialoprotein and development of subepithelial complex deposits similar to those in contralateral control kidneys. These studies demonstrate that properties of the glomerulus itself play an important role in determining the site of complex deposition in experimental AICN and suggest that electrophysical characteristics of the glomerular capillary wall may influence complex localization on the GBM.