The ultrastructure of the glomerular slit diaphragm in autologous immune complex nephritis.
Morphologic alterations of the slit diaphram and glomercular epithelium were examined in rats with experimental autologous immune complex nephritis following perfusion fixation with tannic acid-glutaraldehyde.  The changes observed included a displacemnt by immune complex deposits of foot processes and associated slit diaphragms towards the urinary space.  With the onset of proteinuria, foot processes spreas, resulting in a decrease in spithelial cell surface area and a diminution in the length of interpithelial slits.  Concomiantly, the redundant slit diaphragm became folded and pleated in the residual interpithelial spaces.  No primary defect in the slit diaphragm was observed to account fo the severe proteinuria seen in this disease.  Instead areas of detached epithelial cells and an occasional slit pore lacking a slit diaphragm may consitute sites for substantial protein loss in the urinary space in autologous immune complex nephritis.
D000818:Animals; D000936:Antigen-Antibody Complex; D004195:Disease Models, Animal; D005260:Female; D007105:Immune Complex Diseases / Q000473:pathology* / Q000503:physiopathology; D007678:Kidney Glomerulus / Q000503:physiopathology / Q000648:ultrastructure*; D008297:Male; D009393:Nephritis / Q000473:pathology* / Q000503:physiopathology; D010477:Perfusion; D011507:Proteinuria / Q000503:physiopathology; D051381:Rats
D000936:Antigen-Antibody Complex