Injection of small amounts of
ferritin intravenously, into the aorta (above the renal arteries) or into the left renal artery of rabbits hyperimmunized against this
protein, results in the formation of circulating, insoluble,
antigen-antibody complexes. Some of these complexes localize focally in the renal glomerular capillaries, where they elicit severe lesions. The fate of the complexes and the evolution of the lesions have been followed by immunofluorescent and electron microscopic techniques. Within a few hours, the deposition of complexes in the glomeruli resulted in a massive accumulation of neutrophils platelets, and
fibrin, sometimes leading to acute focal necroses of some loops. These lesions were quite similar to those developing in the small dermal vessels during the
Arthus reaction. Most of the complexes were rapidly phagocytosed and degraded by neutrophils; swelling and proliferation of endothelial and mesangial cells usually followed the acute damage and contributed to the removal of remaining complexes, cell debris, and
fibrin deposits. Later, focal areas of mesangial proliferation and
sclerosis were observed, containing large amounts of basement membrane-like material and sometimes of
collagen fibrils; synechiae and crescent formation were noted in certain places. These observations suggest that the glomerular localization of very large, poorly soluble or insoluble
immune complexes may be responsible for the focal glomerular changes seen in association with
subacute bacterial endocarditis, with
anaphylactoid purpura, or for some of the most severe lesions developing during chronic
immune complex diseases.