Intrarenal insoluble immune complex formation

In the rabbit, intrarenal insoluble immune complex formation results in a mesangiopathic lesion with focal glomerulosclerosis. In swine we have examined in vivo the relation between intrarenal insoluble immune complex formation, glomerular deposition and associated renal vein platelet and basophil changes, pattern of scarring and degree of persistent functional impairment. Swine, as opposed to rabbits, were selected because their platelets more closely resemble human platelets in immune reactions. Direct renal antigen challenge was performed on two occasions at weekly intervals in swine maintained in persistent antibody excess. Immune complex glomerular deposition was observed in renal biopsies performed 20 minutes following antigen challenge. A significant renal vein thrombocytopenia and decline in basophil count was detected at the time of intrarenal insoluble immune complex formation. When basophil count was expressed relative to white cell count change, a weak association was detected. These in vivo changes in contrast to the soluble immune complex challenge in the rabbit has led us to postulate that in this model the direct platelet spontaneously pecipitating (insoluble) immune complex reaction may provide the permeability factors to facilitate glomerular immune complex deposition. A scarring mesangiopathic lesion with a persistent decrement in glomerular filtration is noted in swine studied one week after two consecutive renal antigen challenges. This type of intrarenal immune reaction results in a pattern of functional and histologic damage observed in progressive mesangiopathic forms of glomerulonephritis in man.