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Serum sickness was induced in rats by a modification of previously described methods avoiding i.v. administration of the antigen. All the animals developed a progressive disease characterized by an initial pattern of deposition of IC in the mesangium followed by the appearance of GBM deposits. This change in the deposition of IC was associated with the onset of massive proteinuria and a fall in the titre of precipitating antibodies. Simultaneously, specific desensitization of platelets for a rat PAF could be demonstrated and platelet aggregates were seen in the glomeruli. The presence of homocytotropic IgGa anti-ovalbumin antibodies in rat sera during the induction of the disease was demonstrated by 2 hr PCA. Accordingly, this antibody together with the antigen ovalbumin induced the release of histamine From peritoneal mast cells, suggesting that a similar mechanism might occur in vivo during the induction of the disease. Rat PAF and β glucuronidase could be obtained from peritoneal macrophages under similar conditions to those required for the release of histamine. The data support a role for inflammatory mediators in the increase in vascular permeability needed for the deposition of IC in the GBM and provide evidence for a new role of macrophages and PMNs in glomerular pathology in contributing to an increase in permeability of GBM. [ABSTRACT FROM AUTHOR]

The purpose of this study was to characterize circulating IgA and the IgA deposited in the glomeruli of patients with alcoholic liver disease. In the 6 patients studied there was an increased proportion in monomeric IgA (3.5 fold) and IgA between 9-13S (8.94 fold), 13.17S (4.49 fold) and 17.21S (1.63 fold) fractions on 5.40% sucrose density gradient ultracentrifugation at physiological pH. All fractions between 9-21S decreased at acid pH, however a 3.28 fold increase in fractions where polymeric IgA is expected to appear. IgA eluted at acid pH from autopsy kidney was studied by the same procedures. At pH 7.4 about 55% of that IgA have a molecular weight comprised between 9.21S, decreasing to around 25% at acid pH. The existence of true polymeric IgA in serum and kidney was based on the capacity of high molecular weight IgA to bind human secretory component. The amount of Immune complexes with monomeric IgA were higher than those with polymeric IgA in serum as well as in kidney. However, the percentage of heavy IgA (probably polymeric IgA) in kidney were, in each patient, higher than those observed in serum. Our results show the presence of high amounts of monomeric and polymeric IgA, both partially as immune complexes, in serum and kidneys of patients with alcoholic liver disease and IgA glomerulonephritis. Furthermore, our data suggest a role for human liver in the clearance of serum IgA such as has been demonstrated in some animal species, especially in rats. [ABSTRACT FROM AUTHOR]