Experimental IgA nephropathy.

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Abstract
An animal model for Ig[immunoglobulin]A immune complex nephritis was developed. IgA immune complexes formed in vitro with an IgA anti-dinitrophenyl (DNP) derived from MOPC-315 plasmacytoma and dinitrophenylated bovine serum albumin (DNP-BSA) produced mild focal glomerulonephritis in mice. Similar but more severe pathological changes were produced with complexes formed in vivo in normal mice or MOPC-315 tumor-bearing mice. In contrast to the focal nature of the PAS[periodic acid Schiff]-positive glomerular lesions observed by light microscopy, immunofluorescent examination revealed IgA deposits in all glomeruli. This discrepancy between immunofluorescent and histopathologic findings and the distribution of the immune complexes within the affected glomeruli are some features in which this experimental model resembles human IgA nephropathy. Fixation of complement by DNP-BSA-IgA immune complexes, formed in vitro or in vivo, occurred in the glomeruli of mice with IgA immune complex nephropathy. The pattern of C3 [complement component 3] glomerular deposits was similar to that of IgA although C was nonessential for complex deposition. This conclusion is based on the observation that decomplemented mice, although showing no deposition of C3 in their glomerulus, developed glomerular immunohistological changes similar to those observed in experimental mice that were not decomplemented. Polymeric IgA was critical for renal deposition of complexes and induction of nephritic histological changes. Monomeric IgA immune complexes failed to produce glomerular deposits. Secretory IgA, which is predominantly polymeric, may play a role in human IgA-associated glomerulonephritis.