[Acute experimental glomerulonephritis induced by the glomerular deposition of circulating polymeric IgA-concanavalin A complexes].

The perfusion of polymeric IgA (pIgA)--or secretory IgA (sIgA)--Concanavalin A (ConA) non-immune complexes (apparent Mol.Wt greater than 10(3) Kd) into the aorta of rats led to a dose-dependent and a mannose-dependent deposition of both IgA and lectin into the glomeruli. Rats injected with amounts of those complexes as low as 500 micrograms developed, one hour later, a focal and segmental proliferative glomerulonephritis characterized by: a) the deposition in the mesangial area of most glomeruli of injected complexes and of rat C3; b) small areas of fibrinoïd necrosis in 10 to 15% of glomeruli, confined to the periphery of a single lobule of the tuft; c) a segmental infiltration of those glomeruli by polymorphonuclear leucocytes, mononuclear phagocytes and platelets; d) a hyperactive aspect of mesangial cells; e) the presence of red blood cells in tubular lumens. By contrast, no glomerular lesions were obvious in rats similarly injected either with monomeric IgA (mIgA)-ConA, pIgA-peanut agglutinin (PNA) or sIgA-PNA complexes or with heat-aggregated pIgA or mIgA. The data indicate that preformed polymeric IgA-ConA complexes can specifically bind to glomerular structures in vivo and locally trigger, as antigen-antibody complexes, an acute inflammatory reaction resulting in glomerular lesions similar to those observed in Henoch-Schönlein purpura nephritis.