Disposition of IgA-containing circulating immune complexes.

Two fundamentally different mechanisms may account for the glomerular immune deposits in IgA nephropathy (IgAN): (1) deposition of circulating immune complexes and (2) the in situ formation of immune complexes. In this review the experimental evidence for and against an important role of circulating IgA-containing immune complexes in the pathogenesis of IgAN is summarized. Several physical characteristics, including size, lattice composition, and electrical charge, may influence the deposition of immune complexes in the renal mesangium. Furthermore, the likelihood of deposition of circulating IgA-containing immune complexes in vulnerable locations (such as the kidney) may be increased because of their impaired removal from the circulation by macrophages of the liver and spleen and the erythrocyte-immune complex clearing mechanism. However, the relative contributions of these factors to the pathogenesis of IgAN remain speculative.