ANALYSIS OF IGA FROM IGA-FIBRONECTIN COMPLEX IN THE PATIENT WITH IGA NEPHROPATHY AND ITS EFFECT ON THE FUNCTION OF RENAL CELIS IN CULTURE.

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IgA-fibronectin complex(IgA-F・C) have been in the serum of patients with IgA nephropathy(IgAN) with higher incidence than other serological markers for IgAN.The purpose of this study is ; 1. to determine the incidence of IgA-F・C in pediatric patiens with IgAN in addition to looking at the basis of this assay system using collagen type I -coated microtiter plate, and 2. to analyze the formation of this complex in patients, with Western blot utilizing a set of monoclonal anti-human fibronectin antibodies for materials from heparin-affinity column treated by patient's serum.Result : 1. Significant detection of IgA-F・C in IgAN patients was observed in 52%, which did not correlate with severity of disease or an attack of gross hematuria. Elevated IgA-F・C was also detected in some of patients with Henoch-Schonlein purpura nephritis and active stage of juvenile rheumatoid arthritis. A few of definite IgAN patient with low activity of IgA-F・C turned out to be significant by treatment with gelatin-column.2. Silver-staining of SDS-PAGE for eluate of gelatin-, or heparin-column showed that binding proteins of serum to each column contained proteins of wide-ranged molecular weight, and some of them demonstrated only in patients but not controls. The extra-proteins was shown especially in the material from heparin-affinity column. These findings were confirmed by Western blot procedure, suggesting that serum fibronectin was degraded, which must be neglected in a established protocol for isolation of fibronectin. Reactivity of some monoclonal antibodies to degraded fibronectins was specific to patient.3. Application of purified IgA onto immobilized fibronectin fragments from patient and cathepsin D-digested fibronectin demonstrated that 42 kilodalton fragment, produced both by patient and cathepsin D proteolyis, was bound to IgA.These findings may have ramifications in the origin and possible pathogenetic importance for the etiology of IgAN.