1. Henoch—Schoenlein nephritis and IgA nephropathy share clinical and immunological features, but the pathogenesis of neither condition is established. We have recently described IgG autoantibodies to glomerular components in active IgA nephropathy and have now sought evidence for a similar autoimmune component in Henoch—Schoenlein purpura.

2. Sera from 26 patients with Henoch—Schoenlein nephritis and six patients with Henoch—Schoenlein purpura without accompanying nephritis were studied and compared with sera from 20 patients with other forms of glomerulonephritis and 40 normal subjects. E.l.i.s.a.s were developed to detect IgA and IgG binding to the ligand from whole human glomeruli previously described, laminin, DNA, cardiolipin (diphosphatidylglycerol) and a panel of dietary constituents (BSA, α-caesin, β-lactoglobulin, ovalbumin and wheat gliadin).

3. Sera from 16 of the 26 patients with Henoch—Schoenlein nephritis displayed increased IgG binding to the human glomerular extract compared with the normal control group (P<0.001), whereas IgG binding was not significantly raised in the patients with Henoch—Schoenlein purpura without evidence of renal involvement. IgA binding was not raised compared with control subjects. Serum IgA and IgG binding to other potential autoantigens or antigens present on dietary constituents was not significantly different in patients with Henoch—Schoenlein nephritis or patients with Henoch—Schoenlein purpura without nephritis compared with control subjects.

4. Western blotting of the denatured and reduced glomerular extract revealed binding of IgG, from the sera of patients with active Henoch—Schoenlein nephritis, to glomerular components of Mr 48000 and 58000, similar to the Mr of the glomerular antigens identified in IgA nephropathy. Immunoglobulin binding was shown to be specific antibody binding using F(ab')2 fragments from the IgG fraction of e.l.i.s.a.-positive sera.

5. Clinical associations showed in 10 of 11 patients with Henoch—Schoenlein nephritis whose sera were studied in remission: IgG antiglomerular antibody binding fell to within the normal range (P<0.05).

6. These results demonstrate an autoimmune component in Henoch—Schoenlein nephritis, and the close temporal relationship with active nephritis implies that this may be a critical component in the pathogenesis of glomerular injury. The absence of specific antibody, or non-specific immunoglobulin binding, to any of the range of dietary constituents or other putative autoantigens tested suggests that polyclonal B-cell activation is not an important feature of Henoch—Schoenlein nephritis.

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