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Platelet‐associated IgG in idiopathic glomerulonephritis and the nephritis of systemic lupus erythematosus
Author(s) -
Bennett A.,
Frampton G.,
Cameron J. S.
Publication year - 1986
Publication title -
british journal of haematology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.907
H-Index - 186
eISSN - 1365-2141
pISSN - 0007-1048
DOI - 10.1111/j.1365-2141.1986.tb04093.x
Subject(s) - medicine , platelet , immunology , lupus nephritis , antibody , immune system , nephritis , glomerulonephritis , immune complex , disease , kidney
Summary We studied platelet‐associated IgG (PAIgG) in patients with the nephritis of systemic lupus erythematosus (SLE) and with idiopathic glomerulonephritis (IGN), and found no increase in PAIgG in the patients with IGN, and an increase in only a minority of patients with SLE, all of whom had active disease. Patients with IGN and a nephrotic syndrome had both a low serum IgG and a low PAIgG. The increase in PAlgG in the patients with SLE correlated with the titres of antibody against dsDNA in the serum, but not with the platelet‐agglutinating immune complexes also present. Intraplatelet serotonin, however, was reduced in both groups, and this correlated with the amounts of platelet‐agglutinating complexes in the serum of the SLE patients. Immune complexes may associate with platelets in vivo to cause this release, but if so this must be a reversible phenomenon (‘hit and run’immune platelet injury); alternatively, the Fc binding to the platelet surface may be weak and insufficient to survive the ex vivo washing procedures.