Abnormal expression of complement receptor (CR1) in IgA nephritis: increase in erythrocytes and loss on glomeruli in patients with impaired renal function.
The number of complement receptor for C3b (CR1) molecules in erythrocytes from patients with renal diseases was measured by an immunoradiometric assay using monoclonal antibodies against CR1. IgA nephritis patients with high serum creatinine value (Scr) showed markedly elevated levels of CR1, whereas patients with normal Scr had normal CR1 levels. A similar increase in CR1 number was observed in membranoproliferative glomerular nephritis with high Scr. CR1 of these patients functioned normally as a cofactor of C3b inactivator in cleaving immune complex-bound C3b. In contrast, a high frequency (5/6) of negative staining of glomerular CR1 was observed in IgA nephritis patients with high Scr by immunofluorescence study. We postulate that the disease-associated, acquired factors at least in part contribute to the abnormal expression of CR1: elevated levels in erythrocytes and defective expression on glomeruli.
D000925:Anticoagulants / Q000627:therapeutic use; D003179:Complement C3b / Q000378:metabolism; D000939:Epitopes; D004910:Erythrocyte Membrane / Q000648:ultrastructure; D005455:Fluorescent Antibody Technique; D005922:Glomerulonephritis, IGA / Q000473:pathology*; D006801:Humans; D007678:Kidney Glomerulus / Q000648:ultrastructure; D011951:Receptors, Complement / Q000032:analysis* / Q000097:blood
D000925:Anticoagulants; D000939:Epitopes; D011951:Receptors, Complement; D003179:Complement C3b