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Platelets mediate neutrophil-dependent immune complex nephritis in the rat.

The Journal of clinical investigation

Animals, Binding Sites, Antibody, Blood Platelets, immunology, pathology, Complement System Proteins, metabolism, Glomerulonephritis, etiology, physiopathology, Immune Complex Diseases, Immune Sera, Kidney Function Tests, Kidney Glomerulus, ultrastructure, Male, Neutrophils, Proteinuria, Rats, Rats, Inbred Strains, Thrombocytopenia

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      Abstract

      Neutrophils and platelets are frequently present in glomeruli in immune glomerulonephritis (GN). No role for the platelet in acute neutrophil-mediated renal injury has been defined. We investigated a neutrophil-mediated model of subendothelial immune complex GN in the rat. Rats were platelet-depleted (mean platelet less than 10,000/microliter) with goat anti-platelet IgG before induction of GN by the renal artery perfusion of concanavalin A followed by anti-concanavalin A IgG. Platelet-depletion resulted in a significant reduction in albuminuria (7 +/- 2 vs. 55 +/- 10 mg/24 h) and fractional albumin excretion (0.045 +/- 0.01 vs. 0.410 +/- 0.09) compared with controls. The decrease in albuminuria was not due to differences in blood or glomerular neutrophil counts, complement, renal function, or glomerular antibody binding. Platelet-depleted rats had equivalent subendothelial deposits and glomerular endothelial cell injury but had minimal platelet infiltrates and fibrin deposition compared with controls. These studies demonstrate a role for platelets in mediating acute neutrophil-induced glomerular injury and proteinuria in this model of GN.

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      Journal
      2971672
      10.1172/JCI113720
      442673

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