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

R J Johnson; C E Alpers; P Pritzl; M Schulze; P Baker; C Pruchno; W G Couser

doi:10.1172/JCI113720

Department of Medicine, University of Washington, Seattle 98195.

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Department of Medicine, University of Washington, Seattle 98195.

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Department of Medicine, University of Washington, Seattle 98195.

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Department of Medicine, University of Washington, Seattle 98195.

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Department of Medicine, University of Washington, Seattle 98195.

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Department of Medicine, University of Washington, Seattle 98195.

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Department of Medicine, University of Washington, Seattle 98195.

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Published in Volume 82, Issue 4 on October 1, 1988
J Clin Invest. 1988;82(4):1225–1235. https://doi.org/10.1172/JCI113720.
© 1988 The American Society for Clinical Investigation

Published October 1, 1988 - Version history

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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