Membrane Glomerulonephrit is1 , 2

M acrophages have been shown to mediate glomer­ ular injury in antiglomeruiar basement membrane (anti-GBM) glomerulonephritis in rats and rabbits. To evaluate the role of macrophages and the m ac­ rophage-related cytokines, colony stimulating fac­ tor-1 (CSF-1), monocyte chemoattractant protein-1 (MCP-1) and RANTES, accelerated anti-GBM nephritis was studied in op/op mutant mice, which lack CSF-1 and are severely m acrophage deficient, and in het­ erozygous o p /■ + ■ control mice. Observations were m ade 24 h and 3 days after the injection of rabbit anti-mouse GBM antibody in mice preimmunized with rabbit immunoglobulin G. Proteinuria rose progres­ sively in both groups but did not differ between them (urine protein/creatinine ratio at 3 days: 1.01 ± 0.38 in o p /o p versus 1.45 ± 0.43 in o p /+ ; Ps not significant). In both op/op and o p /+ mice, anti-GBM nephritis was associated with renal expression of mRNA for RANTES and MCP-1 and barely detectable levels of mRNA for CSF-1. In contrast, these cytokines were not expressed in sham-injected mice. Morphologic lesions ap ­ peared earlier in op/op mice but were com parable by Day 3. Glomerular injury consisted of capillary thrombosis and endothelial cell dam age associated with mild to m oderate leukocyte Infiltration. Despite