Glomerular macrophage phagocytic activity in experimental immune complex glomerulonephritis. In rats with the proliferative immune complex glomerulonephritis of chronic serum sickness, kidney function deteriorates in three clearly distinguishable and discrete stages: mild, moderate and severe. The macrophage component of glomerular inflammation in each stage is also quantitatively and qualitatively distinct, with abnormal phenotypic markers appearing in the moderate stage and increasing in the severe stage. To determine whether there were distinct functional differences among macrophages from the three stages, Fcγ receptor-mediated phagocytic capacity was measured. The phagocytic capacity of glomerular macrophages increased significantly in the moderate stage, then significantly decreased, as rats progressed to severe chronic serum sickness. This decline in phagocytic function was not associated with a decrease in the expression of Fcγ receptors on the glomerular macrophage cell surface. Furthermore, the phagocytic function of peritoneal macrophages from rats with severe chronic serum sickness was not impaired. Whether or not this attenuation of glomerular macrophage phagocytic capacity is the cause, or result, of renal disease progression remains unclear. It may indicate a potentially protective role for intraglomerular macrophages, and can serve as an additional functional marker of disease progression.