Monocyte chemoattractant protein-1(MCP-1) has been known to play a role in pathophysiology of inflammatory glomerular disease through selective monocyte attraction and activation. The levels of urine and serum MCP-1 in 20 inflammatory glomerular diseases(IgA nephropathy 16, lupus nephritis 4), 17 non-inflammatory glomerular diseases(membranous nephrothy 9, minimal change disease 8), and 10 normal controls were evaluated by ELISA. The secretion of MCP-1 by peripheral blood mononuclear cells(PBMC) was examined in 5 patients with IgA nephropathy, membranous nephropathy, and minimal change disease respectively and 5 normal controls. After 4 week treatment with steroid, the urine and serum MCP-1 levels were followed up in eighteen patients who received steroid therapy. Urinary excretion of MCP-1 was significantly higher in patients with inflammatory glomerular disease(0.78+/-0.51ng/mg creatinine) compared to normal controls(0.18+/-0.12ng/mg creatinine). There were no differences in serum MCP-1 levels and MCP-1 production by PBMC between normal controls and patients. Positive correlation between urinary excretion of MCP-1 and proteinuria were observed in the patients with inflammatory glomerular disease but not in the patients with non-inflammatory glomerular disease. Any correlation between serum MCP-1 levels and urinary excretion of MCP-1 or proteinuria was not found. Urinary excretion of MCP-1 and proteinuria were decreased after steroid therapy. However, reduction in urinary excretion of MCP-1 does not seem to be related with decrease in proteinuria. Further studies are necessary to clarify the clinical significances of reduction in urinary excretion of MCP-1 with steroid therapy. In conclusion, our data support some role of MCP-1 in the pathophysiology of inflammatory glomerular diseases. MCP-1, however, does not seem to play an important role in those of membranous nephropathy and minimal change disease.