Korean Journal of Nephrology 1999;18(2):247-257.

염증성 및 비염증성 사구체신염에서 요중 MCP-1의 차이와 단백뇨와의 관계 (Difference of Urine MCP-1 in Inflammatory and Non-Inflammatory Glomerular Diseases and Its Realtion to the Proteinuria)

김권기, 홍성표, 이태원, 임천규, 김명재 (Kwon Kee Kim, Seong Pyo Hong, Tae Won Lee, Chun Gyoo Ihm and Myung Jae Kim)

Abstract

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