Korean J Nephrol.
1999 Mar;18(2):247-257.
Difference of Urine MCP-1 in Inflammatory and Non-Inflammatory Glomerular Diseases and Its Realtion to the Proteinuria
- Affiliations
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- 1Department of Internal Medicine, Kachun Medical College, Kyunggyi, Korea.
- 2Department of Internal Medicine, College of Medicine, Kyung Hee University, Seoul, Korea.
Abstract
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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.