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Quantification of Monocyte Chemotactic Activity In Vivo and Characterization of Blood Monocyte Derived Macrophages
Published on: August 12, 2019
Increased urinary excretion of monocyte chemoattractant protein-1 in proteinuric renal diseases
Tsukasa Morii1, Hiroki Fujita, Takuma Narita
1Department of Geriatric Medicine, Akita University School of Medicine, Hondo, Akita, Japan. morii@med.akita-u.ac.jp
Abstract:
Monocyte chemoattractant protein-1 (MCP-1) is a chemokine that is produced mainly by tubular epithelial cells in kidney and contributes to renal interstitial inflammation and fibrosis. More recently, we have demonstrated that urinary MCP-1 excretion is increased in proportion to the degree of albuminuria (proteinuria) and positively correlated with urinary N-acetylglucosaminidase (NAG) levels in type 2 diabetic patients. Based on these findings, we have suggested that heavy proteinuria, itself, probably aggravates renal tubular damage and accelerates the disease progression in diabetic nephropathy by increasing the MCP-1 expression in renal tubuli. In the present study, to evaluate whether urinary MCP-1 excretion is increased in the proteinuric states not only in diabetic nephropathy but also in other renal diseases, we examined urinary MCP-1 levels in IgA nephropathy patients with macroalbuminuria (IgAN group; n = 6), and compared the results with the data obtained from type 2 diabetic patients with overt diabetic nephropathy (DN group; n = 23) and those without diabetic nephropathy (non-DN group; n = 27). Urinary MCP-1 excretion levels in non-DN, DN, IgAN groups were 157.2 (52.8-378.5), 346.1 (147.0-1276.7), and 274.4 (162.2-994.5) ng/g creatinine, median (range), respectively. Expectedly, urinary MCP-1 and NAG excretion levels in DN and IgAN groups were significantly elevated as compared with non-DN group. Therefore, we suggest that MCP-1 expression in renal tubuli is enhanced in proteinuric states,irrespective of the types of renal disease, and that increased MCP-1 expression probably contributes to renal tubular damage in proteinuric states.
Insights
Monocyte chemoattractant protein-1 (MCP-1) is elevated in proteinuric kidney diseases, including diabetic nephropathy and IgA nephropathy. This suggests MCP-1 contributes to kidney tubule damage in these conditions.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Monocyte chemoattractant protein-1 (MCP-1) is a key chemokine implicated in renal interstitial inflammation and fibrosis.
- Elevated urinary MCP-1 correlates with albuminuria and N-acetylglucosaminidase (NAG) in type 2 diabetic patients, suggesting it exacerbates tubular damage in diabetic nephropathy.
- The role of MCP-1 in other proteinuric kidney diseases remains less understood.
Purpose of the Study:
- To investigate whether urinary MCP-1 excretion is increased in proteinuric states beyond diabetic nephropathy.
- To compare MCP-1 levels in IgA nephropathy patients with macroalbuminuria to those with and without diabetic nephropathy.
Main Methods:
- Urinary MCP-1 levels were measured in three groups: non-diabetic nephropathy (non-DN, n=27), diabetic nephropathy (DN, n=23), and IgA nephropathy with macroalbuminuria (IgAN, n=6).
- Urinary NAG levels were also assessed.
- Statistical comparison of MCP-1 and NAG excretion between groups was performed.
Main Results:
- Urinary MCP-1 excretion levels were significantly higher in both the DN group (346.1 ng/g creatinine) and the IgAN group (274.4 ng/g creatinine) compared to the non-DN group (157.2 ng/g creatinine).
- Urinary NAG levels were also significantly elevated in DN and IgAN groups compared to the non-DN group.
- MCP-1 levels showed a median range of 147.0-1276.7 in DN and 162.2-994.5 in IgAN.
Conclusions:
- Urinary MCP-1 expression is enhanced in proteinuric states, irrespective of the underlying renal disease type.
- Increased MCP-1 likely contributes to renal tubular damage in various proteinuric kidney conditions.
- MCP-1 serves as a potential biomarker for tubular damage in proteinuric kidney diseases.
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