ArticlePediatric nephrology (Berlin, Germany)2004
Monocyte chemoattractant protein-1 and interleukin-8 levels in children with acute poststreptococcal glomerulonephritis.
Article in Pediatric nephrology (Berlin, Germany), 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 19 citations in OpenAlex.
- Article
- Elevated expressions of 15-lipoxygenase and lipoxin A4 in children with acute poststreptococcal glomerulonephritis.The American journal of pathology · 2009Article
- Streptococcal exotoxin B increases interleukin-6, tumor necrosis factor alpha, interleukin-8 and transforming growth factor beta-1 in leukocytes.Pediatric nephrology (Berlin, Germany) · 2007Article
- Apoptosis and proliferation in childhood acute proliferative glomerulonephritis.Pediatric nephrology (Berlin, Germany) · 2005Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The infiltration of leukocytes into the glomeruli is a major factor in inflammatory glomerular damage in acute poststreptococcal glomerulonephritis (APSGN). Chemokines participate in leukocyte infiltration. The aim of the present study was to investigate the role of monocyte chemoattractant protein-1 (CCL2/MCP-1) and interleukin-8 (CXL8/IL-8) in APSGN with special emphasis on their role in the clinical course of renal disease. Twenty-one children with APSGN were studied. Serum and urinary CCL2/MCP-1 and CXL8/IL-8 levels were measured by ELISA. The relationships between urinary chemokines and the degree of proteinuria were investigated. Serum and urinary CCL2/MCP-1 levels were significantly higher in the acute phase than in the resolution phase and in controls ( P<0.05). Urinary CCL2/MCP-1 levels in the control group were significantly lower than in both the acute and resolution phases ( P=0.01 and P =0.001, respectively). In the acute phase, urinary CCL2/MCP-1 correlated with the extent of proteinuria ( r=0.58, P =0.006) but not with serum CCL2/MCP-1 levels ( r=0.21, P =0.36). Urinary and serum CXL8/IL-8 levels were significantly elevated in the acute phase compared with the resolution phase and controls ( P<0.05). A consistent increase in urinary CCL2/MCP-1 was found in the acute phase of patients with APSGN, and this correlates with the degree of proteinuria. Our results emphasize the important role of locally produced chemokines in immune-mediated glomerular injury.
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