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Intrarenal gene expression of proinflammatory chemokines and cytokines in chronic proteinuric glomerulopathies
Irena Brabcová, Katja Kotsch, Petra Hřibová, Alena Loužecká, Kateřina Bartošová, Kateřina Hyklová, Jiří Lácha, Hans-Dieter Volk, Ondřej Viklický
Language English Country Czech Republic
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NR8913
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- MeSH
- Biopsy methods utilization MeSH
- Chemokines physiology genetics immunology MeSH
- Cytokinins physiology genetics immunology MeSH
- Gene Expression physiology genetics drug effects MeSH
- Research Support as Topic MeSH
- Glomerulonephritis etiology complications metabolism MeSH
- Hypertension etiology physiopathology MeSH
- Humans MeSH
- Reverse Transcriptase Polymerase Chain Reaction methods utilization MeSH
- Proteinuria etiology microbiology physiopathology MeSH
- Check Tag
- Humans MeSH
Proteinuria has been recently shown to be an independent risk factor for the progression of chronic nephropathies, but the actual mechanisms by which urinary protein load damages renal tissue in humans remain unsolved. Using real-time RT-PCR method we evaluated intrarenal mRNA expression of various cytokines and chemokines in patients with biopsy-proven IgA nephropathy (IgAN, n=11), membranous nephropathy (MN, n=6) and focal and segmental glomerulosclerosis (FSGS, n=6) who exhibited proteinuria over 0.5 g/day. There was a significant positive correlation between the proteinuria extent and the intrarenal RANTES (regulated upon activation normal T cell expressed and secreted) mRNA expression in patients with IgAN, a similar trend was also observed in patients with MN and FSGS. There were no clear relationships between the proteinuria and intrarenal mRNA expression of tumor necrosis factor ?, transforming growth factor ß1 and monocyte chemoattractant peptide-1. There were no differences in the pattern of cytokine mRNA expression between different glomerulopathies. In conclusion, our results support the hypothesis that lymphocytes, macrophages and their products provoke tissue injury in response to proteinuria independently of the nature of renal diseases in man.
Department of Nephrology Institute for Clinical and Experimental Medicine Prague Czech Republic
Institute of Medical Immunology Medical University Charité Humboldt University Berlin Germany
Transplant Laboratory Institute for Clinical and Experimental Medicine Prague
Transplant Laboratory Institute for Clinical and Experimental Medicine Prague Czech Republic
Grant č. NR/8913-4 Ministerstvo zdravotnictví České republiky
Bibliography, etc.Lit.: 19
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- $a Proteinuria has been recently shown to be an independent risk factor for the progression of chronic nephropathies, but the actual mechanisms by which urinary protein load damages renal tissue in humans remain unsolved. Using real-time RT-PCR method we evaluated intrarenal mRNA expression of various cytokines and chemokines in patients with biopsy-proven IgA nephropathy (IgAN, n=11), membranous nephropathy (MN, n=6) and focal and segmental glomerulosclerosis (FSGS, n=6) who exhibited proteinuria over 0.5 g/day. There was a significant positive correlation between the proteinuria extent and the intrarenal RANTES (regulated upon activation normal T cell expressed and secreted) mRNA expression in patients with IgAN, a similar trend was also observed in patients with MN and FSGS. There were no clear relationships between the proteinuria and intrarenal mRNA expression of tumor necrosis factor ?, transforming growth factor ß1 and monocyte chemoattractant peptide-1. There were no differences in the pattern of cytokine mRNA expression between different glomerulopathies. In conclusion, our results support the hypothesis that lymphocytes, macrophages and their products provoke tissue injury in response to proteinuria independently of the nature of renal diseases in man.
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