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TWEAK/Fn14 system and crescent formation in IgA nephropathy
Yohei Sasaki1, Yoshio Shimizu2, Yusuke Suzuki3
1Division of Nephrology, Department of Internal Medicine, Juntendo University Faculty of Medicine, 2-1-1, Hongo, Bunkyo-ku, Tokyo, 113-8421, Japan. yhsasaki@juntendo.ac.jp.
BMC Nephrology
|April 18, 2015
Summary
Elevated urinary TWEAK (TNF-like weak inducer of apoptosis) levels correlate with kidney damage in IgA nephropathy (IgAN). This suggests the TWEAK/Fn14 pathway is involved in IgAN progression and severity.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Kidney inflammation involves the TNF-like weak inducer of apoptosis (TWEAK), secreted by renal cells.
- IgA nephropathy (IgAN) is a common kidney disease characterized by inflammation.
Purpose of the Study:
- To investigate the association between urinary TWEAK levels and histological findings in IgA nephropathy (IgAN) patients.
- To explore the role of the TWEAK/Fn14 system in IgAN pathogenesis.
Main Methods:
- Measured urinary TWEAK (uTWEAK) levels in 116 IgAN patients, 50 non-IgAN kidney disease patients, and 50 healthy controls using ELISA.
- Assessed renal biopsy histology using Oxford and Japanese classifications.
- Investigated TWEAK/Fn14 expression in renal tissues and TWEAK's effect on glomerular cells.
Main Results:
- Urinary TWEAK levels were significantly higher in IgAN and other kidney disease patients compared to healthy individuals.
- uTWEAK levels correlated with proteinuria and extracapillary proliferation in IgAN patients.
- Decreased uTWEAK levels were observed in patients achieving remission, with increased TWEAK/Fn14 expression in those with glomerular crescents.
Conclusions:
- The TWEAK/Fn14 system is implicated in crescent formation and proteinuria in IgAN.
- Urinary TWEAK levels serve as a potential biomarker for IgAN activity and severity.
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