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Glucocorticoids Reduce Aberrant O-Glycosylation of IgA1 in IgA Nephropathy Patients
P. Kosztyu, M. Hill, J. Jemelkova, L. Czernekova, LR. Kafkova, M. Hruby, K. Matousovic, K. Vondrak, J. Zadrazil, I. Sterzl, J. Mestecky, M. Raska,
Jazyk angličtina Země Švýcarsko
Typ dokumentu časopisecké články
Grantová podpora
NV15-33686A
MZ0
CEP - Centrální evidence projektů
Digitální knihovna NLK
Plný text - Článek
Zdroj
NLK
Directory of Open Access Journals
od 2013
Free Medical Journals
od 2010
ProQuest Central
od 1994-05-01 do Před 1 rokem
Open Access Digital Library
od 2013-01-01
Medline Complete (EBSCOhost)
od 2005-01-01
Health & Medicine (ProQuest)
od 1994-05-01 do Před 1 rokem
Karger Open Access
od 2013-01-01
ROAD: Directory of Open Access Scholarly Resources
od 1996
PubMed
29529610
DOI
10.1159/000487903
Knihovny.cz E-zdroje
- MeSH
- glukokortikoidy farmakologie terapeutické užití MeSH
- glykosylace účinky léků MeSH
- IgA nefropatie diagnóza farmakoterapie MeSH
- imunoglobulin A krev imunologie metabolismus MeSH
- imunokomplex krev MeSH
- lidé MeSH
- prednison terapeutické užití MeSH
- prognóza MeSH
- protilátky krev MeSH
- studie případů a kontrol MeSH
- Check Tag
- lidé MeSH
- Publikační typ
- časopisecké články MeSH
BACKGROUND/AIMS: IgA nephropathy is associated with aberrant O-glycosylation of IgA1, which is recognized by autoantibodies leading to the formation of circulating immune complexes. Some of them, after deposition into kidney mesangium, trigger glomerular injury. In patients with active disease nonresponding to angiotensin-converting enzyme inhibitors or angiotensin II blockers, corticosteroids are recommended. METHODS: The relationship between the corticosteroid therapy and serum levels of IgA, aberrantly O-glycosylated IgA1, IgA-containing immune complexes and their mesangioproliferative activity was analyzed in IgA nephropathy patients and disease and healthy controls. RESULTS: Prednisone therapy significantly reduced proteinuria and levels of serum IgA, galactose-deficient IgA1, and IgA-IgG immune complexes in IgA nephropathy patients and thus reduced differences in all of the above parameters between IgAN patients and control groups. A moderate but not significant reduction of mesangioproliferative potential of IgA-IgG immune complexes and IgA sialylation was detected. CONCLUSION: The prednisone therapy reduces overall aberrancy in IgA1 O-glycosylation in IgA nephropathy patients, but the measurement of IgA1 parameters does not allow us to predict the prednisone therapy outcome in individual patients.
Citace poskytuje Crossref.org
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- $a Kosztyu, Petr $7 xx0239748 $u Department of Immunology, Faculty of Medicine and Dentistry, Palacky University, Olomouc and University Hospital Olomouc, Olomouc, Czech Republic.
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- $a BACKGROUND/AIMS: IgA nephropathy is associated with aberrant O-glycosylation of IgA1, which is recognized by autoantibodies leading to the formation of circulating immune complexes. Some of them, after deposition into kidney mesangium, trigger glomerular injury. In patients with active disease nonresponding to angiotensin-converting enzyme inhibitors or angiotensin II blockers, corticosteroids are recommended. METHODS: The relationship between the corticosteroid therapy and serum levels of IgA, aberrantly O-glycosylated IgA1, IgA-containing immune complexes and their mesangioproliferative activity was analyzed in IgA nephropathy patients and disease and healthy controls. RESULTS: Prednisone therapy significantly reduced proteinuria and levels of serum IgA, galactose-deficient IgA1, and IgA-IgG immune complexes in IgA nephropathy patients and thus reduced differences in all of the above parameters between IgAN patients and control groups. A moderate but not significant reduction of mesangioproliferative potential of IgA-IgG immune complexes and IgA sialylation was detected. CONCLUSION: The prednisone therapy reduces overall aberrancy in IgA1 O-glycosylation in IgA nephropathy patients, but the measurement of IgA1 parameters does not allow us to predict the prednisone therapy outcome in individual patients.
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