Glucocorticoids Reduce Aberrant O-Glycosylation of IgA1 in IgA Nephropathy Patients
Identifikátory výsledku
Kód výsledku v IS VaVaI
<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F00216208%3A11110%2F18%3A10376089" target="_blank" >RIV/00216208:11110/18:10376089 - isvavai.cz</a>
Nalezeny alternativní kódy
RIV/61388971:_____/18:00494330 RIV/00216208:11130/18:10376089 RIV/61989592:15110/18:73592333 RIV/00023761:_____/18:N0000017 a 3 dalších
Výsledek na webu
<a href="https://doi.org/10.1159/000487903" target="_blank" >https://doi.org/10.1159/000487903</a>
DOI - Digital Object Identifier
<a href="http://dx.doi.org/10.1159/000487903" target="_blank" >10.1159/000487903</a>
Alternativní jazyky
Jazyk výsledku
angličtina
Název v původním jazyce
Glucocorticoids Reduce Aberrant O-Glycosylation of IgA1 in IgA Nephropathy Patients
Popis výsledku v původním jazyce
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. (C) 2018 The Author(s) Published by S. Karger AG, Basel.
Název v anglickém jazyce
Glucocorticoids Reduce Aberrant O-Glycosylation of IgA1 in IgA Nephropathy Patients
Popis výsledku anglicky
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. (C) 2018 The Author(s) Published by S. Karger AG, Basel.
Klasifikace
Druh
J<sub>imp</sub> - Článek v periodiku v databázi Web of Science
CEP obor
—
OECD FORD obor
30217 - Urology and nephrology
Návaznosti výsledku
Projekt
Výsledek vznikl pri realizaci vícero projektů. Více informací v záložce Projekty.
Návaznosti
I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace
Ostatní
Rok uplatnění
2018
Kód důvěrnosti údajů
S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů
Údaje specifické pro druh výsledku
Název periodika
Kidney & Blood Pressure Research
ISSN
1420-4096
e-ISSN
—
Svazek periodika
43
Číslo periodika v rámci svazku
2
Stát vydavatele periodika
CH - Švýcarská konfederace
Počet stran výsledku
10
Strana od-do
350-359
Kód UT WoS článku
000434716500005
EID výsledku v databázi Scopus
2-s2.0-85054692240