Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes

IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, frequently leads to end-stage renal disease and kidney transplantation. However, disease recurrence often occurs after transplantation. Here we evaluated the predictive value of three markers for IgAN recurrence: the prese...

Ausführliche Beschreibung

Gespeichert in:
Bibliographische Detailangaben
Veröffentlicht in:Kidney international 2015-10, Vol.88 (4), p.815-822
Hauptverfasser: Berthelot, Laureline, Robert, Thomas, Vuiblet, Vincent, Tabary, Thierry, Braconnier, Antoine, Dramé, Moustapha, Toupance, Olivier, Rieu, Philippe, Monteiro, Renato C., Touré, Fatouma
Format: Artikel
Sprache:eng
Schlagworte:
Online-Zugang:Volltext
Tags: Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
container_end_page 822
container_issue 4
container_start_page 815
container_title Kidney international
container_volume 88
creator Berthelot, Laureline
Robert, Thomas
Vuiblet, Vincent
Tabary, Thierry
Braconnier, Antoine
Dramé, Moustapha
Toupance, Olivier
Rieu, Philippe
Monteiro, Renato C.
Touré, Fatouma
description IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, frequently leads to end-stage renal disease and kidney transplantation. However, disease recurrence often occurs after transplantation. Here we evaluated the predictive value of three markers for IgAN recurrence: the presence of galactose-deficient IgA1, IgG anti-IgA autoantibodies, and IgA-soluble (s) CD89 complexes. This was analyzed in 38 kidney transplant recipients with IgAN recurrence and compared with 22 patients transplanted for IgAN but without recurrence and with 17 healthy controls. Pre-transplantation galactose-deficient IgA1 serum levels were significantly higher in the recurrence compared with the no recurrence or control groups. IgA–IgG complexes were significantly elevated in the recurrence group. Both the recurrence and no recurrence groups had increased values of IgA–sCD89 complexes compared with healthy controls, but values were significantly lower in patients with recurrence compared with no recurrence. Areas under the receiver operating curve of the markers in pre-transplantation sera were 0.86 for galactose-deficient-IgA, 0.82 for IgA–IgG, and 0.78 for sCD89–IgA; all significant. Disease recurrence was associated with decreased serum galactose-deficient IgA1 and appearance of mesangial-galactose-deficient IgA1 deposits, whereas increased serum IgA–sCD89 complexes were associated with mesangial sCD89 deposits. Thus, galactose-deficient-IgA1, IgG autoantibodies, and IgA–sCD89 complexes are valuable biomarkers to predict disease recurrence, highlighting major pathogenic mechanisms in IgAN.
doi_str_mv 10.1038/ki.2015.158
format Article
fullrecord <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1718912742</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S2157171615322437</els_id><sourcerecordid>1718912742</sourcerecordid><originalsourceid>FETCH-LOGICAL-c536t-cfaa8a63df1387b7acdb709faeb77842dd564a2240525253f6cc75c282c19433</originalsourceid><addsrcrecordid>eNptkc2LFDEQxYMo7rh68i4BL4L2mI9OJ31cxq-FBUH2HtJJ9W520502Scv2f2-GWT2I1KGo4leP4j2EXlOyp4Srj_d-zwgVeyrUE7SjgvGGSiGeoh0hSjRMcHWGXuR8R-rcc_IcnbGOdFS07Q5NP8CuKcFc8OXNBZ5huU1xMeV2wz7jJYHztoDDw4ZNKFBnfBM2G_MWzHFfjz5gs5Zo5uKH6DxkbGaHcwzrEAAfPqke2zgtAR4gv0TPRhMyvHrs5-j6y-frw7fm6vvXy8PFVWMF70pjR2OU6bgbKVdykMa6QZJ-NDBIqVrmnOhaw1hLBKvFx85aKSxTzNK-5fwcvTvJLin-XCEXPflsIQQzQ1yzppKqnjLZsoq-_Qe9i2ua63NHSoq2Ul2l3p8om2LOCUa9JD-ZtGlK9DEEfe_1MQRdQ6j0m0fNdZjA_WX_uF4BcQKgevDLQ9LZephtNTuBLdpF_1_h34Ggk8w</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1717542746</pqid></control><display><type>article</type><title>Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Berthelot, Laureline ; Robert, Thomas ; Vuiblet, Vincent ; Tabary, Thierry ; Braconnier, Antoine ; Dramé, Moustapha ; Toupance, Olivier ; Rieu, Philippe ; Monteiro, Renato C. ; Touré, Fatouma</creator><creatorcontrib>Berthelot, Laureline ; Robert, Thomas ; Vuiblet, Vincent ; Tabary, Thierry ; Braconnier, Antoine ; Dramé, Moustapha ; Toupance, Olivier ; Rieu, Philippe ; Monteiro, Renato C. ; Touré, Fatouma</creatorcontrib><description>IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, frequently leads to end-stage renal disease and kidney transplantation. However, disease recurrence often occurs after transplantation. Here we evaluated the predictive value of three markers for IgAN recurrence: the presence of galactose-deficient IgA1, IgG anti-IgA autoantibodies, and IgA-soluble (s) CD89 complexes. This was analyzed in 38 kidney transplant recipients with IgAN recurrence and compared with 22 patients transplanted for IgAN but without recurrence and with 17 healthy controls. Pre-transplantation galactose-deficient IgA1 serum levels were significantly higher in the recurrence compared with the no recurrence or control groups. IgA–IgG complexes were significantly elevated in the recurrence group. Both the recurrence and no recurrence groups had increased values of IgA–sCD89 complexes compared with healthy controls, but values were significantly lower in patients with recurrence compared with no recurrence. Areas under the receiver operating curve of the markers in pre-transplantation sera were 0.86 for galactose-deficient-IgA, 0.82 for IgA–IgG, and 0.78 for sCD89–IgA; all significant. Disease recurrence was associated with decreased serum galactose-deficient IgA1 and appearance of mesangial-galactose-deficient IgA1 deposits, whereas increased serum IgA–sCD89 complexes were associated with mesangial sCD89 deposits. Thus, galactose-deficient-IgA1, IgG autoantibodies, and IgA–sCD89 complexes are valuable biomarkers to predict disease recurrence, highlighting major pathogenic mechanisms in IgAN.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.2015.158</identifier><identifier>PMID: 26061544</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Adult ; Aged ; Antigen-Antibody Complex - blood ; Antigens, CD - blood ; Area Under Curve ; Autoantibodies - blood ; autoantibody ; Biomarkers - blood ; Biopsy ; Case-Control Studies ; Disease Progression ; Female ; Glomerulonephritis, IGA - blood ; Glomerulonephritis, IGA - diagnosis ; Glomerulonephritis, IGA - immunology ; Glomerulonephritis, IGA - surgery ; Humans ; IgA glycosylation ; IgA nephropathy ; Immunoglobulin A - blood ; Kidney - immunology ; Kidney - pathology ; Kidney Failure, Chronic - blood ; Kidney Failure, Chronic - diagnosis ; Kidney Failure, Chronic - immunology ; Kidney Failure, Chronic - surgery ; Kidney Transplantation ; Male ; Middle Aged ; Predictive Value of Tests ; Receptors, Fc - blood ; Recurrence ; Risk Factors ; ROC Curve ; sCD89 ; Treatment Outcome</subject><ispartof>Kidney international, 2015-10, Vol.88 (4), p.815-822</ispartof><rights>2015 International Society of Nephrology</rights><rights>Copyright Nature Publishing Group Oct 2015</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c536t-cfaa8a63df1387b7acdb709faeb77842dd564a2240525253f6cc75c282c19433</citedby><cites>FETCH-LOGICAL-c536t-cfaa8a63df1387b7acdb709faeb77842dd564a2240525253f6cc75c282c19433</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26061544$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Berthelot, Laureline</creatorcontrib><creatorcontrib>Robert, Thomas</creatorcontrib><creatorcontrib>Vuiblet, Vincent</creatorcontrib><creatorcontrib>Tabary, Thierry</creatorcontrib><creatorcontrib>Braconnier, Antoine</creatorcontrib><creatorcontrib>Dramé, Moustapha</creatorcontrib><creatorcontrib>Toupance, Olivier</creatorcontrib><creatorcontrib>Rieu, Philippe</creatorcontrib><creatorcontrib>Monteiro, Renato C.</creatorcontrib><creatorcontrib>Touré, Fatouma</creatorcontrib><title>Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, frequently leads to end-stage renal disease and kidney transplantation. However, disease recurrence often occurs after transplantation. Here we evaluated the predictive value of three markers for IgAN recurrence: the presence of galactose-deficient IgA1, IgG anti-IgA autoantibodies, and IgA-soluble (s) CD89 complexes. This was analyzed in 38 kidney transplant recipients with IgAN recurrence and compared with 22 patients transplanted for IgAN but without recurrence and with 17 healthy controls. Pre-transplantation galactose-deficient IgA1 serum levels were significantly higher in the recurrence compared with the no recurrence or control groups. IgA–IgG complexes were significantly elevated in the recurrence group. Both the recurrence and no recurrence groups had increased values of IgA–sCD89 complexes compared with healthy controls, but values were significantly lower in patients with recurrence compared with no recurrence. Areas under the receiver operating curve of the markers in pre-transplantation sera were 0.86 for galactose-deficient-IgA, 0.82 for IgA–IgG, and 0.78 for sCD89–IgA; all significant. Disease recurrence was associated with decreased serum galactose-deficient IgA1 and appearance of mesangial-galactose-deficient IgA1 deposits, whereas increased serum IgA–sCD89 complexes were associated with mesangial sCD89 deposits. Thus, galactose-deficient-IgA1, IgG autoantibodies, and IgA–sCD89 complexes are valuable biomarkers to predict disease recurrence, highlighting major pathogenic mechanisms in IgAN.</description><subject>Adult</subject><subject>Aged</subject><subject>Antigen-Antibody Complex - blood</subject><subject>Antigens, CD - blood</subject><subject>Area Under Curve</subject><subject>Autoantibodies - blood</subject><subject>autoantibody</subject><subject>Biomarkers - blood</subject><subject>Biopsy</subject><subject>Case-Control Studies</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Glomerulonephritis, IGA - blood</subject><subject>Glomerulonephritis, IGA - diagnosis</subject><subject>Glomerulonephritis, IGA - immunology</subject><subject>Glomerulonephritis, IGA - surgery</subject><subject>Humans</subject><subject>IgA glycosylation</subject><subject>IgA nephropathy</subject><subject>Immunoglobulin A - blood</subject><subject>Kidney - immunology</subject><subject>Kidney - pathology</subject><subject>Kidney Failure, Chronic - blood</subject><subject>Kidney Failure, Chronic - diagnosis</subject><subject>Kidney Failure, Chronic - immunology</subject><subject>Kidney Failure, Chronic - surgery</subject><subject>Kidney Transplantation</subject><subject>Male</subject><subject>Middle Aged</subject><subject>Predictive Value of Tests</subject><subject>Receptors, Fc - blood</subject><subject>Recurrence</subject><subject>Risk Factors</subject><subject>ROC Curve</subject><subject>sCD89</subject><subject>Treatment Outcome</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2015</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNptkc2LFDEQxYMo7rh68i4BL4L2mI9OJ31cxq-FBUH2HtJJ9W520502Scv2f2-GWT2I1KGo4leP4j2EXlOyp4Srj_d-zwgVeyrUE7SjgvGGSiGeoh0hSjRMcHWGXuR8R-rcc_IcnbGOdFS07Q5NP8CuKcFc8OXNBZ5huU1xMeV2wz7jJYHztoDDw4ZNKFBnfBM2G_MWzHFfjz5gs5Zo5uKH6DxkbGaHcwzrEAAfPqke2zgtAR4gv0TPRhMyvHrs5-j6y-frw7fm6vvXy8PFVWMF70pjR2OU6bgbKVdykMa6QZJ-NDBIqVrmnOhaw1hLBKvFx85aKSxTzNK-5fwcvTvJLin-XCEXPflsIQQzQ1yzppKqnjLZsoq-_Qe9i2ua63NHSoq2Ul2l3p8om2LOCUa9JD-ZtGlK9DEEfe_1MQRdQ6j0m0fNdZjA_WX_uF4BcQKgevDLQ9LZephtNTuBLdpF_1_h34Ggk8w</recordid><startdate>20151001</startdate><enddate>20151001</enddate><creator>Berthelot, Laureline</creator><creator>Robert, Thomas</creator><creator>Vuiblet, Vincent</creator><creator>Tabary, Thierry</creator><creator>Braconnier, Antoine</creator><creator>Dramé, Moustapha</creator><creator>Toupance, Olivier</creator><creator>Rieu, Philippe</creator><creator>Monteiro, Renato C.</creator><creator>Touré, Fatouma</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PHGZM</scope><scope>PHGZT</scope><scope>PJZUB</scope><scope>PKEHL</scope><scope>PPXIY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20151001</creationdate><title>Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes</title><author>Berthelot, Laureline ; Robert, Thomas ; Vuiblet, Vincent ; Tabary, Thierry ; Braconnier, Antoine ; Dramé, Moustapha ; Toupance, Olivier ; Rieu, Philippe ; Monteiro, Renato C. ; Touré, Fatouma</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c536t-cfaa8a63df1387b7acdb709faeb77842dd564a2240525253f6cc75c282c19433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2015</creationdate><topic>Adult</topic><topic>Aged</topic><topic>Antigen-Antibody Complex - blood</topic><topic>Antigens, CD - blood</topic><topic>Area Under Curve</topic><topic>Autoantibodies - blood</topic><topic>autoantibody</topic><topic>Biomarkers - blood</topic><topic>Biopsy</topic><topic>Case-Control Studies</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Glomerulonephritis, IGA - blood</topic><topic>Glomerulonephritis, IGA - diagnosis</topic><topic>Glomerulonephritis, IGA - immunology</topic><topic>Glomerulonephritis, IGA - surgery</topic><topic>Humans</topic><topic>IgA glycosylation</topic><topic>IgA nephropathy</topic><topic>Immunoglobulin A - blood</topic><topic>Kidney - immunology</topic><topic>Kidney - pathology</topic><topic>Kidney Failure, Chronic - blood</topic><topic>Kidney Failure, Chronic - diagnosis</topic><topic>Kidney Failure, Chronic - immunology</topic><topic>Kidney Failure, Chronic - surgery</topic><topic>Kidney Transplantation</topic><topic>Male</topic><topic>Middle Aged</topic><topic>Predictive Value of Tests</topic><topic>Receptors, Fc - blood</topic><topic>Recurrence</topic><topic>Risk Factors</topic><topic>ROC Curve</topic><topic>sCD89</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Berthelot, Laureline</creatorcontrib><creatorcontrib>Robert, Thomas</creatorcontrib><creatorcontrib>Vuiblet, Vincent</creatorcontrib><creatorcontrib>Tabary, Thierry</creatorcontrib><creatorcontrib>Braconnier, Antoine</creatorcontrib><creatorcontrib>Dramé, Moustapha</creatorcontrib><creatorcontrib>Toupance, Olivier</creatorcontrib><creatorcontrib>Rieu, Philippe</creatorcontrib><creatorcontrib>Monteiro, Renato C.</creatorcontrib><creatorcontrib>Touré, Fatouma</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Calcium &amp; Calcified Tissue Abstracts</collection><collection>Nursing &amp; Allied Health Database</collection><collection>Health &amp; Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Health &amp; Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing &amp; Allied Health Premium</collection><collection>ProQuest Central (New)</collection><collection>ProQuest One Academic (New)</collection><collection>ProQuest Health &amp; Medical Research Collection</collection><collection>ProQuest One Academic Middle East (New)</collection><collection>ProQuest One Health &amp; Nursing</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Berthelot, Laureline</au><au>Robert, Thomas</au><au>Vuiblet, Vincent</au><au>Tabary, Thierry</au><au>Braconnier, Antoine</au><au>Dramé, Moustapha</au><au>Toupance, Olivier</au><au>Rieu, Philippe</au><au>Monteiro, Renato C.</au><au>Touré, Fatouma</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2015-10-01</date><risdate>2015</risdate><volume>88</volume><issue>4</issue><spage>815</spage><epage>822</epage><pages>815-822</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><abstract>IgA nephropathy (IgAN), the most common primary glomerulonephritis worldwide, frequently leads to end-stage renal disease and kidney transplantation. However, disease recurrence often occurs after transplantation. Here we evaluated the predictive value of three markers for IgAN recurrence: the presence of galactose-deficient IgA1, IgG anti-IgA autoantibodies, and IgA-soluble (s) CD89 complexes. This was analyzed in 38 kidney transplant recipients with IgAN recurrence and compared with 22 patients transplanted for IgAN but without recurrence and with 17 healthy controls. Pre-transplantation galactose-deficient IgA1 serum levels were significantly higher in the recurrence compared with the no recurrence or control groups. IgA–IgG complexes were significantly elevated in the recurrence group. Both the recurrence and no recurrence groups had increased values of IgA–sCD89 complexes compared with healthy controls, but values were significantly lower in patients with recurrence compared with no recurrence. Areas under the receiver operating curve of the markers in pre-transplantation sera were 0.86 for galactose-deficient-IgA, 0.82 for IgA–IgG, and 0.78 for sCD89–IgA; all significant. Disease recurrence was associated with decreased serum galactose-deficient IgA1 and appearance of mesangial-galactose-deficient IgA1 deposits, whereas increased serum IgA–sCD89 complexes were associated with mesangial sCD89 deposits. Thus, galactose-deficient-IgA1, IgG autoantibodies, and IgA–sCD89 complexes are valuable biomarkers to predict disease recurrence, highlighting major pathogenic mechanisms in IgAN.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>26061544</pmid><doi>10.1038/ki.2015.158</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record>
fulltext fulltext
identifier ISSN: 0085-2538
ispartof Kidney international, 2015-10, Vol.88 (4), p.815-822
issn 0085-2538
1523-1755
language eng
recordid cdi_proquest_miscellaneous_1718912742
source MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
subjects Adult
Aged
Antigen-Antibody Complex - blood
Antigens, CD - blood
Area Under Curve
Autoantibodies - blood
autoantibody
Biomarkers - blood
Biopsy
Case-Control Studies
Disease Progression
Female
Glomerulonephritis, IGA - blood
Glomerulonephritis, IGA - diagnosis
Glomerulonephritis, IGA - immunology
Glomerulonephritis, IGA - surgery
Humans
IgA glycosylation
IgA nephropathy
Immunoglobulin A - blood
Kidney - immunology
Kidney - pathology
Kidney Failure, Chronic - blood
Kidney Failure, Chronic - diagnosis
Kidney Failure, Chronic - immunology
Kidney Failure, Chronic - surgery
Kidney Transplantation
Male
Middle Aged
Predictive Value of Tests
Receptors, Fc - blood
Recurrence
Risk Factors
ROC Curve
sCD89
Treatment Outcome
title Recurrent IgA nephropathy is predicted by altered glycosylated IgA, autoantibodies and soluble CD89 complexes
url https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-21T23%3A01%3A58IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Recurrent%20IgA%20nephropathy%20is%20predicted%20by%20altered%20glycosylated%20IgA,%20autoantibodies%20and%20soluble%20CD89%20complexes&rft.jtitle=Kidney%20international&rft.au=Berthelot,%20Laureline&rft.date=2015-10-01&rft.volume=88&rft.issue=4&rft.spage=815&rft.epage=822&rft.pages=815-822&rft.issn=0085-2538&rft.eissn=1523-1755&rft_id=info:doi/10.1038/ki.2015.158&rft_dat=%3Cproquest_cross%3E1718912742%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1717542746&rft_id=info:pmid/26061544&rft_els_id=S2157171615322437&rfr_iscdi=true