Resistance factors for the treatment of immunoglobulin A nephropathy with diffuse mesangial proliferation
Aim Some patients with severe immunoglobulin A nephropathy (IgAN) are resistant to multi‐drug combination therapy; however, there have been few reports on the risk factors for non‐responsiveness to treatment for severe IgAN. We, therefore, evaluated the risk factors for non‐responsiveness to treatme...
Gespeichert in:
Veröffentlicht in: | Nephrology (Carlton, Vic.) Vic.), 2014-07, Vol.19 (7), p.384-391 |
---|---|
Hauptverfasser: | , , , , , , , , |
Format: | Artikel |
Sprache: | eng |
Schlagworte: | |
Online-Zugang: | Volltext |
Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
container_end_page | 391 |
---|---|
container_issue | 7 |
container_start_page | 384 |
container_title | Nephrology (Carlton, Vic.) |
container_volume | 19 |
creator | Kawasaki, Yukihiko Suyama, Kazuhide Miyazaki, Kyohei Kanno, Shuto Ono, Atsushi Suzuki, Yuichi Sato, Masatoki Hashimoto, Koichi Hosoya, Mitsuaki |
description | Aim
Some patients with severe immunoglobulin A nephropathy (IgAN) are resistant to multi‐drug combination therapy; however, there have been few reports on the risk factors for non‐responsiveness to treatment for severe IgAN. We, therefore, evaluated the risk factors for non‐responsiveness to treatment in cases of severe IgAN.
Methods
We collected data on 44 children who had been diagnosed with IgAN with diffuse mesangial proliferation and treated with multi‐drug combination therapy. The children were divided into two groups based on the prognosis at the latest follow‐up. Group 1 consisted of 30 children with normal urine and nine children with minor urinary abnormalities and Group 2 consisted of four children with persistent nephropathy and one child with renal insufficiency. The clinical, laboratory, and pathological findings for both groups were analyzed.
Results
The age at the onset in Group 2 was higher than that in Group 1. C3 deposits and high chronicity index values at the first renal biopsy were more frequently found in Group 2 than in Group 1 patients. IgA deposits, serum IgA and myeloid‐related protein (MRP) 8/14 levels, and glomerular and interstitial MRP8+CD68+ scores at the second biopsy were all higher in Group 2 than in Group 1 patients.
Conclusions
Our results, although based on only a small number of patients in a retrospective study, suggest that age, presence of C3 deposits and interstitial changes at the onset, and persistent renal inflammatory activation may be risk factors for non‐responsiveness to treatment for IgAN with diffuse mesangial proliferation.
Summary at a Glance
This paper identifies a number of clinical, laboratory and pathological risk factors for persistence of IgA nephropathy despite treatment in children. |
doi_str_mv | 10.1111/nep.12232 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1551643748</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1551643748</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3962-446df2c30c19a8286b3c4e0e13a50bc83f3d84e3fd19e3f2306d46ac12cfb3453</originalsourceid><addsrcrecordid>eNqNkUFv1DAQhS0EoqVw4A8gH-GQ1vY4TnKsVqUgVW0FtD1ajjPuGpJ4azsq--8x3bY3JOYwM4dv3pPmEfKes0Ne6mjGzSEXAsQLss-lZBVvuuZl2UGwqoa63SNvUvrJGG-E4q_JnpBKKsHlPvHfMPmUzWyROmNziIm6EGleI80RTZ5wzjQ46qdpmcPtGPpl9DM9psV0HcPG5PWW3vu8poN3bklIJ0xmvvVmpJsYRu8wmuzD_Ja8cmZM-O5xHpCrzyc_Vl-qs4vTr6vjs8pCp0QlpRqcsMAs70wrWtWDlciQg6lZb1twMLQSwQ28K10AU4NUxnJhXQ-yhgPycadb3O8WTFlPPlkcRzNjWJLmdc2VhEa2_4GCUq3oJCvopx1qY0gpotOb6CcTt5oz_TcEXf6hH0Io7IdH2aWfcHgmn75egKMdcO9H3P5bSZ-fXD5JVruLkhX-fr4w8ZdWDTS1vjk_1TfN5fdVB1Jfwx8k1KEv</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1536682940</pqid></control><display><type>article</type><title>Resistance factors for the treatment of immunoglobulin A nephropathy with diffuse mesangial proliferation</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Kawasaki, Yukihiko ; Suyama, Kazuhide ; Miyazaki, Kyohei ; Kanno, Shuto ; Ono, Atsushi ; Suzuki, Yuichi ; Sato, Masatoki ; Hashimoto, Koichi ; Hosoya, Mitsuaki</creator><creatorcontrib>Kawasaki, Yukihiko ; Suyama, Kazuhide ; Miyazaki, Kyohei ; Kanno, Shuto ; Ono, Atsushi ; Suzuki, Yuichi ; Sato, Masatoki ; Hashimoto, Koichi ; Hosoya, Mitsuaki</creatorcontrib><description>Aim
Some patients with severe immunoglobulin A nephropathy (IgAN) are resistant to multi‐drug combination therapy; however, there have been few reports on the risk factors for non‐responsiveness to treatment for severe IgAN. We, therefore, evaluated the risk factors for non‐responsiveness to treatment in cases of severe IgAN.
Methods
We collected data on 44 children who had been diagnosed with IgAN with diffuse mesangial proliferation and treated with multi‐drug combination therapy. The children were divided into two groups based on the prognosis at the latest follow‐up. Group 1 consisted of 30 children with normal urine and nine children with minor urinary abnormalities and Group 2 consisted of four children with persistent nephropathy and one child with renal insufficiency. The clinical, laboratory, and pathological findings for both groups were analyzed.
Results
The age at the onset in Group 2 was higher than that in Group 1. C3 deposits and high chronicity index values at the first renal biopsy were more frequently found in Group 2 than in Group 1 patients. IgA deposits, serum IgA and myeloid‐related protein (MRP) 8/14 levels, and glomerular and interstitial MRP8+CD68+ scores at the second biopsy were all higher in Group 2 than in Group 1 patients.
Conclusions
Our results, although based on only a small number of patients in a retrospective study, suggest that age, presence of C3 deposits and interstitial changes at the onset, and persistent renal inflammatory activation may be risk factors for non‐responsiveness to treatment for IgAN with diffuse mesangial proliferation.
Summary at a Glance
This paper identifies a number of clinical, laboratory and pathological risk factors for persistence of IgA nephropathy despite treatment in children.</description><identifier>ISSN: 1320-5358</identifier><identifier>EISSN: 1440-1797</identifier><identifier>DOI: 10.1111/nep.12232</identifier><identifier>PMID: 24646214</identifier><language>eng</language><publisher>Australia: Blackwell Publishing Ltd</publisher><subject>Age of Onset ; Antigens, CD - metabolism ; Antigens, Differentiation, Myelomonocytic - metabolism ; Biopsy - methods ; Calgranulin A - metabolism ; Calgranulin B - metabolism ; Child ; Dilazep - administration & dosage ; Drug Resistance, Multiple ; Drug Therapy, Combination - methods ; Female ; Glomerulonephritis, IGA - blood ; Glomerulonephritis, IGA - diagnosis ; Glomerulonephritis, IGA - drug therapy ; Glomerulonephritis, IGA - epidemiology ; Humans ; Immunoglobulin A - metabolism ; immunoglobulin A nephropathy ; Immunosuppressive Agents - administration & dosage ; Japan - epidemiology ; Kidney Function Tests - methods ; Male ; Mesangial Cells - metabolism ; Mesangial Cells - pathology ; Mizoribine ; multi-drugs combination therapy ; Prednisolone - administration & dosage ; resistant factors ; Retrospective Studies ; Ribonucleosides - administration & dosage ; Risk Factors ; serum myeloid-related protein8/14 ; Severity of Illness Index ; Vasodilator Agents - administration & dosage</subject><ispartof>Nephrology (Carlton, Vic.), 2014-07, Vol.19 (7), p.384-391</ispartof><rights>2014 Asian Pacific Society of Nephrology</rights><rights>2014 Asian Pacific Society of Nephrology.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3962-446df2c30c19a8286b3c4e0e13a50bc83f3d84e3fd19e3f2306d46ac12cfb3453</citedby><cites>FETCH-LOGICAL-c3962-446df2c30c19a8286b3c4e0e13a50bc83f3d84e3fd19e3f2306d46ac12cfb3453</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://onlinelibrary.wiley.com/doi/pdf/10.1111%2Fnep.12232$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnep.12232$$EHTML$$P50$$Gwiley$$H</linktohtml><link.rule.ids>314,780,784,1417,27924,27925,45574,45575</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24646214$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kawasaki, Yukihiko</creatorcontrib><creatorcontrib>Suyama, Kazuhide</creatorcontrib><creatorcontrib>Miyazaki, Kyohei</creatorcontrib><creatorcontrib>Kanno, Shuto</creatorcontrib><creatorcontrib>Ono, Atsushi</creatorcontrib><creatorcontrib>Suzuki, Yuichi</creatorcontrib><creatorcontrib>Sato, Masatoki</creatorcontrib><creatorcontrib>Hashimoto, Koichi</creatorcontrib><creatorcontrib>Hosoya, Mitsuaki</creatorcontrib><title>Resistance factors for the treatment of immunoglobulin A nephropathy with diffuse mesangial proliferation</title><title>Nephrology (Carlton, Vic.)</title><addtitle>Nephrology</addtitle><description>Aim
Some patients with severe immunoglobulin A nephropathy (IgAN) are resistant to multi‐drug combination therapy; however, there have been few reports on the risk factors for non‐responsiveness to treatment for severe IgAN. We, therefore, evaluated the risk factors for non‐responsiveness to treatment in cases of severe IgAN.
Methods
We collected data on 44 children who had been diagnosed with IgAN with diffuse mesangial proliferation and treated with multi‐drug combination therapy. The children were divided into two groups based on the prognosis at the latest follow‐up. Group 1 consisted of 30 children with normal urine and nine children with minor urinary abnormalities and Group 2 consisted of four children with persistent nephropathy and one child with renal insufficiency. The clinical, laboratory, and pathological findings for both groups were analyzed.
Results
The age at the onset in Group 2 was higher than that in Group 1. C3 deposits and high chronicity index values at the first renal biopsy were more frequently found in Group 2 than in Group 1 patients. IgA deposits, serum IgA and myeloid‐related protein (MRP) 8/14 levels, and glomerular and interstitial MRP8+CD68+ scores at the second biopsy were all higher in Group 2 than in Group 1 patients.
Conclusions
Our results, although based on only a small number of patients in a retrospective study, suggest that age, presence of C3 deposits and interstitial changes at the onset, and persistent renal inflammatory activation may be risk factors for non‐responsiveness to treatment for IgAN with diffuse mesangial proliferation.
Summary at a Glance
This paper identifies a number of clinical, laboratory and pathological risk factors for persistence of IgA nephropathy despite treatment in children.</description><subject>Age of Onset</subject><subject>Antigens, CD - metabolism</subject><subject>Antigens, Differentiation, Myelomonocytic - metabolism</subject><subject>Biopsy - methods</subject><subject>Calgranulin A - metabolism</subject><subject>Calgranulin B - metabolism</subject><subject>Child</subject><subject>Dilazep - administration & dosage</subject><subject>Drug Resistance, Multiple</subject><subject>Drug Therapy, Combination - methods</subject><subject>Female</subject><subject>Glomerulonephritis, IGA - blood</subject><subject>Glomerulonephritis, IGA - diagnosis</subject><subject>Glomerulonephritis, IGA - drug therapy</subject><subject>Glomerulonephritis, IGA - epidemiology</subject><subject>Humans</subject><subject>Immunoglobulin A - metabolism</subject><subject>immunoglobulin A nephropathy</subject><subject>Immunosuppressive Agents - administration & dosage</subject><subject>Japan - epidemiology</subject><subject>Kidney Function Tests - methods</subject><subject>Male</subject><subject>Mesangial Cells - metabolism</subject><subject>Mesangial Cells - pathology</subject><subject>Mizoribine</subject><subject>multi-drugs combination therapy</subject><subject>Prednisolone - administration & dosage</subject><subject>resistant factors</subject><subject>Retrospective Studies</subject><subject>Ribonucleosides - administration & dosage</subject><subject>Risk Factors</subject><subject>serum myeloid-related protein8/14</subject><subject>Severity of Illness Index</subject><subject>Vasodilator Agents - administration & dosage</subject><issn>1320-5358</issn><issn>1440-1797</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkUFv1DAQhS0EoqVw4A8gH-GQ1vY4TnKsVqUgVW0FtD1ajjPuGpJ4azsq--8x3bY3JOYwM4dv3pPmEfKes0Ne6mjGzSEXAsQLss-lZBVvuuZl2UGwqoa63SNvUvrJGG-E4q_JnpBKKsHlPvHfMPmUzWyROmNziIm6EGleI80RTZ5wzjQ46qdpmcPtGPpl9DM9psV0HcPG5PWW3vu8poN3bklIJ0xmvvVmpJsYRu8wmuzD_Ja8cmZM-O5xHpCrzyc_Vl-qs4vTr6vjs8pCp0QlpRqcsMAs70wrWtWDlciQg6lZb1twMLQSwQ28K10AU4NUxnJhXQ-yhgPycadb3O8WTFlPPlkcRzNjWJLmdc2VhEa2_4GCUq3oJCvopx1qY0gpotOb6CcTt5oz_TcEXf6hH0Io7IdH2aWfcHgmn75egKMdcO9H3P5bSZ-fXD5JVruLkhX-fr4w8ZdWDTS1vjk_1TfN5fdVB1Jfwx8k1KEv</recordid><startdate>201407</startdate><enddate>201407</enddate><creator>Kawasaki, Yukihiko</creator><creator>Suyama, Kazuhide</creator><creator>Miyazaki, Kyohei</creator><creator>Kanno, Shuto</creator><creator>Ono, Atsushi</creator><creator>Suzuki, Yuichi</creator><creator>Sato, Masatoki</creator><creator>Hashimoto, Koichi</creator><creator>Hosoya, Mitsuaki</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</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>7X8</scope><scope>7T5</scope><scope>H94</scope></search><sort><creationdate>201407</creationdate><title>Resistance factors for the treatment of immunoglobulin A nephropathy with diffuse mesangial proliferation</title><author>Kawasaki, Yukihiko ; Suyama, Kazuhide ; Miyazaki, Kyohei ; Kanno, Shuto ; Ono, Atsushi ; Suzuki, Yuichi ; Sato, Masatoki ; Hashimoto, Koichi ; Hosoya, Mitsuaki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3962-446df2c30c19a8286b3c4e0e13a50bc83f3d84e3fd19e3f2306d46ac12cfb3453</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Age of Onset</topic><topic>Antigens, CD - metabolism</topic><topic>Antigens, Differentiation, Myelomonocytic - metabolism</topic><topic>Biopsy - methods</topic><topic>Calgranulin A - metabolism</topic><topic>Calgranulin B - metabolism</topic><topic>Child</topic><topic>Dilazep - administration & dosage</topic><topic>Drug Resistance, Multiple</topic><topic>Drug Therapy, Combination - methods</topic><topic>Female</topic><topic>Glomerulonephritis, IGA - blood</topic><topic>Glomerulonephritis, IGA - diagnosis</topic><topic>Glomerulonephritis, IGA - drug therapy</topic><topic>Glomerulonephritis, IGA - epidemiology</topic><topic>Humans</topic><topic>Immunoglobulin A - metabolism</topic><topic>immunoglobulin A nephropathy</topic><topic>Immunosuppressive Agents - administration & dosage</topic><topic>Japan - epidemiology</topic><topic>Kidney Function Tests - methods</topic><topic>Male</topic><topic>Mesangial Cells - metabolism</topic><topic>Mesangial Cells - pathology</topic><topic>Mizoribine</topic><topic>multi-drugs combination therapy</topic><topic>Prednisolone - administration & dosage</topic><topic>resistant factors</topic><topic>Retrospective Studies</topic><topic>Ribonucleosides - administration & dosage</topic><topic>Risk Factors</topic><topic>serum myeloid-related protein8/14</topic><topic>Severity of Illness Index</topic><topic>Vasodilator Agents - administration & dosage</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kawasaki, Yukihiko</creatorcontrib><creatorcontrib>Suyama, Kazuhide</creatorcontrib><creatorcontrib>Miyazaki, Kyohei</creatorcontrib><creatorcontrib>Kanno, Shuto</creatorcontrib><creatorcontrib>Ono, Atsushi</creatorcontrib><creatorcontrib>Suzuki, Yuichi</creatorcontrib><creatorcontrib>Sato, Masatoki</creatorcontrib><creatorcontrib>Hashimoto, Koichi</creatorcontrib><creatorcontrib>Hosoya, Mitsuaki</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Nephrology (Carlton, Vic.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kawasaki, Yukihiko</au><au>Suyama, Kazuhide</au><au>Miyazaki, Kyohei</au><au>Kanno, Shuto</au><au>Ono, Atsushi</au><au>Suzuki, Yuichi</au><au>Sato, Masatoki</au><au>Hashimoto, Koichi</au><au>Hosoya, Mitsuaki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Resistance factors for the treatment of immunoglobulin A nephropathy with diffuse mesangial proliferation</atitle><jtitle>Nephrology (Carlton, Vic.)</jtitle><addtitle>Nephrology</addtitle><date>2014-07</date><risdate>2014</risdate><volume>19</volume><issue>7</issue><spage>384</spage><epage>391</epage><pages>384-391</pages><issn>1320-5358</issn><eissn>1440-1797</eissn><abstract>Aim
Some patients with severe immunoglobulin A nephropathy (IgAN) are resistant to multi‐drug combination therapy; however, there have been few reports on the risk factors for non‐responsiveness to treatment for severe IgAN. We, therefore, evaluated the risk factors for non‐responsiveness to treatment in cases of severe IgAN.
Methods
We collected data on 44 children who had been diagnosed with IgAN with diffuse mesangial proliferation and treated with multi‐drug combination therapy. The children were divided into two groups based on the prognosis at the latest follow‐up. Group 1 consisted of 30 children with normal urine and nine children with minor urinary abnormalities and Group 2 consisted of four children with persistent nephropathy and one child with renal insufficiency. The clinical, laboratory, and pathological findings for both groups were analyzed.
Results
The age at the onset in Group 2 was higher than that in Group 1. C3 deposits and high chronicity index values at the first renal biopsy were more frequently found in Group 2 than in Group 1 patients. IgA deposits, serum IgA and myeloid‐related protein (MRP) 8/14 levels, and glomerular and interstitial MRP8+CD68+ scores at the second biopsy were all higher in Group 2 than in Group 1 patients.
Conclusions
Our results, although based on only a small number of patients in a retrospective study, suggest that age, presence of C3 deposits and interstitial changes at the onset, and persistent renal inflammatory activation may be risk factors for non‐responsiveness to treatment for IgAN with diffuse mesangial proliferation.
Summary at a Glance
This paper identifies a number of clinical, laboratory and pathological risk factors for persistence of IgA nephropathy despite treatment in children.</abstract><cop>Australia</cop><pub>Blackwell Publishing Ltd</pub><pmid>24646214</pmid><doi>10.1111/nep.12232</doi><tpages>8</tpages></addata></record> |
fulltext | fulltext |
identifier | ISSN: 1320-5358 |
ispartof | Nephrology (Carlton, Vic.), 2014-07, Vol.19 (7), p.384-391 |
issn | 1320-5358 1440-1797 |
language | eng |
recordid | cdi_proquest_miscellaneous_1551643748 |
source | MEDLINE; Access via Wiley Online Library |
subjects | Age of Onset Antigens, CD - metabolism Antigens, Differentiation, Myelomonocytic - metabolism Biopsy - methods Calgranulin A - metabolism Calgranulin B - metabolism Child Dilazep - administration & dosage Drug Resistance, Multiple Drug Therapy, Combination - methods Female Glomerulonephritis, IGA - blood Glomerulonephritis, IGA - diagnosis Glomerulonephritis, IGA - drug therapy Glomerulonephritis, IGA - epidemiology Humans Immunoglobulin A - metabolism immunoglobulin A nephropathy Immunosuppressive Agents - administration & dosage Japan - epidemiology Kidney Function Tests - methods Male Mesangial Cells - metabolism Mesangial Cells - pathology Mizoribine multi-drugs combination therapy Prednisolone - administration & dosage resistant factors Retrospective Studies Ribonucleosides - administration & dosage Risk Factors serum myeloid-related protein8/14 Severity of Illness Index Vasodilator Agents - administration & dosage |
title | Resistance factors for the treatment of immunoglobulin A nephropathy with diffuse mesangial proliferation |
url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2024-12-20T07%3A47%3A05IST&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=Resistance%20factors%20for%20the%20treatment%20of%20immunoglobulin%20A%20nephropathy%20with%20diffuse%20mesangial%20proliferation&rft.jtitle=Nephrology%20(Carlton,%20Vic.)&rft.au=Kawasaki,%20Yukihiko&rft.date=2014-07&rft.volume=19&rft.issue=7&rft.spage=384&rft.epage=391&rft.pages=384-391&rft.issn=1320-5358&rft.eissn=1440-1797&rft_id=info:doi/10.1111/nep.12232&rft_dat=%3Cproquest_cross%3E1551643748%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=1536682940&rft_id=info:pmid/24646214&rfr_iscdi=true |