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...

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Veröffentlicht in:Nephrology (Carlton, Vic.) Vic.), 2014-07, Vol.19 (7), p.384-391
Hauptverfasser: Kawasaki, Yukihiko, Suyama, Kazuhide, Miyazaki, Kyohei, Kanno, Shuto, Ono, Atsushi, Suzuki, Yuichi, Sato, Masatoki, Hashimoto, Koichi, Hosoya, Mitsuaki
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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
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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 &amp; 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 &amp; dosage ; Japan - epidemiology ; Kidney Function Tests - methods ; Male ; Mesangial Cells - metabolism ; Mesangial Cells - pathology ; Mizoribine ; multi-drugs combination therapy ; Prednisolone - administration &amp; dosage ; resistant factors ; Retrospective Studies ; Ribonucleosides - administration &amp; dosage ; Risk Factors ; serum myeloid-related protein8/14 ; Severity of Illness Index ; Vasodilator Agents - administration &amp; 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. 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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 &amp; 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 &amp; 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 &amp; dosage</topic><topic>resistant factors</topic><topic>Retrospective Studies</topic><topic>Ribonucleosides - administration &amp; dosage</topic><topic>Risk Factors</topic><topic>serum myeloid-related protein8/14</topic><topic>Severity of Illness Index</topic><topic>Vasodilator Agents - administration &amp; 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>
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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
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