Clinical and pathological analyses of interstitial fibrosis and tubular atrophy cases after kidney transplantation
Aim We carried out a clinicopathological analysis of cases presenting with interstitial fibrosis and tubular atrophy (IF/TA) after renal transplantation in an attempt to clarify the mechanisms underlying the development and prognostic significance of IF/TA. Methods IF/TA was diagnosed in 35 renal al...
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creator | Shimizu, Tomokazu Toma, Hiroshi Hayakawa, Nozomi Shibahara, Rumi Ishiyama, Ryou Hayashida, Akihiro Fujimori, Daiji Tsunoyama, Kuniko Ikezawa, Eri Kitajima, Shoji Iida, Shoichi Ishida, Hideki Tanabe, Kazunari Honda, Kazuho Koike, Junki |
description | Aim
We carried out a clinicopathological analysis of cases presenting with interstitial fibrosis and tubular atrophy (IF/TA) after renal transplantation in an attempt to clarify the mechanisms underlying the development and prognostic significance of IF/TA.
Methods
IF/TA was diagnosed in 35 renal allograft biopsy specimens (BS) obtained from 35 renal transplant recipients under follow up at the Department of Transplant Surgery, Kidney Center, Toda Chuo General Hospital, between January 2014 and March 2015.
Results
IF/TA was diagnosed at a median of 39.9 months after the transplantation. Among the 35 patients with IF/TA, 19 (54%) had a history of acute rejection. Among the 35 BS showing evidence of IF/TA, the IF/TA was grade I in 25, grade II in 9, and grade III in 1. Arteriosclerosis of the middle‐sized arteries was observed in 30 BS (86%). We then classified the 35 BS showing evidence of IF/TA according to their overall histopathological features, as follows; IF/TA alone (6 BS; 17%), IF/TA + medullary ray injury (12 BS; 34%), and IF/TA + rejection (12 BS; 34%). Loss of the renal allograft occurred during the observation period in one of the patients (3%). Of the remaining patients with functioning grafts, deterioration of the renal allograft function after the biopsies occurred in 15 patients (43%).
Conclusions
The results of our study suggests that rejection contributes to IF/TA in 30–40% of cases, medullary ray injury in 30–40% of cases, and nonspecific injury in 20% of cases. IF/TA contributes significantly to deterioration of renal allograft function. |
doi_str_mv | 10.1111/nep.12766 |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1799561864</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1799561864</sourcerecordid><originalsourceid>FETCH-LOGICAL-c3986-e006bb3e333b4a1ecc44fa522bd7590401b7271ed2cbd077112634d4a888b2343</originalsourceid><addsrcrecordid>eNp1kMtO3DAYhS1UVCh00ReosiyLgG-x42U74tKCuEhUldhYvxOnuHiSYDsqeXs8zMAOb2zZ3zn6_SH0heBDktdRb8dDQqUQW2iXcI5LIpX8kM-M4rJiVb2DPsX4D2MiqSAf0Q4VSlIl1C4KC-9614AvoG-LEdL94Ie_mwvwc7SxGLrC9cmGmFxy-aFzJgzRxZdImszkIRSQwjDez0UDqwh0mS8eXNvbuUgB-jh66BMkN_T7aLsDH-3nzb6Hfp8c3y7Oyour05-L7xdlw1QtSouxMIZZxpjhQGzTcN5BRalpZaUwx8RIKoltaWNaLCUhVDDecqjr2lDG2R76tu4dw_A42Zj00sXG-jyIHaaosyRVCVKLFXqwRpv8sRhsp8fglhBmTbBeKdZZsX5RnNmvm9rJLG37Rr46zcDRGvjvvJ3fb9KXx9evleU64WKyT28JCA9aSCYr_efyVP9Qd-z87EbpX-wZ0qGWug</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1799561864</pqid></control><display><type>article</type><title>Clinical and pathological analyses of interstitial fibrosis and tubular atrophy cases after kidney transplantation</title><source>MEDLINE</source><source>Access via Wiley Online Library</source><creator>Shimizu, Tomokazu ; Toma, Hiroshi ; Hayakawa, Nozomi ; Shibahara, Rumi ; Ishiyama, Ryou ; Hayashida, Akihiro ; Fujimori, Daiji ; Tsunoyama, Kuniko ; Ikezawa, Eri ; Kitajima, Shoji ; Iida, Shoichi ; Ishida, Hideki ; Tanabe, Kazunari ; Honda, Kazuho ; Koike, Junki</creator><creatorcontrib>Shimizu, Tomokazu ; Toma, Hiroshi ; Hayakawa, Nozomi ; Shibahara, Rumi ; Ishiyama, Ryou ; Hayashida, Akihiro ; Fujimori, Daiji ; Tsunoyama, Kuniko ; Ikezawa, Eri ; Kitajima, Shoji ; Iida, Shoichi ; Ishida, Hideki ; Tanabe, Kazunari ; Honda, Kazuho ; Koike, Junki</creatorcontrib><description>Aim
We carried out a clinicopathological analysis of cases presenting with interstitial fibrosis and tubular atrophy (IF/TA) after renal transplantation in an attempt to clarify the mechanisms underlying the development and prognostic significance of IF/TA.
Methods
IF/TA was diagnosed in 35 renal allograft biopsy specimens (BS) obtained from 35 renal transplant recipients under follow up at the Department of Transplant Surgery, Kidney Center, Toda Chuo General Hospital, between January 2014 and March 2015.
Results
IF/TA was diagnosed at a median of 39.9 months after the transplantation. Among the 35 patients with IF/TA, 19 (54%) had a history of acute rejection. Among the 35 BS showing evidence of IF/TA, the IF/TA was grade I in 25, grade II in 9, and grade III in 1. Arteriosclerosis of the middle‐sized arteries was observed in 30 BS (86%). We then classified the 35 BS showing evidence of IF/TA according to their overall histopathological features, as follows; IF/TA alone (6 BS; 17%), IF/TA + medullary ray injury (12 BS; 34%), and IF/TA + rejection (12 BS; 34%). Loss of the renal allograft occurred during the observation period in one of the patients (3%). Of the remaining patients with functioning grafts, deterioration of the renal allograft function after the biopsies occurred in 15 patients (43%).
Conclusions
The results of our study suggests that rejection contributes to IF/TA in 30–40% of cases, medullary ray injury in 30–40% of cases, and nonspecific injury in 20% of cases. IF/TA contributes significantly to deterioration of renal allograft function.</description><identifier>ISSN: 1320-5358</identifier><identifier>EISSN: 1440-1797</identifier><identifier>DOI: 10.1111/nep.12766</identifier><identifier>PMID: 26972969</identifier><language>eng</language><publisher>Australia: Blackwell Publishing Ltd</publisher><subject>Adolescent ; Adult ; Aged ; Allografts ; Atrophy ; Biopsy ; calcineurin inhibitor arteriolopathy ; Disease Progression ; Female ; Fibrosis ; Graft Rejection - etiology ; Graft Rejection - pathology ; Graft Rejection - physiopathology ; Graft Survival ; Hospitals, General ; Humans ; interstitial fibrosis and tubular atrophy ; Japan ; Kidney Diseases - etiology ; Kidney Diseases - pathology ; Kidney Diseases - physiopathology ; Kidney Function Tests ; kidney transplantation ; Kidney Transplantation - adverse effects ; Kidney Tubules - pathology ; Kidney Tubules - physiopathology ; Male ; medullary ray injury ; Middle Aged ; rejection ; Retrospective Studies ; Risk Factors ; Severity of Illness Index ; Time Factors ; Treatment Outcome ; Young Adult</subject><ispartof>Nephrology (Carlton, Vic.), 2016-07, Vol.21 (S1), p.26-30</ispartof><rights>2016 Asian Pacific Society of Nephrology</rights><rights>2016 Asian Pacific Society of Nephrology.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c3986-e006bb3e333b4a1ecc44fa522bd7590401b7271ed2cbd077112634d4a888b2343</citedby><cites>FETCH-LOGICAL-c3986-e006bb3e333b4a1ecc44fa522bd7590401b7271ed2cbd077112634d4a888b2343</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.12766$$EPDF$$P50$$Gwiley$$H</linktopdf><linktohtml>$$Uhttps://onlinelibrary.wiley.com/doi/full/10.1111%2Fnep.12766$$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/26972969$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Shimizu, Tomokazu</creatorcontrib><creatorcontrib>Toma, Hiroshi</creatorcontrib><creatorcontrib>Hayakawa, Nozomi</creatorcontrib><creatorcontrib>Shibahara, Rumi</creatorcontrib><creatorcontrib>Ishiyama, Ryou</creatorcontrib><creatorcontrib>Hayashida, Akihiro</creatorcontrib><creatorcontrib>Fujimori, Daiji</creatorcontrib><creatorcontrib>Tsunoyama, Kuniko</creatorcontrib><creatorcontrib>Ikezawa, Eri</creatorcontrib><creatorcontrib>Kitajima, Shoji</creatorcontrib><creatorcontrib>Iida, Shoichi</creatorcontrib><creatorcontrib>Ishida, Hideki</creatorcontrib><creatorcontrib>Tanabe, Kazunari</creatorcontrib><creatorcontrib>Honda, Kazuho</creatorcontrib><creatorcontrib>Koike, Junki</creatorcontrib><title>Clinical and pathological analyses of interstitial fibrosis and tubular atrophy cases after kidney transplantation</title><title>Nephrology (Carlton, Vic.)</title><addtitle>Nephrology</addtitle><description>Aim
We carried out a clinicopathological analysis of cases presenting with interstitial fibrosis and tubular atrophy (IF/TA) after renal transplantation in an attempt to clarify the mechanisms underlying the development and prognostic significance of IF/TA.
Methods
IF/TA was diagnosed in 35 renal allograft biopsy specimens (BS) obtained from 35 renal transplant recipients under follow up at the Department of Transplant Surgery, Kidney Center, Toda Chuo General Hospital, between January 2014 and March 2015.
Results
IF/TA was diagnosed at a median of 39.9 months after the transplantation. Among the 35 patients with IF/TA, 19 (54%) had a history of acute rejection. Among the 35 BS showing evidence of IF/TA, the IF/TA was grade I in 25, grade II in 9, and grade III in 1. Arteriosclerosis of the middle‐sized arteries was observed in 30 BS (86%). We then classified the 35 BS showing evidence of IF/TA according to their overall histopathological features, as follows; IF/TA alone (6 BS; 17%), IF/TA + medullary ray injury (12 BS; 34%), and IF/TA + rejection (12 BS; 34%). Loss of the renal allograft occurred during the observation period in one of the patients (3%). Of the remaining patients with functioning grafts, deterioration of the renal allograft function after the biopsies occurred in 15 patients (43%).
Conclusions
The results of our study suggests that rejection contributes to IF/TA in 30–40% of cases, medullary ray injury in 30–40% of cases, and nonspecific injury in 20% of cases. IF/TA contributes significantly to deterioration of renal allograft function.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Allografts</subject><subject>Atrophy</subject><subject>Biopsy</subject><subject>calcineurin inhibitor arteriolopathy</subject><subject>Disease Progression</subject><subject>Female</subject><subject>Fibrosis</subject><subject>Graft Rejection - etiology</subject><subject>Graft Rejection - pathology</subject><subject>Graft Rejection - physiopathology</subject><subject>Graft Survival</subject><subject>Hospitals, General</subject><subject>Humans</subject><subject>interstitial fibrosis and tubular atrophy</subject><subject>Japan</subject><subject>Kidney Diseases - etiology</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Diseases - physiopathology</subject><subject>Kidney Function Tests</subject><subject>kidney transplantation</subject><subject>Kidney Transplantation - adverse effects</subject><subject>Kidney Tubules - pathology</subject><subject>Kidney Tubules - physiopathology</subject><subject>Male</subject><subject>medullary ray injury</subject><subject>Middle Aged</subject><subject>rejection</subject><subject>Retrospective Studies</subject><subject>Risk Factors</subject><subject>Severity of Illness Index</subject><subject>Time Factors</subject><subject>Treatment Outcome</subject><subject>Young Adult</subject><issn>1320-5358</issn><issn>1440-1797</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kMtO3DAYhS1UVCh00ReosiyLgG-x42U74tKCuEhUldhYvxOnuHiSYDsqeXs8zMAOb2zZ3zn6_SH0heBDktdRb8dDQqUQW2iXcI5LIpX8kM-M4rJiVb2DPsX4D2MiqSAf0Q4VSlIl1C4KC-9614AvoG-LEdL94Ie_mwvwc7SxGLrC9cmGmFxy-aFzJgzRxZdImszkIRSQwjDez0UDqwh0mS8eXNvbuUgB-jh66BMkN_T7aLsDH-3nzb6Hfp8c3y7Oyour05-L7xdlw1QtSouxMIZZxpjhQGzTcN5BRalpZaUwx8RIKoltaWNaLCUhVDDecqjr2lDG2R76tu4dw_A42Zj00sXG-jyIHaaosyRVCVKLFXqwRpv8sRhsp8fglhBmTbBeKdZZsX5RnNmvm9rJLG37Rr46zcDRGvjvvJ3fb9KXx9evleU64WKyT28JCA9aSCYr_efyVP9Qd-z87EbpX-wZ0qGWug</recordid><startdate>201607</startdate><enddate>201607</enddate><creator>Shimizu, Tomokazu</creator><creator>Toma, Hiroshi</creator><creator>Hayakawa, Nozomi</creator><creator>Shibahara, Rumi</creator><creator>Ishiyama, Ryou</creator><creator>Hayashida, Akihiro</creator><creator>Fujimori, Daiji</creator><creator>Tsunoyama, Kuniko</creator><creator>Ikezawa, Eri</creator><creator>Kitajima, Shoji</creator><creator>Iida, Shoichi</creator><creator>Ishida, Hideki</creator><creator>Tanabe, Kazunari</creator><creator>Honda, Kazuho</creator><creator>Koike, Junki</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></search><sort><creationdate>201607</creationdate><title>Clinical and pathological analyses of interstitial fibrosis and tubular atrophy cases after kidney transplantation</title><author>Shimizu, Tomokazu ; Toma, Hiroshi ; Hayakawa, Nozomi ; Shibahara, Rumi ; Ishiyama, Ryou ; Hayashida, Akihiro ; Fujimori, Daiji ; Tsunoyama, Kuniko ; Ikezawa, Eri ; Kitajima, Shoji ; Iida, Shoichi ; Ishida, Hideki ; Tanabe, Kazunari ; Honda, Kazuho ; Koike, Junki</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c3986-e006bb3e333b4a1ecc44fa522bd7590401b7271ed2cbd077112634d4a888b2343</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Allografts</topic><topic>Atrophy</topic><topic>Biopsy</topic><topic>calcineurin inhibitor arteriolopathy</topic><topic>Disease Progression</topic><topic>Female</topic><topic>Fibrosis</topic><topic>Graft Rejection - etiology</topic><topic>Graft Rejection - pathology</topic><topic>Graft Rejection - physiopathology</topic><topic>Graft Survival</topic><topic>Hospitals, General</topic><topic>Humans</topic><topic>interstitial fibrosis and tubular atrophy</topic><topic>Japan</topic><topic>Kidney Diseases - etiology</topic><topic>Kidney Diseases - pathology</topic><topic>Kidney Diseases - physiopathology</topic><topic>Kidney Function Tests</topic><topic>kidney transplantation</topic><topic>Kidney Transplantation - adverse effects</topic><topic>Kidney Tubules - pathology</topic><topic>Kidney Tubules - physiopathology</topic><topic>Male</topic><topic>medullary ray injury</topic><topic>Middle Aged</topic><topic>rejection</topic><topic>Retrospective Studies</topic><topic>Risk Factors</topic><topic>Severity of Illness Index</topic><topic>Time Factors</topic><topic>Treatment Outcome</topic><topic>Young Adult</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Shimizu, Tomokazu</creatorcontrib><creatorcontrib>Toma, Hiroshi</creatorcontrib><creatorcontrib>Hayakawa, Nozomi</creatorcontrib><creatorcontrib>Shibahara, Rumi</creatorcontrib><creatorcontrib>Ishiyama, Ryou</creatorcontrib><creatorcontrib>Hayashida, Akihiro</creatorcontrib><creatorcontrib>Fujimori, Daiji</creatorcontrib><creatorcontrib>Tsunoyama, Kuniko</creatorcontrib><creatorcontrib>Ikezawa, Eri</creatorcontrib><creatorcontrib>Kitajima, Shoji</creatorcontrib><creatorcontrib>Iida, Shoichi</creatorcontrib><creatorcontrib>Ishida, Hideki</creatorcontrib><creatorcontrib>Tanabe, Kazunari</creatorcontrib><creatorcontrib>Honda, Kazuho</creatorcontrib><creatorcontrib>Koike, Junki</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><jtitle>Nephrology (Carlton, Vic.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Shimizu, Tomokazu</au><au>Toma, Hiroshi</au><au>Hayakawa, Nozomi</au><au>Shibahara, Rumi</au><au>Ishiyama, Ryou</au><au>Hayashida, Akihiro</au><au>Fujimori, Daiji</au><au>Tsunoyama, Kuniko</au><au>Ikezawa, Eri</au><au>Kitajima, Shoji</au><au>Iida, Shoichi</au><au>Ishida, Hideki</au><au>Tanabe, Kazunari</au><au>Honda, Kazuho</au><au>Koike, Junki</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Clinical and pathological analyses of interstitial fibrosis and tubular atrophy cases after kidney transplantation</atitle><jtitle>Nephrology (Carlton, Vic.)</jtitle><addtitle>Nephrology</addtitle><date>2016-07</date><risdate>2016</risdate><volume>21</volume><issue>S1</issue><spage>26</spage><epage>30</epage><pages>26-30</pages><issn>1320-5358</issn><eissn>1440-1797</eissn><abstract>Aim
We carried out a clinicopathological analysis of cases presenting with interstitial fibrosis and tubular atrophy (IF/TA) after renal transplantation in an attempt to clarify the mechanisms underlying the development and prognostic significance of IF/TA.
Methods
IF/TA was diagnosed in 35 renal allograft biopsy specimens (BS) obtained from 35 renal transplant recipients under follow up at the Department of Transplant Surgery, Kidney Center, Toda Chuo General Hospital, between January 2014 and March 2015.
Results
IF/TA was diagnosed at a median of 39.9 months after the transplantation. Among the 35 patients with IF/TA, 19 (54%) had a history of acute rejection. Among the 35 BS showing evidence of IF/TA, the IF/TA was grade I in 25, grade II in 9, and grade III in 1. Arteriosclerosis of the middle‐sized arteries was observed in 30 BS (86%). We then classified the 35 BS showing evidence of IF/TA according to their overall histopathological features, as follows; IF/TA alone (6 BS; 17%), IF/TA + medullary ray injury (12 BS; 34%), and IF/TA + rejection (12 BS; 34%). Loss of the renal allograft occurred during the observation period in one of the patients (3%). Of the remaining patients with functioning grafts, deterioration of the renal allograft function after the biopsies occurred in 15 patients (43%).
Conclusions
The results of our study suggests that rejection contributes to IF/TA in 30–40% of cases, medullary ray injury in 30–40% of cases, and nonspecific injury in 20% of cases. IF/TA contributes significantly to deterioration of renal allograft function.</abstract><cop>Australia</cop><pub>Blackwell Publishing Ltd</pub><pmid>26972969</pmid><doi>10.1111/nep.12766</doi><tpages>5</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Aged Allografts Atrophy Biopsy calcineurin inhibitor arteriolopathy Disease Progression Female Fibrosis Graft Rejection - etiology Graft Rejection - pathology Graft Rejection - physiopathology Graft Survival Hospitals, General Humans interstitial fibrosis and tubular atrophy Japan Kidney Diseases - etiology Kidney Diseases - pathology Kidney Diseases - physiopathology Kidney Function Tests kidney transplantation Kidney Transplantation - adverse effects Kidney Tubules - pathology Kidney Tubules - physiopathology Male medullary ray injury Middle Aged rejection Retrospective Studies Risk Factors Severity of Illness Index Time Factors Treatment Outcome Young Adult |
title | Clinical and pathological analyses of interstitial fibrosis and tubular atrophy cases after kidney transplantation |
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