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De novo thrombotic microangiopathy in renal transplant patients
Objectives: Thrombotic microangiopathy is a form of renal capillary injury possibly associated with calcineurin inhibitor toxicity, acute humoral rejection, infections, and recurrent diseases. Here, we examined its incidence in patients diagnosed with acute and chronic active humoral rejection, poly...
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Published in: | Experimental and clinical transplantation 2018-03, Vol.16 (1), p.131-135 |
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container_title | Experimental and clinical transplantation |
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creator | Haberal,Mehmet Özdemir,Binnaz Handan Akdur,Aydıncan Ayvazoğlu Soy,Ebru Hatice Özdemir,Gökçe Ok Atılgan,Alev Yılmaz Akçay,Eda |
description | Objectives: Thrombotic microangiopathy is a form of
renal capillary injury possibly associated with
calcineurin inhibitor toxicity, acute humoral rejection,
infections, and recurrent diseases. Here, we examined
its incidence in patients diagnosed with acute and
chronic active humoral rejection, polyomavirus
nephropathy, acute cellular rejection, and im -
munoglobulin A recurrence.
Materials and Methods: In total, 272 renal allograft
recipients who met the inclusion criteria were
reevaluated for presence of renal thrombotic
microangiopathy. Thrombotic microangiopathy
diagnosis was established by clinical, laboratory, and
histologic features. C4d expression in peritubular
capillaries was determined. Clinical data were
collected from medical records.
Results: Of 272 patients (mean age of 42.8 ± 12.7 years),
only 74 patients (27.2%) had de novo thrombotic
microangiopathy, which was found in 30/90 patients
(33.3%) with acute humoral rejection, 9/51 (17.6%)
with acute cellular rejection, 22/53 (41.5%) with
chronic active humoral rejection, 10/55 (18.2%) with
polyomavirus nephropathy, and 3/23 (13%) with
immunoglobulin A nephropathy. Significant differences
were shown between therapy type and thrombotic
microangiopathy development (P = .02). Patients who
received cyclosporine (38.5%) tended to show higher
incidence of thrombotic microangiopathy than
patients who received tacrolimus (20.7%) or sirolimus
(7.7%). Patients with C4d-positive acute humoral (97.6%
vs 2.4%) and chronic active humoral rejection (68.2%
vs 31.8%) had greater incidence of thrombotic
microangiopathy versus those who were C4d-negative.
Graft loss was significantly higher in C4d-positive
than in C4d-negative thrombotic microangiopathy
groups (P< .001). Overall 1-, 3-, and 5-year graft survival
was 94%, 85%, and 85% versus 83%, 51%, and
51% in thrombotic microangiopathy-negative
versus thrombotic microangiopathy-positive patients
(P < .001).
Conclusions: Acute humoral rejection and chronic
active humoral rejection were the most common and
therefore most important causes of de novo
thrombotic microangiopathy in renal transplant
patients. Its presence in the renal allograft biopsy
should arouse suspicion for underlying acute or
chronic active humoral rejection. |
doi_str_mv | 10.6002/ect.TOND-TDTD2017.P27 |
format | article |
fullrecord | <record><control><sourceid>idealonline</sourceid><recordid>TN_cdi_idealonline_journals_IDEAL_69418</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>IDEAL_69418</sourcerecordid><originalsourceid>FETCH-LOGICAL-c295t-8d8ffc02fb2d7b3e9e41a73cf163cd097a4e3e06266474b72db29a12b849ec023</originalsourceid><addsrcrecordid>eNotjkFLwzAYhoMoWOZ-gpCbp9bkS5qkJxnrnIPiPNRzSdLURbpktFHw31vQ03t4eB5ehO4pKQQh8OhsKtrja523dVsDobJ4A3mFMqBc5IqDvEYZZYTnRJXlLVrPszeEcymBC5Whp9rhEL8jTqcpnk1M3uKzt1PU4cPHi06nH-wDnlzQI06TDvNl1CHhhXgX0nyHbgY9zm79vyv0_rxrty95c9wftpsmt1CVKVe9GgZLYDDQS8Nc5TjVktmBCmZ7UknNHXNEgBBcciOhN1BpCkbxyi0eW6GHv67vnR5jGH1w3Wf8mpZfc3eod5umExWniv0CvJ5Qqg</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>De novo thrombotic microangiopathy in renal transplant patients</title><source>Freely Accessible Science Journals</source><creator>Haberal,Mehmet ; Özdemir,Binnaz Handan ; Akdur,Aydıncan ; Ayvazoğlu Soy,Ebru Hatice ; Özdemir,Gökçe ; Ok Atılgan,Alev ; Yılmaz Akçay,Eda</creator><contributor>Haberal,Mehmet</contributor><creatorcontrib>Haberal,Mehmet ; Özdemir,Binnaz Handan ; Akdur,Aydıncan ; Ayvazoğlu Soy,Ebru Hatice ; Özdemir,Gökçe ; Ok Atılgan,Alev ; Yılmaz Akçay,Eda ; Haberal,Mehmet</creatorcontrib><description>Objectives: Thrombotic microangiopathy is a form of
renal capillary injury possibly associated with
calcineurin inhibitor toxicity, acute humoral rejection,
infections, and recurrent diseases. Here, we examined
its incidence in patients diagnosed with acute and
chronic active humoral rejection, polyomavirus
nephropathy, acute cellular rejection, and im -
munoglobulin A recurrence.
Materials and Methods: In total, 272 renal allograft
recipients who met the inclusion criteria were
reevaluated for presence of renal thrombotic
microangiopathy. Thrombotic microangiopathy
diagnosis was established by clinical, laboratory, and
histologic features. C4d expression in peritubular
capillaries was determined. Clinical data were
collected from medical records.
Results: Of 272 patients (mean age of 42.8 ± 12.7 years),
only 74 patients (27.2%) had de novo thrombotic
microangiopathy, which was found in 30/90 patients
(33.3%) with acute humoral rejection, 9/51 (17.6%)
with acute cellular rejection, 22/53 (41.5%) with
chronic active humoral rejection, 10/55 (18.2%) with
polyomavirus nephropathy, and 3/23 (13%) with
immunoglobulin A nephropathy. Significant differences
were shown between therapy type and thrombotic
microangiopathy development (P = .02). Patients who
received cyclosporine (38.5%) tended to show higher
incidence of thrombotic microangiopathy than
patients who received tacrolimus (20.7%) or sirolimus
(7.7%). Patients with C4d-positive acute humoral (97.6%
vs 2.4%) and chronic active humoral rejection (68.2%
vs 31.8%) had greater incidence of thrombotic
microangiopathy versus those who were C4d-negative.
Graft loss was significantly higher in C4d-positive
than in C4d-negative thrombotic microangiopathy
groups (P< .001). Overall 1-, 3-, and 5-year graft survival
was 94%, 85%, and 85% versus 83%, 51%, and
51% in thrombotic microangiopathy-negative
versus thrombotic microangiopathy-positive patients
(P < .001).
Conclusions: Acute humoral rejection and chronic
active humoral rejection were the most common and
therefore most important causes of de novo
thrombotic microangiopathy in renal transplant
patients. Its presence in the renal allograft biopsy
should arouse suspicion for underlying acute or
chronic active humoral rejection.</description><identifier>ISSN: 1304-0855</identifier><identifier>EISSN: 2146-8427</identifier><identifier>DOI: 10.6002/ect.TOND-TDTD2017.P27</identifier><language>eng</language><publisher>Başkent Üniversitesi</publisher><subject>Tıp</subject><ispartof>Experimental and clinical transplantation, 2018-03, Vol.16 (1), p.131-135</ispartof><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c295t-8d8ffc02fb2d7b3e9e41a73cf163cd097a4e3e06266474b72db29a12b849ec023</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids></links><search><contributor>Haberal,Mehmet</contributor><creatorcontrib>Haberal,Mehmet</creatorcontrib><creatorcontrib>Özdemir,Binnaz Handan</creatorcontrib><creatorcontrib>Akdur,Aydıncan</creatorcontrib><creatorcontrib>Ayvazoğlu Soy,Ebru Hatice</creatorcontrib><creatorcontrib>Özdemir,Gökçe</creatorcontrib><creatorcontrib>Ok Atılgan,Alev</creatorcontrib><creatorcontrib>Yılmaz Akçay,Eda</creatorcontrib><title>De novo thrombotic microangiopathy in renal transplant patients</title><title>Experimental and clinical transplantation</title><description>Objectives: Thrombotic microangiopathy is a form of
renal capillary injury possibly associated with
calcineurin inhibitor toxicity, acute humoral rejection,
infections, and recurrent diseases. Here, we examined
its incidence in patients diagnosed with acute and
chronic active humoral rejection, polyomavirus
nephropathy, acute cellular rejection, and im -
munoglobulin A recurrence.
Materials and Methods: In total, 272 renal allograft
recipients who met the inclusion criteria were
reevaluated for presence of renal thrombotic
microangiopathy. Thrombotic microangiopathy
diagnosis was established by clinical, laboratory, and
histologic features. C4d expression in peritubular
capillaries was determined. Clinical data were
collected from medical records.
Results: Of 272 patients (mean age of 42.8 ± 12.7 years),
only 74 patients (27.2%) had de novo thrombotic
microangiopathy, which was found in 30/90 patients
(33.3%) with acute humoral rejection, 9/51 (17.6%)
with acute cellular rejection, 22/53 (41.5%) with
chronic active humoral rejection, 10/55 (18.2%) with
polyomavirus nephropathy, and 3/23 (13%) with
immunoglobulin A nephropathy. Significant differences
were shown between therapy type and thrombotic
microangiopathy development (P = .02). Patients who
received cyclosporine (38.5%) tended to show higher
incidence of thrombotic microangiopathy than
patients who received tacrolimus (20.7%) or sirolimus
(7.7%). Patients with C4d-positive acute humoral (97.6%
vs 2.4%) and chronic active humoral rejection (68.2%
vs 31.8%) had greater incidence of thrombotic
microangiopathy versus those who were C4d-negative.
Graft loss was significantly higher in C4d-positive
than in C4d-negative thrombotic microangiopathy
groups (P< .001). Overall 1-, 3-, and 5-year graft survival
was 94%, 85%, and 85% versus 83%, 51%, and
51% in thrombotic microangiopathy-negative
versus thrombotic microangiopathy-positive patients
(P < .001).
Conclusions: Acute humoral rejection and chronic
active humoral rejection were the most common and
therefore most important causes of de novo
thrombotic microangiopathy in renal transplant
patients. Its presence in the renal allograft biopsy
should arouse suspicion for underlying acute or
chronic active humoral rejection.</description><subject>Tıp</subject><issn>1304-0855</issn><issn>2146-8427</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><recordid>eNotjkFLwzAYhoMoWOZ-gpCbp9bkS5qkJxnrnIPiPNRzSdLURbpktFHw31vQ03t4eB5ehO4pKQQh8OhsKtrja523dVsDobJ4A3mFMqBc5IqDvEYZZYTnRJXlLVrPszeEcymBC5Whp9rhEL8jTqcpnk1M3uKzt1PU4cPHi06nH-wDnlzQI06TDvNl1CHhhXgX0nyHbgY9zm79vyv0_rxrty95c9wftpsmt1CVKVe9GgZLYDDQS8Nc5TjVktmBCmZ7UknNHXNEgBBcciOhN1BpCkbxyi0eW6GHv67vnR5jGH1w3Wf8mpZfc3eod5umExWniv0CvJ5Qqg</recordid><startdate>201803</startdate><enddate>201803</enddate><creator>Haberal,Mehmet</creator><creator>Özdemir,Binnaz Handan</creator><creator>Akdur,Aydıncan</creator><creator>Ayvazoğlu Soy,Ebru Hatice</creator><creator>Özdemir,Gökçe</creator><creator>Ok Atılgan,Alev</creator><creator>Yılmaz Akçay,Eda</creator><general>Başkent Üniversitesi</general><scope>IEBAR</scope></search><sort><creationdate>201803</creationdate><title>De novo thrombotic microangiopathy in renal transplant patients</title><author>Haberal,Mehmet ; Özdemir,Binnaz Handan ; Akdur,Aydıncan ; Ayvazoğlu Soy,Ebru Hatice ; Özdemir,Gökçe ; Ok Atılgan,Alev ; Yılmaz Akçay,Eda</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c295t-8d8ffc02fb2d7b3e9e41a73cf163cd097a4e3e06266474b72db29a12b849ec023</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Tıp</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Haberal,Mehmet</creatorcontrib><creatorcontrib>Özdemir,Binnaz Handan</creatorcontrib><creatorcontrib>Akdur,Aydıncan</creatorcontrib><creatorcontrib>Ayvazoğlu Soy,Ebru Hatice</creatorcontrib><creatorcontrib>Özdemir,Gökçe</creatorcontrib><creatorcontrib>Ok Atılgan,Alev</creatorcontrib><creatorcontrib>Yılmaz Akçay,Eda</creatorcontrib><collection>Idealonline online kütüphane - Journals</collection><jtitle>Experimental and clinical transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Haberal,Mehmet</au><au>Özdemir,Binnaz Handan</au><au>Akdur,Aydıncan</au><au>Ayvazoğlu Soy,Ebru Hatice</au><au>Özdemir,Gökçe</au><au>Ok Atılgan,Alev</au><au>Yılmaz Akçay,Eda</au><au>Haberal,Mehmet</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>De novo thrombotic microangiopathy in renal transplant patients</atitle><jtitle>Experimental and clinical transplantation</jtitle><date>2018-03</date><risdate>2018</risdate><volume>16</volume><issue>1</issue><spage>131</spage><epage>135</epage><pages>131-135</pages><issn>1304-0855</issn><eissn>2146-8427</eissn><abstract>Objectives: Thrombotic microangiopathy is a form of
renal capillary injury possibly associated with
calcineurin inhibitor toxicity, acute humoral rejection,
infections, and recurrent diseases. Here, we examined
its incidence in patients diagnosed with acute and
chronic active humoral rejection, polyomavirus
nephropathy, acute cellular rejection, and im -
munoglobulin A recurrence.
Materials and Methods: In total, 272 renal allograft
recipients who met the inclusion criteria were
reevaluated for presence of renal thrombotic
microangiopathy. Thrombotic microangiopathy
diagnosis was established by clinical, laboratory, and
histologic features. C4d expression in peritubular
capillaries was determined. Clinical data were
collected from medical records.
Results: Of 272 patients (mean age of 42.8 ± 12.7 years),
only 74 patients (27.2%) had de novo thrombotic
microangiopathy, which was found in 30/90 patients
(33.3%) with acute humoral rejection, 9/51 (17.6%)
with acute cellular rejection, 22/53 (41.5%) with
chronic active humoral rejection, 10/55 (18.2%) with
polyomavirus nephropathy, and 3/23 (13%) with
immunoglobulin A nephropathy. Significant differences
were shown between therapy type and thrombotic
microangiopathy development (P = .02). Patients who
received cyclosporine (38.5%) tended to show higher
incidence of thrombotic microangiopathy than
patients who received tacrolimus (20.7%) or sirolimus
(7.7%). Patients with C4d-positive acute humoral (97.6%
vs 2.4%) and chronic active humoral rejection (68.2%
vs 31.8%) had greater incidence of thrombotic
microangiopathy versus those who were C4d-negative.
Graft loss was significantly higher in C4d-positive
than in C4d-negative thrombotic microangiopathy
groups (P< .001). Overall 1-, 3-, and 5-year graft survival
was 94%, 85%, and 85% versus 83%, 51%, and
51% in thrombotic microangiopathy-negative
versus thrombotic microangiopathy-positive patients
(P < .001).
Conclusions: Acute humoral rejection and chronic
active humoral rejection were the most common and
therefore most important causes of de novo
thrombotic microangiopathy in renal transplant
patients. Its presence in the renal allograft biopsy
should arouse suspicion for underlying acute or
chronic active humoral rejection.</abstract><pub>Başkent Üniversitesi</pub><doi>10.6002/ect.TOND-TDTD2017.P27</doi><tpages>5</tpages></addata></record> |
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language | eng |
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source | Freely Accessible Science Journals |
subjects | Tıp |
title | De novo thrombotic microangiopathy in renal transplant patients |
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