Cold ischemia in the absence of alloreactivity induces chronic transplant nephropathy through a process mediated by the platelet-activating factor
Ischemia-reperfusion injury is considered a risk factor for the development of chronic transplant nephropathy (CTN) although the mechanisms that mediate its effects have not been completely established. We have previously shown that treatment with a platelet-activating factor (PAF) receptor antagoni...
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| Veröffentlicht in: | Transplantation 2000-12, Vol.70 (11), p.1624-1631 |
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| creator | HERRERO-FRESNEDA, Immaculada TORRAS, Joan LLOBERAS, Nuria RIERA, Marta CRUZADO, Josep M CONDOM, Enric MERLOS, Manel ALSINA, Jeroni GRINYO, Josep M |
| description | Ischemia-reperfusion injury is considered a risk factor for the development of chronic transplant nephropathy (CTN) although the mechanisms that mediate its effects have not been completely established. We have previously shown that treatment with a platelet-activating factor (PAF) receptor antagonist (UR12670) protected kidneys from the progression to chronic nephropathy induced by warm ischemia. Here we examine the contribution of cold ischemia to the development of late functional and structural kidney changes in rats subjected to syngeneic renal transplantation and the role of PAF in this chronic nephropathy.
Lewis rats were used as kidney donors and recipients, which were transplanted either immediately or after a cold ischemia period of 5 hr. Contralateral nephrectomy was performed on the seventh day after transplantation. Cyclosporine was administered for 15 days after transplantation. Groups were as follows: Sy, immediate transplantation; SyI, transplantation after 5 hr of cold ischemia; SyIUr, transplantation after 5 hr of cold ischemia plus UR12670 from the transplantation day to the end of the study, at 24 weeks. Serum creatinine, creatinine clearance, and proteinuria were determined every 4 weeks. Urinary |
| doi_str_mv | 10.1097/00007890-200012150-00015 |
| format | Article |
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Lewis rats were used as kidney donors and recipients, which were transplanted either immediately or after a cold ischemia period of 5 hr. Contralateral nephrectomy was performed on the seventh day after transplantation. Cyclosporine was administered for 15 days after transplantation. Groups were as follows: Sy, immediate transplantation; SyI, transplantation after 5 hr of cold ischemia; SyIUr, transplantation after 5 hr of cold ischemia plus UR12670 from the transplantation day to the end of the study, at 24 weeks. Serum creatinine, creatinine clearance, and proteinuria were determined every 4 weeks. Urinary</description><identifier>ISSN: 0041-1337</identifier><identifier>EISSN: 1534-6080</identifier><identifier>DOI: 10.1097/00007890-200012150-00015</identifier><identifier>PMID: 11190497</identifier><identifier>CODEN: TRPLAU</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott</publisher><subject>Animals ; Biological and medical sciences ; Cold Temperature - adverse effects ; Creatinine - blood ; Kidney - blood supply ; Kidney - physiology ; Kidney Transplantation - immunology ; Kidney Transplantation - pathology ; Kidneys ; Male ; Medical sciences ; Nephrology. Urinary tract diseases ; Platelet Activating Factor - pharmacology ; Platelet Activating Factor - urine ; platelet-activating factor ; Rats ; Rats, Inbred Lew ; Reperfusion Injury - chemically induced ; Reperfusion Injury - complications ; Reperfusion Injury - etiology ; Time Factors ; Urinary system involvement in other diseases. Miscellaneous</subject><ispartof>Transplantation, 2000-12, Vol.70 (11), p.1624-1631</ispartof><rights>2001 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=901661$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11190497$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>HERRERO-FRESNEDA, Immaculada</creatorcontrib><creatorcontrib>TORRAS, Joan</creatorcontrib><creatorcontrib>LLOBERAS, Nuria</creatorcontrib><creatorcontrib>RIERA, Marta</creatorcontrib><creatorcontrib>CRUZADO, Josep M</creatorcontrib><creatorcontrib>CONDOM, Enric</creatorcontrib><creatorcontrib>MERLOS, Manel</creatorcontrib><creatorcontrib>ALSINA, Jeroni</creatorcontrib><creatorcontrib>GRINYO, Josep M</creatorcontrib><title>Cold ischemia in the absence of alloreactivity induces chronic transplant nephropathy through a process mediated by the platelet-activating factor</title><title>Transplantation</title><addtitle>Transplantation</addtitle><description>Ischemia-reperfusion injury is considered a risk factor for the development of chronic transplant nephropathy (CTN) although the mechanisms that mediate its effects have not been completely established. We have previously shown that treatment with a platelet-activating factor (PAF) receptor antagonist (UR12670) protected kidneys from the progression to chronic nephropathy induced by warm ischemia. Here we examine the contribution of cold ischemia to the development of late functional and structural kidney changes in rats subjected to syngeneic renal transplantation and the role of PAF in this chronic nephropathy.
Lewis rats were used as kidney donors and recipients, which were transplanted either immediately or after a cold ischemia period of 5 hr. Contralateral nephrectomy was performed on the seventh day after transplantation. Cyclosporine was administered for 15 days after transplantation. Groups were as follows: Sy, immediate transplantation; SyI, transplantation after 5 hr of cold ischemia; SyIUr, transplantation after 5 hr of cold ischemia plus UR12670 from the transplantation day to the end of the study, at 24 weeks. Serum creatinine, creatinine clearance, and proteinuria were determined every 4 weeks. Urinary</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cold Temperature - adverse effects</subject><subject>Creatinine - blood</subject><subject>Kidney - blood supply</subject><subject>Kidney - physiology</subject><subject>Kidney Transplantation - immunology</subject><subject>Kidney Transplantation - pathology</subject><subject>Kidneys</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Platelet Activating Factor - pharmacology</subject><subject>Platelet Activating Factor - urine</subject><subject>platelet-activating factor</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Reperfusion Injury - chemically induced</subject><subject>Reperfusion Injury - complications</subject><subject>Reperfusion Injury - etiology</subject><subject>Time Factors</subject><subject>Urinary system involvement in other diseases. 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Urinary tract diseases</topic><topic>Platelet Activating Factor - pharmacology</topic><topic>Platelet Activating Factor - urine</topic><topic>platelet-activating factor</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Reperfusion Injury - chemically induced</topic><topic>Reperfusion Injury - complications</topic><topic>Reperfusion Injury - etiology</topic><topic>Time Factors</topic><topic>Urinary system involvement in other diseases. Miscellaneous</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HERRERO-FRESNEDA, Immaculada</creatorcontrib><creatorcontrib>TORRAS, Joan</creatorcontrib><creatorcontrib>LLOBERAS, Nuria</creatorcontrib><creatorcontrib>RIERA, Marta</creatorcontrib><creatorcontrib>CRUZADO, Josep M</creatorcontrib><creatorcontrib>CONDOM, Enric</creatorcontrib><creatorcontrib>MERLOS, Manel</creatorcontrib><creatorcontrib>ALSINA, Jeroni</creatorcontrib><creatorcontrib>GRINYO, Josep M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>Immunology Abstracts</collection><collection>AIDS and Cancer Research Abstracts</collection><jtitle>Transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HERRERO-FRESNEDA, Immaculada</au><au>TORRAS, Joan</au><au>LLOBERAS, Nuria</au><au>RIERA, Marta</au><au>CRUZADO, Josep M</au><au>CONDOM, Enric</au><au>MERLOS, Manel</au><au>ALSINA, Jeroni</au><au>GRINYO, Josep M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cold ischemia in the absence of alloreactivity induces chronic transplant nephropathy through a process mediated by the platelet-activating factor</atitle><jtitle>Transplantation</jtitle><addtitle>Transplantation</addtitle><date>2000-12-15</date><risdate>2000</risdate><volume>70</volume><issue>11</issue><spage>1624</spage><epage>1631</epage><pages>1624-1631</pages><issn>0041-1337</issn><eissn>1534-6080</eissn><coden>TRPLAU</coden><abstract>Ischemia-reperfusion injury is considered a risk factor for the development of chronic transplant nephropathy (CTN) although the mechanisms that mediate its effects have not been completely established. We have previously shown that treatment with a platelet-activating factor (PAF) receptor antagonist (UR12670) protected kidneys from the progression to chronic nephropathy induced by warm ischemia. Here we examine the contribution of cold ischemia to the development of late functional and structural kidney changes in rats subjected to syngeneic renal transplantation and the role of PAF in this chronic nephropathy.
Lewis rats were used as kidney donors and recipients, which were transplanted either immediately or after a cold ischemia period of 5 hr. Contralateral nephrectomy was performed on the seventh day after transplantation. Cyclosporine was administered for 15 days after transplantation. Groups were as follows: Sy, immediate transplantation; SyI, transplantation after 5 hr of cold ischemia; SyIUr, transplantation after 5 hr of cold ischemia plus UR12670 from the transplantation day to the end of the study, at 24 weeks. Serum creatinine, creatinine clearance, and proteinuria were determined every 4 weeks. Urinary</abstract><cop>Hagerstown, MD</cop><pub>Lippincott</pub><pmid>11190497</pmid><doi>10.1097/00007890-200012150-00015</doi><tpages>8</tpages></addata></record> |
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| ispartof | Transplantation, 2000-12, Vol.70 (11), p.1624-1631 |
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| subjects | Animals Biological and medical sciences Cold Temperature - adverse effects Creatinine - blood Kidney - blood supply Kidney - physiology Kidney Transplantation - immunology Kidney Transplantation - pathology Kidneys Male Medical sciences Nephrology. Urinary tract diseases Platelet Activating Factor - pharmacology Platelet Activating Factor - urine platelet-activating factor Rats Rats, Inbred Lew Reperfusion Injury - chemically induced Reperfusion Injury - complications Reperfusion Injury - etiology Time Factors Urinary system involvement in other diseases. Miscellaneous |
| title | Cold ischemia in the absence of alloreactivity induces chronic transplant nephropathy through a process mediated by the platelet-activating factor |
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