Effect of the Direct Renin Inhibitor Aliskiren in the Prevention of Experimental Contrast-Induced Nephropathy in the Rat
Background: Renal vasoconstriction, activated by the renin-angiotensin system, plays a pivotal role in the pathogenesis of contrast-induced nephropathy (CIN). The purpose of this study was to evaluate the effect of aliskiren, a direct renin inhibitor, for the prophylaxis of experimental CIN in the r...
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| Veröffentlicht in: | Kidney & blood pressure research 2012-01, Vol.35 (6), p.425-430 |
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| creator | Kedrah, Alla Eldeen Ari, Elif Alahdab, Yesim Gul, Cuma Bulent Macunluoglu, Beyza Atakan, Aydin Asicioglu, Ebru Cakalagaoglu, Fulya Koc, Mehmet |
| description | Background: Renal vasoconstriction, activated by the renin-angiotensin system, plays a pivotal role in the pathogenesis of contrast-induced nephropathy (CIN). The purpose of this study was to evaluate the effect of aliskiren, a direct renin inhibitor, for the prophylaxis of experimental CIN in the rat. Methods: Thirty-two Wistar albino rats were divided into four groups of 8 rats each, namely the control (C), aliskiren (A), contrast media (CM) and aliskiren plus contrast media (ACM) groups. Aliskiren was given orally at a dose of 50 mg/kg/day once daily for 5 consecutive days. CIN was induced by intravenous administration of indomethacin, N-nitro-L-arginine methyl ester and high-osmolar contrast medium meglumine amidotrizoate. Renal function parameters, kidney histology and tubular expression of vascular endothelial growth factor were determined. Results: Mean serum creatinine was significantly lower (p < 0.001) and mean creatinine clearance was higher (p < 0.001) in the ACM group compared with the CM group. However, there were no differences between the ACM and CM groups in terms of tubular necrosis, proteinaceous casts, medullary congestion and vascular endothelial growth factor expression. Conclusion: Our preliminary data seem to suggest a potential role of aliskiren for the prophylaxis of CIN in an experimental rat model. |
| doi_str_mv | 10.1159/000336104 |
| format | Article |
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The purpose of this study was to evaluate the effect of aliskiren, a direct renin inhibitor, for the prophylaxis of experimental CIN in the rat. Methods: Thirty-two Wistar albino rats were divided into four groups of 8 rats each, namely the control (C), aliskiren (A), contrast media (CM) and aliskiren plus contrast media (ACM) groups. Aliskiren was given orally at a dose of 50 mg/kg/day once daily for 5 consecutive days. CIN was induced by intravenous administration of indomethacin, N-nitro-L-arginine methyl ester and high-osmolar contrast medium meglumine amidotrizoate. Renal function parameters, kidney histology and tubular expression of vascular endothelial growth factor were determined. Results: Mean serum creatinine was significantly lower (p < 0.001) and mean creatinine clearance was higher (p < 0.001) in the ACM group compared with the CM group. However, there were no differences between the ACM and CM groups in terms of tubular necrosis, proteinaceous casts, medullary congestion and vascular endothelial growth factor expression. Conclusion: Our preliminary data seem to suggest a potential role of aliskiren for the prophylaxis of CIN in an experimental rat model.</description><identifier>ISSN: 1420-4096</identifier><identifier>EISSN: 1423-0143</identifier><identifier>DOI: 10.1159/000336104</identifier><identifier>PMID: 22677784</identifier><identifier>CODEN: RPBIEL</identifier><language>eng</language><publisher>Basel, Switzerland: S. Karger AG</publisher><subject>Amides - pharmacology ; Amides - therapeutic use ; Animals ; Contrast Media - toxicity ; Fumarates - pharmacology ; Fumarates - therapeutic use ; Kidney Diseases - chemically induced ; Kidney Diseases - pathology ; Kidney Diseases - prevention & control ; Male ; Original Paper ; Random Allocation ; Rats ; Rats, Wistar ; Renin - antagonists & inhibitors ; Renin - metabolism ; Treatment Outcome</subject><ispartof>Kidney & blood pressure research, 2012-01, Vol.35 (6), p.425-430</ispartof><rights>2012 S. Karger AG, Basel</rights><rights>Copyright © 2012 S. Karger AG, Basel.</rights><rights>Copyright (c) 2013 S. Karger AG, Basel</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c369t-9c5c38effdb89e039fb5e3b33ba37377eca5805de95b36fa723760fbef63da1d3</citedby><cites>FETCH-LOGICAL-c369t-9c5c38effdb89e039fb5e3b33ba37377eca5805de95b36fa723760fbef63da1d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,777,781,27905,27906</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/22677784$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Kedrah, Alla Eldeen</creatorcontrib><creatorcontrib>Ari, Elif</creatorcontrib><creatorcontrib>Alahdab, Yesim</creatorcontrib><creatorcontrib>Gul, Cuma Bulent</creatorcontrib><creatorcontrib>Macunluoglu, Beyza</creatorcontrib><creatorcontrib>Atakan, Aydin</creatorcontrib><creatorcontrib>Asicioglu, Ebru</creatorcontrib><creatorcontrib>Cakalagaoglu, Fulya</creatorcontrib><creatorcontrib>Koc, Mehmet</creatorcontrib><title>Effect of the Direct Renin Inhibitor Aliskiren in the Prevention of Experimental Contrast-Induced Nephropathy in the Rat</title><title>Kidney & blood pressure research</title><addtitle>Kidney Blood Press Res</addtitle><description>Background: Renal vasoconstriction, activated by the renin-angiotensin system, plays a pivotal role in the pathogenesis of contrast-induced nephropathy (CIN). The purpose of this study was to evaluate the effect of aliskiren, a direct renin inhibitor, for the prophylaxis of experimental CIN in the rat. Methods: Thirty-two Wistar albino rats were divided into four groups of 8 rats each, namely the control (C), aliskiren (A), contrast media (CM) and aliskiren plus contrast media (ACM) groups. Aliskiren was given orally at a dose of 50 mg/kg/day once daily for 5 consecutive days. CIN was induced by intravenous administration of indomethacin, N-nitro-L-arginine methyl ester and high-osmolar contrast medium meglumine amidotrizoate. Renal function parameters, kidney histology and tubular expression of vascular endothelial growth factor were determined. Results: Mean serum creatinine was significantly lower (p < 0.001) and mean creatinine clearance was higher (p < 0.001) in the ACM group compared with the CM group. However, there were no differences between the ACM and CM groups in terms of tubular necrosis, proteinaceous casts, medullary congestion and vascular endothelial growth factor expression. Conclusion: Our preliminary data seem to suggest a potential role of aliskiren for the prophylaxis of CIN in an experimental rat model.</description><subject>Amides - pharmacology</subject><subject>Amides - therapeutic use</subject><subject>Animals</subject><subject>Contrast Media - toxicity</subject><subject>Fumarates - pharmacology</subject><subject>Fumarates - therapeutic use</subject><subject>Kidney Diseases - chemically induced</subject><subject>Kidney Diseases - pathology</subject><subject>Kidney Diseases - prevention & control</subject><subject>Male</subject><subject>Original Paper</subject><subject>Random Allocation</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renin - antagonists & inhibitors</subject><subject>Renin - metabolism</subject><subject>Treatment Outcome</subject><issn>1420-4096</issn><issn>1423-0143</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2012</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpd0TtPwzAQAGALgSgUBnaEIrHAELBzcR5jVQpUQoAqmCMnOdNAagfbQeXf49LSgcn2-buTfUfICaNXjPH8mlIKkDAa75ADFkcQUhbD7u-ehjHNkwE5tPbdM05ptE8GUZSkaZrFB2Q5kRIrF2gZuDkGN41ZnWaoGhVM1bwpG6dNMGob--GvVODDK_ds8AuVa7RaZU6WHZpm4QOiDcZaOSOsC6eq7iusg0fs5kZ3ws2__9Jnwh2RPSlai8ebdUhebycv4_vw4eluOh49hBUkuQvzileQoZR1meVIIZclRygBSgEppClWgmeU15jzEhIp0gjShMoSZQK1YDUMycW6bmf0Z4_WFYvGVti2QqHubcGiLAOWMB57ev6PvuveKP-6wncyo3FGGfPqcq0qo601KIvO_12Y74LRYjWOYjsOb882FftygfVW_vXfg9M1-BDmDc0WbPJ_ADYKjiw</recordid><startdate>20120101</startdate><enddate>20120101</enddate><creator>Kedrah, Alla Eldeen</creator><creator>Ari, Elif</creator><creator>Alahdab, Yesim</creator><creator>Gul, Cuma Bulent</creator><creator>Macunluoglu, Beyza</creator><creator>Atakan, Aydin</creator><creator>Asicioglu, Ebru</creator><creator>Cakalagaoglu, Fulya</creator><creator>Koc, Mehmet</creator><general>S. 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Gul, Cuma Bulent ; Macunluoglu, Beyza ; Atakan, Aydin ; Asicioglu, Ebru ; Cakalagaoglu, Fulya ; Koc, Mehmet</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c369t-9c5c38effdb89e039fb5e3b33ba37377eca5805de95b36fa723760fbef63da1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2012</creationdate><topic>Amides - pharmacology</topic><topic>Amides - therapeutic use</topic><topic>Animals</topic><topic>Contrast Media - toxicity</topic><topic>Fumarates - pharmacology</topic><topic>Fumarates - therapeutic use</topic><topic>Kidney Diseases - chemically induced</topic><topic>Kidney Diseases - pathology</topic><topic>Kidney Diseases - prevention & control</topic><topic>Male</topic><topic>Original Paper</topic><topic>Random Allocation</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renin - antagonists & inhibitors</topic><topic>Renin - metabolism</topic><topic>Treatment Outcome</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Kedrah, Alla Eldeen</creatorcontrib><creatorcontrib>Ari, Elif</creatorcontrib><creatorcontrib>Alahdab, Yesim</creatorcontrib><creatorcontrib>Gul, Cuma Bulent</creatorcontrib><creatorcontrib>Macunluoglu, Beyza</creatorcontrib><creatorcontrib>Atakan, Aydin</creatorcontrib><creatorcontrib>Asicioglu, Ebru</creatorcontrib><creatorcontrib>Cakalagaoglu, Fulya</creatorcontrib><creatorcontrib>Koc, Mehmet</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Bacteriology Abstracts (Microbiology B)</collection><collection>Industrial and Applied Microbiology Abstracts (Microbiology A)</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Technology Research Database</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>Environmental Sciences and Pollution Management</collection><collection>ProQuest One Community College</collection><collection>Engineering Research Database</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Algology Mycology and Protozoology Abstracts (Microbiology C)</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>SIRS Editorial</collection><collection>MEDLINE - Academic</collection><jtitle>Kidney & blood pressure research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Kedrah, Alla Eldeen</au><au>Ari, Elif</au><au>Alahdab, Yesim</au><au>Gul, Cuma Bulent</au><au>Macunluoglu, Beyza</au><au>Atakan, Aydin</au><au>Asicioglu, Ebru</au><au>Cakalagaoglu, Fulya</au><au>Koc, Mehmet</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of the Direct Renin Inhibitor Aliskiren in the Prevention of Experimental Contrast-Induced Nephropathy in the Rat</atitle><jtitle>Kidney & blood pressure research</jtitle><addtitle>Kidney Blood Press Res</addtitle><date>2012-01-01</date><risdate>2012</risdate><volume>35</volume><issue>6</issue><spage>425</spage><epage>430</epage><pages>425-430</pages><issn>1420-4096</issn><eissn>1423-0143</eissn><coden>RPBIEL</coden><abstract>Background: Renal vasoconstriction, activated by the renin-angiotensin system, plays a pivotal role in the pathogenesis of contrast-induced nephropathy (CIN). The purpose of this study was to evaluate the effect of aliskiren, a direct renin inhibitor, for the prophylaxis of experimental CIN in the rat. Methods: Thirty-two Wistar albino rats were divided into four groups of 8 rats each, namely the control (C), aliskiren (A), contrast media (CM) and aliskiren plus contrast media (ACM) groups. Aliskiren was given orally at a dose of 50 mg/kg/day once daily for 5 consecutive days. CIN was induced by intravenous administration of indomethacin, N-nitro-L-arginine methyl ester and high-osmolar contrast medium meglumine amidotrizoate. Renal function parameters, kidney histology and tubular expression of vascular endothelial growth factor were determined. Results: Mean serum creatinine was significantly lower (p < 0.001) and mean creatinine clearance was higher (p < 0.001) in the ACM group compared with the CM group. However, there were no differences between the ACM and CM groups in terms of tubular necrosis, proteinaceous casts, medullary congestion and vascular endothelial growth factor expression. Conclusion: Our preliminary data seem to suggest a potential role of aliskiren for the prophylaxis of CIN in an experimental rat model.</abstract><cop>Basel, Switzerland</cop><pub>S. Karger AG</pub><pmid>22677784</pmid><doi>10.1159/000336104</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Amides - pharmacology Amides - therapeutic use Animals Contrast Media - toxicity Fumarates - pharmacology Fumarates - therapeutic use Kidney Diseases - chemically induced Kidney Diseases - pathology Kidney Diseases - prevention & control Male Original Paper Random Allocation Rats Rats, Wistar Renin - antagonists & inhibitors Renin - metabolism Treatment Outcome |
| title | Effect of the Direct Renin Inhibitor Aliskiren in the Prevention of Experimental Contrast-Induced Nephropathy in the Rat |
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