Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model
Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4. We used the nephrectomy...
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| Veröffentlicht in: | Brazilian Journal of Nephrology 2018-04, Vol.40 (2), p.105-111 |
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| creator | Dionísio, Laura Mattana Luvizoto, Mateus Justi Gribner, Caroline Carneiro, Danielle Carvalho, Viviane Robes, Franciele Sheidemantel, Marcos Rego, Fabiane Noronha, Lúcia de Pecoits-Filho, Roberto Hauser, Aline Borsato |
| description | Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4.
We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium.
Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W.
TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4. |
| doi_str_mv | 10.1590/2175-8239-jbn-3878 |
| format | Article |
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We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium.
Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W.
TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4.</description><identifier>ISSN: 0101-2800</identifier><identifier>ISSN: 2175-8239</identifier><identifier>EISSN: 2175-8239</identifier><identifier>DOI: 10.1590/2175-8239-jbn-3878</identifier><identifier>PMID: 29738042</identifier><language>eng</language><publisher>Brazil: Sociedade Brasileira de Nefrologia</publisher><subject>Animals ; análises imunoistoquímicas, marcadores cardíacos ; Biomarkers - blood ; Cardio-Renal Syndrome - blood ; Cardio-Renal Syndrome - etiology ; Cardiomyopathies - blood ; Cardiomyopathies - etiology ; Disease Models, Animal ; doenças renais ; Male ; Natriuretic Peptide, Brain - blood ; Original ; Peptide Fragments - blood ; Rats ; Rats, Wistar ; síndrome cardiorrenal ; Troponin I - blood ; Tumor Necrosis Factor-alpha - blood ; Uremia - blood ; Uremia - complications</subject><ispartof>Brazilian Journal of Nephrology, 2018-04, Vol.40 (2), p.105-111</ispartof><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4888-abf053c6390c7079402fef8370524b256583995ef660715634a7254bea1191e93</citedby><cites>FETCH-LOGICAL-c4888-abf053c6390c7079402fef8370524b256583995ef660715634a7254bea1191e93</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6533987/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6533987/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,864,885,27924,27925,53791,53793</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29738042$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dionísio, Laura Mattana</creatorcontrib><creatorcontrib>Luvizoto, Mateus Justi</creatorcontrib><creatorcontrib>Gribner, Caroline</creatorcontrib><creatorcontrib>Carneiro, Danielle</creatorcontrib><creatorcontrib>Carvalho, Viviane</creatorcontrib><creatorcontrib>Robes, Franciele</creatorcontrib><creatorcontrib>Sheidemantel, Marcos</creatorcontrib><creatorcontrib>Rego, Fabiane</creatorcontrib><creatorcontrib>Noronha, Lúcia de</creatorcontrib><creatorcontrib>Pecoits-Filho, Roberto</creatorcontrib><creatorcontrib>Hauser, Aline Borsato</creatorcontrib><title>Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model</title><title>Brazilian Journal of Nephrology</title><addtitle>J Bras Nefrol</addtitle><description>Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4.
We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium.
Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W.
TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4.</description><subject>Animals</subject><subject>análises imunoistoquímicas, marcadores cardíacos</subject><subject>Biomarkers - blood</subject><subject>Cardio-Renal Syndrome - blood</subject><subject>Cardio-Renal Syndrome - etiology</subject><subject>Cardiomyopathies - blood</subject><subject>Cardiomyopathies - etiology</subject><subject>Disease Models, Animal</subject><subject>doenças renais</subject><subject>Male</subject><subject>Natriuretic Peptide, Brain - blood</subject><subject>Original</subject><subject>Peptide Fragments - blood</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>síndrome cardiorrenal</subject><subject>Troponin I - blood</subject><subject>Tumor Necrosis Factor-alpha - blood</subject><subject>Uremia - blood</subject><subject>Uremia - complications</subject><issn>0101-2800</issn><issn>2175-8239</issn><issn>2175-8239</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>DOA</sourceid><recordid>eNpVkV1LwzAUhoMoOqZ_wAvpH6iefCc3gg4_BoI3eh1O23TLbJuRTqH_3s7pcFeBk_M-74GHkEsK11RauGFUy9wwbvNV0eXcaHNEJvvhMZkABZozA3BGLvo-FMCBWqENPyVnzGpuQLAJmd-H2GL68KnPYp2VmKoQ8-Q7bLJ-6KoUW5-FLvtMvg1l1g5xt7LGzXLIsAvtuNjGyjfn5KTGpvcXv--UvD8-vM2e85fXp_ns7iUvhTEmx6IGyUvFLZQatBXAal8brkEyUTCppOHWSl8rBZpKxQVqJkXhkVJLveVTMt9xq4grt07jBWlwEYP7GcS0cJg2oWy8k5TXKIuxBpVAqgqsxkJhKFUV9RpG1u2Otf4sWl-VvtskbA6ghz9dWLpF_HJKcm6NHgFsByhT7Pvk632Wgtt6clslbqvEjZ7c1tMYuvrfuo_8WeHfTYqOeQ</recordid><startdate>20180401</startdate><enddate>20180401</enddate><creator>Dionísio, Laura Mattana</creator><creator>Luvizoto, Mateus Justi</creator><creator>Gribner, Caroline</creator><creator>Carneiro, Danielle</creator><creator>Carvalho, Viviane</creator><creator>Robes, Franciele</creator><creator>Sheidemantel, Marcos</creator><creator>Rego, Fabiane</creator><creator>Noronha, Lúcia de</creator><creator>Pecoits-Filho, Roberto</creator><creator>Hauser, Aline Borsato</creator><general>Sociedade Brasileira de Nefrologia</general><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>5PM</scope><scope>DOA</scope></search><sort><creationdate>20180401</creationdate><title>Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model</title><author>Dionísio, Laura Mattana ; Luvizoto, Mateus Justi ; Gribner, Caroline ; Carneiro, Danielle ; Carvalho, Viviane ; Robes, Franciele ; Sheidemantel, Marcos ; Rego, Fabiane ; Noronha, Lúcia de ; Pecoits-Filho, Roberto ; Hauser, Aline Borsato</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4888-abf053c6390c7079402fef8370524b256583995ef660715634a7254bea1191e93</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>análises imunoistoquímicas, marcadores cardíacos</topic><topic>Biomarkers - blood</topic><topic>Cardio-Renal Syndrome - blood</topic><topic>Cardio-Renal Syndrome - etiology</topic><topic>Cardiomyopathies - blood</topic><topic>Cardiomyopathies - etiology</topic><topic>Disease Models, Animal</topic><topic>doenças renais</topic><topic>Male</topic><topic>Natriuretic Peptide, Brain - blood</topic><topic>Original</topic><topic>Peptide Fragments - blood</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>síndrome cardiorrenal</topic><topic>Troponin I - blood</topic><topic>Tumor Necrosis Factor-alpha - blood</topic><topic>Uremia - blood</topic><topic>Uremia - complications</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dionísio, Laura Mattana</creatorcontrib><creatorcontrib>Luvizoto, Mateus Justi</creatorcontrib><creatorcontrib>Gribner, Caroline</creatorcontrib><creatorcontrib>Carneiro, Danielle</creatorcontrib><creatorcontrib>Carvalho, Viviane</creatorcontrib><creatorcontrib>Robes, Franciele</creatorcontrib><creatorcontrib>Sheidemantel, Marcos</creatorcontrib><creatorcontrib>Rego, Fabiane</creatorcontrib><creatorcontrib>Noronha, Lúcia de</creatorcontrib><creatorcontrib>Pecoits-Filho, Roberto</creatorcontrib><creatorcontrib>Hauser, Aline Borsato</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>PubMed Central (Full Participant titles)</collection><collection>DOAJ Directory of Open Access Journals</collection><jtitle>Brazilian Journal of Nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dionísio, Laura Mattana</au><au>Luvizoto, Mateus Justi</au><au>Gribner, Caroline</au><au>Carneiro, Danielle</au><au>Carvalho, Viviane</au><au>Robes, Franciele</au><au>Sheidemantel, Marcos</au><au>Rego, Fabiane</au><au>Noronha, Lúcia de</au><au>Pecoits-Filho, Roberto</au><au>Hauser, Aline Borsato</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model</atitle><jtitle>Brazilian Journal of Nephrology</jtitle><addtitle>J Bras Nefrol</addtitle><date>2018-04-01</date><risdate>2018</risdate><volume>40</volume><issue>2</issue><spage>105</spage><epage>111</epage><pages>105-111</pages><issn>0101-2800</issn><issn>2175-8239</issn><eissn>2175-8239</eissn><abstract>Cardio-renal syndrome subtype 4 (CRS4) is a condition of primary chronic kidney disease that leads to reduction of cardiac function, ventricular hypertrophy, and risk of cardiovascular events. Objective: Our aim was to understand the mechanisms involved on the onset of CRS4.
We used the nephrectomy 5/6 (CKD) animal model and compared to control (SHAM). Serum biomarkers were analyzed at baseline, 4, and 8 weeks. After euthanasia, histology and immunohistochemistry were performed in the myocardium.
Troponin I (TnI) was increased at 4 weeks (W) and 8W, but nt-proBNP showed no difference. The greater diameter of cardiomyocytes indicated left ventricular hypertrophy and the highest levels of TNF-α were found at 4W declining in 8W while fibrosis was more intense in 8W. Angiotensin expression showed an increase at 8W.
TnI seems to reflect cardiac injury as a consequence of the CKD however nt-proBNP did not change because it reflects stretching. TNF-α characterized an inflammatory peak and fibrosis increased over time in a process connecting heart and kidneys. The angiotensin showed increased activity of the renin-angiotensin axis and corroborates the hypothesis that the inflammatory process and its involvement with CRS4. Therefore, this animal study reinforces the need for renin-angiotensin blockade strategies and the control of CKD to avoid the development of CRS4.</abstract><cop>Brazil</cop><pub>Sociedade Brasileira de Nefrologia</pub><pmid>29738042</pmid><doi>10.1590/2175-8239-jbn-3878</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Animals análises imunoistoquímicas, marcadores cardíacos Biomarkers - blood Cardio-Renal Syndrome - blood Cardio-Renal Syndrome - etiology Cardiomyopathies - blood Cardiomyopathies - etiology Disease Models, Animal doenças renais Male Natriuretic Peptide, Brain - blood Original Peptide Fragments - blood Rats Rats, Wistar síndrome cardiorrenal Troponin I - blood Tumor Necrosis Factor-alpha - blood Uremia - blood Uremia - complications |
| title | Biomarkers of cardio-renal syndrome in uremic myocardiopathy animal model |
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