Dietary protein causes a decline in the glomerular filtration rate of the remnant kidney mediated by metabolic acidosis and endothelin receptors
Dietary casein promotes a progressive decline in the glomerular filtration rate (GFR) of remnant kidneys associated with metabolic acidosis and an endothelin-mediated increase in renal acidification. We tested whether diets that affect the acid–base status contributes to the decline of GFR through e...
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| Veröffentlicht in: | Kidney international 2008-01, Vol.73 (2), p.192-199 |
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| creator | Phisitkul, S. Hacker, C. Simoni, J. Tran, R.M. Wesson, D.E. |
| description | Dietary casein promotes a progressive decline in the glomerular filtration rate (GFR) of remnant kidneys associated with metabolic acidosis and an endothelin-mediated increase in renal acidification. We tested whether diets that affect the acid–base status contributes to the decline of GFR through endothelin receptors in rats with a remnant kidney. Rats on a casein diet had metabolic acidosis at baseline and developed a progressive decline in GFR after renal mass reduction. Dietary sodium bicarbonate but not sodium chloride ameliorated metabolic acidosis and prevented the decrease in GFR but only after the sodium bicarbonate-induced increase in blood pressure was treated. Dietary soy protein did not induce baseline metabolic acidosis and rats with remnant kidney on a soy diet had no decrease in their GFR. By contrast, rats with a remnant kidney on soy protein given dietary acid developed metabolic acidosis and a decreased GFR. This decline in GFR was prevented in either case by endothelin A but not endothelin A/B receptor antagonism. Our study suggests that the casein-induced decline in GFR of the remnant kidney is mediated by metabolic acidosis through endothelin A receptors. |
| doi_str_mv | 10.1038/sj.ki.5002647 |
| format | Article |
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We tested whether diets that affect the acid–base status contributes to the decline of GFR through endothelin receptors in rats with a remnant kidney. Rats on a casein diet had metabolic acidosis at baseline and developed a progressive decline in GFR after renal mass reduction. Dietary sodium bicarbonate but not sodium chloride ameliorated metabolic acidosis and prevented the decrease in GFR but only after the sodium bicarbonate-induced increase in blood pressure was treated. Dietary soy protein did not induce baseline metabolic acidosis and rats with remnant kidney on a soy diet had no decrease in their GFR. By contrast, rats with a remnant kidney on soy protein given dietary acid developed metabolic acidosis and a decreased GFR. This decline in GFR was prevented in either case by endothelin A but not endothelin A/B receptor antagonism. Our study suggests that the casein-induced decline in GFR of the remnant kidney is mediated by metabolic acidosis through endothelin A receptors.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/sj.ki.5002647</identifier><identifier>PMID: 17978813</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>acid ; Acidosis - physiopathology ; albuminuria ; alkali ; Animals ; Bicarbonates - pharmacology ; Biological and medical sciences ; Blood Pressure ; bosentan ; Carbon Dioxide - blood ; Caseins - adverse effects ; darusentan ; Dietary Proteins - adverse effects ; Endothelin-1 - urine ; Glomerular Filtration Rate ; Kidneys ; Male ; Malformations of the urinary system ; Medical sciences ; Nephrectomy ; Nephrology. Urinary tract diseases ; Rats ; Receptors, Endothelin - physiology ; Sodium Chloride - pharmacology</subject><ispartof>Kidney international, 2008-01, Vol.73 (2), p.192-199</ispartof><rights>2008 International Society of Nephrology</rights><rights>2008 INIST-CNRS</rights><rights>Copyright Nature Publishing Group Jan 2008</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c501t-e7290829817ce52ab256276dd5b1d46b61bec27deaaf4825bd793d9ed5e7af433</citedby><cites>FETCH-LOGICAL-c501t-e7290829817ce52ab256276dd5b1d46b61bec27deaaf4825bd793d9ed5e7af433</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=20057581$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17978813$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Phisitkul, S.</creatorcontrib><creatorcontrib>Hacker, C.</creatorcontrib><creatorcontrib>Simoni, J.</creatorcontrib><creatorcontrib>Tran, R.M.</creatorcontrib><creatorcontrib>Wesson, D.E.</creatorcontrib><title>Dietary protein causes a decline in the glomerular filtration rate of the remnant kidney mediated by metabolic acidosis and endothelin receptors</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Dietary casein promotes a progressive decline in the glomerular filtration rate (GFR) of remnant kidneys associated with metabolic acidosis and an endothelin-mediated increase in renal acidification. We tested whether diets that affect the acid–base status contributes to the decline of GFR through endothelin receptors in rats with a remnant kidney. Rats on a casein diet had metabolic acidosis at baseline and developed a progressive decline in GFR after renal mass reduction. Dietary sodium bicarbonate but not sodium chloride ameliorated metabolic acidosis and prevented the decrease in GFR but only after the sodium bicarbonate-induced increase in blood pressure was treated. Dietary soy protein did not induce baseline metabolic acidosis and rats with remnant kidney on a soy diet had no decrease in their GFR. By contrast, rats with a remnant kidney on soy protein given dietary acid developed metabolic acidosis and a decreased GFR. This decline in GFR was prevented in either case by endothelin A but not endothelin A/B receptor antagonism. Our study suggests that the casein-induced decline in GFR of the remnant kidney is mediated by metabolic acidosis through endothelin A receptors.</description><subject>acid</subject><subject>Acidosis - physiopathology</subject><subject>albuminuria</subject><subject>alkali</subject><subject>Animals</subject><subject>Bicarbonates - pharmacology</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>bosentan</subject><subject>Carbon Dioxide - blood</subject><subject>Caseins - adverse effects</subject><subject>darusentan</subject><subject>Dietary Proteins - adverse effects</subject><subject>Endothelin-1 - urine</subject><subject>Glomerular Filtration Rate</subject><subject>Kidneys</subject><subject>Male</subject><subject>Malformations of the urinary system</subject><subject>Medical sciences</subject><subject>Nephrectomy</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Rats</subject><subject>Receptors, Endothelin - physiology</subject><subject>Sodium Chloride - pharmacology</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2008</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kU2PFCEQholx446rR6-GmKy3HoEeGvpo1vUj2cSLngkN1cpMN4xAm-y_8CdvjdPRxMRTQfFUvcVbhLzgbMtZq9-U_fYQtpIx0e3UI7LhUrQNV1I-JhvGtGyEbPUleVrKnuG9b9kTcslVr7Tm7Yb8eheg2nxPjzlVCJE6uxQo1FIPbgoRKObqd6DfpjRDXiab6Rimmm0NKVIMQNP4m8gwRxsrPQQf4Z7O4AO-ejqcztUOaQqOWhd8KgEFoqcQfcJKlMFiB8eacnlGLkY7FXi-xivy9f3tl5uPzd3nD59u3t41TjJeG1CiZ1r0misHUthByE6ozns5cL_rho4P4ITyYO2400IOXvWt78FLUJhp2yvy-twXP_5jgVLNHIqDabIR0lKMYrzTrVYIvvoH3KclR5zNCM64YIJxhJoz5HIqJcNojjnM6KvhzJz2ZMreHIJZ94T8y7XpMqBRf-l1MQhcr4Atzk5jttGF8ocTjEkl9UlYnTlAr34GyKa4ANGh-WhpNT6F_4zwAH2KsSU</recordid><startdate>20080101</startdate><enddate>20080101</enddate><creator>Phisitkul, S.</creator><creator>Hacker, C.</creator><creator>Simoni, J.</creator><creator>Tran, R.M.</creator><creator>Wesson, D.E.</creator><general>Elsevier Inc</general><general>Nature Publishing</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</scope><scope>IQODW</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>3V.</scope><scope>7QP</scope><scope>7RV</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>NAPCQ</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20080101</creationdate><title>Dietary protein causes a decline in the glomerular filtration rate of the remnant kidney mediated by metabolic acidosis and endothelin receptors</title><author>Phisitkul, S. ; Hacker, C. ; Simoni, J. ; Tran, R.M. ; Wesson, D.E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c501t-e7290829817ce52ab256276dd5b1d46b61bec27deaaf4825bd793d9ed5e7af433</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2008</creationdate><topic>acid</topic><topic>Acidosis - physiopathology</topic><topic>albuminuria</topic><topic>alkali</topic><topic>Animals</topic><topic>Bicarbonates - pharmacology</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>bosentan</topic><topic>Carbon Dioxide - blood</topic><topic>Caseins - adverse effects</topic><topic>darusentan</topic><topic>Dietary Proteins - adverse effects</topic><topic>Endothelin-1 - urine</topic><topic>Glomerular Filtration Rate</topic><topic>Kidneys</topic><topic>Male</topic><topic>Malformations of the urinary system</topic><topic>Medical sciences</topic><topic>Nephrectomy</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Rats</topic><topic>Receptors, Endothelin - physiology</topic><topic>Sodium Chloride - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Phisitkul, S.</creatorcontrib><creatorcontrib>Hacker, C.</creatorcontrib><creatorcontrib>Simoni, J.</creatorcontrib><creatorcontrib>Tran, R.M.</creatorcontrib><creatorcontrib>Wesson, D.E.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><collection>Pascal-Francis</collection><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>Calcium & Calcified Tissue Abstracts</collection><collection>Nursing & Allied Health Database</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>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>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Nursing & Allied Health Premium</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>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Phisitkul, S.</au><au>Hacker, C.</au><au>Simoni, J.</au><au>Tran, R.M.</au><au>Wesson, D.E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Dietary protein causes a decline in the glomerular filtration rate of the remnant kidney mediated by metabolic acidosis and endothelin receptors</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2008-01-01</date><risdate>2008</risdate><volume>73</volume><issue>2</issue><spage>192</spage><epage>199</epage><pages>192-199</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Dietary casein promotes a progressive decline in the glomerular filtration rate (GFR) of remnant kidneys associated with metabolic acidosis and an endothelin-mediated increase in renal acidification. We tested whether diets that affect the acid–base status contributes to the decline of GFR through endothelin receptors in rats with a remnant kidney. Rats on a casein diet had metabolic acidosis at baseline and developed a progressive decline in GFR after renal mass reduction. Dietary sodium bicarbonate but not sodium chloride ameliorated metabolic acidosis and prevented the decrease in GFR but only after the sodium bicarbonate-induced increase in blood pressure was treated. Dietary soy protein did not induce baseline metabolic acidosis and rats with remnant kidney on a soy diet had no decrease in their GFR. By contrast, rats with a remnant kidney on soy protein given dietary acid developed metabolic acidosis and a decreased GFR. This decline in GFR was prevented in either case by endothelin A but not endothelin A/B receptor antagonism. Our study suggests that the casein-induced decline in GFR of the remnant kidney is mediated by metabolic acidosis through endothelin A receptors.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>17978813</pmid><doi>10.1038/sj.ki.5002647</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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| ispartof | Kidney international, 2008-01, Vol.73 (2), p.192-199 |
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| subjects | acid Acidosis - physiopathology albuminuria alkali Animals Bicarbonates - pharmacology Biological and medical sciences Blood Pressure bosentan Carbon Dioxide - blood Caseins - adverse effects darusentan Dietary Proteins - adverse effects Endothelin-1 - urine Glomerular Filtration Rate Kidneys Male Malformations of the urinary system Medical sciences Nephrectomy Nephrology. Urinary tract diseases Rats Receptors, Endothelin - physiology Sodium Chloride - pharmacology |
| title | Dietary protein causes a decline in the glomerular filtration rate of the remnant kidney mediated by metabolic acidosis and endothelin receptors |
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