P-398: Loss of renal reserve in obese hypertensive patients
To demonstrate the effects of obesity on renal hemodynamics and the role of renal kallikrein (rKal) and nitric oxide (NO) on renal response to oral protein load (renal reserve, RR), we studied 14 obese (BMI: 32.9 ±1.1, age: 50.5 ±0.9 yrs, SBP: 152.8 ±2.4mmHg, DBP 96.2 ±2.2mmHg, 5 males and 9 females...
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| Veröffentlicht in: | American journal of hypertension 2002-04, Vol.15 (S3), p.174A-175A |
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| creator | Pecly, I.M.D. Genelhu, V. Rodrigues, M.L.G. Duarte, A.V.B. Barroso, S.G. Castro, R.S.P. Lau, C.S.C. Bazhuni, C.A. Francischetti, E.A. |
| description | To demonstrate the effects of obesity on renal hemodynamics and the role of renal kallikrein (rKal) and nitric oxide (NO) on renal response to oral protein load (renal reserve, RR), we studied 14 obese (BMI: 32.9 ±1.1, age: 50.5 ±0.9 yrs, SBP: 152.8 ±2.4mmHg, DBP 96.2 ±2.2mmHg, 5 males and 9 females) and 9 non obese hypertensive patients (BMI=22.9±1.1, age 50.6±2.7yrs, SBP=151.2±2.8 mmHg, DBP: 97.9±2.1mmHg, 4 males and 5 females). Hemodynamic and metabolic evaluations were conducted at basal conditions and after protein challenge moment (1g/kg of weight). Glomerular filtration rate (GFR) was estimated by clearance of inulin, and renal plasma flow (RPF) was calculated by the clearance of 131 orthoiodohippurate. We measured the levels of serum NO by the Griess reaction modified, and the urinary excretion of Kallikrein (Kal) by chromogenic substrate. After protein load there were significant increases of urinary Kal /Creat in both obese individuals (0.12±0.04 vs 0.29±0.06, p=0.002) and lean subjects (0.052±0.008 vs 0.22±0.02, p |
| doi_str_mv | 10.1016/S0895-7061(02)02749-8 |
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Hemodynamic and metabolic evaluations were conducted at basal conditions and after protein challenge moment (1g/kg of weight). Glomerular filtration rate (GFR) was estimated by clearance of inulin, and renal plasma flow (RPF) was calculated by the clearance of 131 orthoiodohippurate. We measured the levels of serum NO by the Griess reaction modified, and the urinary excretion of Kallikrein (Kal) by chromogenic substrate. After protein load there were significant increases of urinary Kal /Creat in both obese individuals (0.12±0.04 vs 0.29±0.06, p=0.002) and lean subjects (0.052±0.008 vs 0.22±0.02, p<0.05) with no differences in response between groups. RPF significantly increased in both groups (374.2±25.5 vs 438.8±27.2 ml/min, p=0.02 in obese, and 496.1±19.9 vs 637.1±40.4 ml/min p= 0.001 in lean subjects) accompanied by increases in GFR (130.9±3.3 vs 138.5±3.5ml/min, p<0.001 in obese and 101.4±3.6 vs 112.9±3.5ml/min, p<0.001 in lean subjects). Serum NO increased in lean subjects but not in obese individuals (19.5±1.2 vs 23.4±3.4 μM, p<0.04 and 23.2±0.9 vs 22.1±1.2 μM, respectively). The NO changes after protein challenge correlated significantly to RR (r=0.51, p <0.03). The mean RR was lower in obese (7.1±0.9) compared to lean hypertensive individuals (11.3±0.8, p=0.005). In our group of obese hypertensive individuals renal reserve is deteriorated compared to lean hypertensive individuals, which appears to be related to differences on vasodilator capacity of renal vasculature after protein load. This effect may be mediated by renal kallikrein and NO, pointing out a deleterious role of obesity on renal reserve.</description><identifier>ISSN: 0895-7061</identifier><identifier>EISSN: 1941-7225</identifier><identifier>DOI: 10.1016/S0895-7061(02)02749-8</identifier><identifier>CODEN: AJHYE6</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Kallikrein ; Obesity ; Renal Reserve</subject><ispartof>American journal of hypertension, 2002-04, Vol.15 (S3), p.174A-175A</ispartof><rights>Copyright Nature Publishing Group Apr 2002</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>314,776,780,27901,27902</link.rule.ids></links><search><creatorcontrib>Pecly, I.M.D.</creatorcontrib><creatorcontrib>Genelhu, V.</creatorcontrib><creatorcontrib>Rodrigues, M.L.G.</creatorcontrib><creatorcontrib>Duarte, A.V.B.</creatorcontrib><creatorcontrib>Barroso, S.G.</creatorcontrib><creatorcontrib>Castro, R.S.P.</creatorcontrib><creatorcontrib>Lau, C.S.C.</creatorcontrib><creatorcontrib>Bazhuni, C.A.</creatorcontrib><creatorcontrib>Francischetti, E.A.</creatorcontrib><title>P-398: Loss of renal reserve in obese hypertensive patients</title><title>American journal of hypertension</title><addtitle>AJH</addtitle><description>To demonstrate the effects of obesity on renal hemodynamics and the role of renal kallikrein (rKal) and nitric oxide (NO) on renal response to oral protein load (renal reserve, RR), we studied 14 obese (BMI: 32.9 ±1.1, age: 50.5 ±0.9 yrs, SBP: 152.8 ±2.4mmHg, DBP 96.2 ±2.2mmHg, 5 males and 9 females) and 9 non obese hypertensive patients (BMI=22.9±1.1, age 50.6±2.7yrs, SBP=151.2±2.8 mmHg, DBP: 97.9±2.1mmHg, 4 males and 5 females). Hemodynamic and metabolic evaluations were conducted at basal conditions and after protein challenge moment (1g/kg of weight). Glomerular filtration rate (GFR) was estimated by clearance of inulin, and renal plasma flow (RPF) was calculated by the clearance of 131 orthoiodohippurate. We measured the levels of serum NO by the Griess reaction modified, and the urinary excretion of Kallikrein (Kal) by chromogenic substrate. After protein load there were significant increases of urinary Kal /Creat in both obese individuals (0.12±0.04 vs 0.29±0.06, p=0.002) and lean subjects (0.052±0.008 vs 0.22±0.02, p<0.05) with no differences in response between groups. RPF significantly increased in both groups (374.2±25.5 vs 438.8±27.2 ml/min, p=0.02 in obese, and 496.1±19.9 vs 637.1±40.4 ml/min p= 0.001 in lean subjects) accompanied by increases in GFR (130.9±3.3 vs 138.5±3.5ml/min, p<0.001 in obese and 101.4±3.6 vs 112.9±3.5ml/min, p<0.001 in lean subjects). Serum NO increased in lean subjects but not in obese individuals (19.5±1.2 vs 23.4±3.4 μM, p<0.04 and 23.2±0.9 vs 22.1±1.2 μM, respectively). The NO changes after protein challenge correlated significantly to RR (r=0.51, p <0.03). The mean RR was lower in obese (7.1±0.9) compared to lean hypertensive individuals (11.3±0.8, p=0.005). In our group of obese hypertensive individuals renal reserve is deteriorated compared to lean hypertensive individuals, which appears to be related to differences on vasodilator capacity of renal vasculature after protein load. This effect may be mediated by renal kallikrein and NO, pointing out a deleterious role of obesity on renal reserve.</description><subject>Kallikrein</subject><subject>Obesity</subject><subject>Renal Reserve</subject><issn>0895-7061</issn><issn>1941-7225</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>BENPR</sourceid><recordid>eNo9jk1LAzEYhIMoWKs_QVjwoofom2STbPQki7Zi_QB7EC8h27zBrXV3TbZi_70LFS8zw_AwDCHHDM4ZMHXxAoWRVINip8DPgOvc0GKHjJjJGdWcy10y-kf2yUFKSwDIlWIjcvVMhSkus1mbUtaGLGLjVoMmjN-Y1U3WVkPO3jcdxh6bVA9t5_oamz4dkr3gVgmP_nxM5rc383JKZ0-Tu_J6RmulcsohFJV2EKRHX6EsUMpQMKY8mkUIQgrPHYKRTDhYaI0LUWHBtOeehdxXYkxOtrNdbL_WmHq7bNdxuJksA66kYUblA0W3VJ16_LFdrD9d3FgXP6zSQks7fX2zpb5_fFATZYX4BbzCWQE</recordid><startdate>200204</startdate><enddate>200204</enddate><creator>Pecly, I.M.D.</creator><creator>Genelhu, V.</creator><creator>Rodrigues, M.L.G.</creator><creator>Duarte, A.V.B.</creator><creator>Barroso, S.G.</creator><creator>Castro, R.S.P.</creator><creator>Lau, C.S.C.</creator><creator>Bazhuni, C.A.</creator><creator>Francischetti, E.A.</creator><general>Oxford University Press</general><scope>BSCLL</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</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>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope></search><sort><creationdate>200204</creationdate><title>P-398: Loss of renal reserve in obese hypertensive patients</title><author>Pecly, I.M.D. ; Genelhu, V. ; Rodrigues, M.L.G. ; Duarte, A.V.B. ; Barroso, S.G. ; Castro, R.S.P. ; Lau, C.S.C. ; Bazhuni, C.A. ; Francischetti, E.A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-i664-20f8b7a0f5dedbe58e55f8116de9cff353d2ae09513a0c77ec3be817d2d1f4db3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Kallikrein</topic><topic>Obesity</topic><topic>Renal Reserve</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pecly, I.M.D.</creatorcontrib><creatorcontrib>Genelhu, V.</creatorcontrib><creatorcontrib>Rodrigues, M.L.G.</creatorcontrib><creatorcontrib>Duarte, A.V.B.</creatorcontrib><creatorcontrib>Barroso, S.G.</creatorcontrib><creatorcontrib>Castro, R.S.P.</creatorcontrib><creatorcontrib>Lau, C.S.C.</creatorcontrib><creatorcontrib>Bazhuni, C.A.</creatorcontrib><creatorcontrib>Francischetti, E.A.</creatorcontrib><collection>Istex</collection><collection>ProQuest Central (Corporate)</collection><collection>ProQuest Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</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)</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>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><jtitle>American journal of hypertension</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pecly, I.M.D.</au><au>Genelhu, V.</au><au>Rodrigues, M.L.G.</au><au>Duarte, A.V.B.</au><au>Barroso, S.G.</au><au>Castro, R.S.P.</au><au>Lau, C.S.C.</au><au>Bazhuni, C.A.</au><au>Francischetti, E.A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>P-398: Loss of renal reserve in obese hypertensive patients</atitle><jtitle>American journal of hypertension</jtitle><addtitle>AJH</addtitle><date>2002-04</date><risdate>2002</risdate><volume>15</volume><issue>S3</issue><spage>174A</spage><epage>175A</epage><pages>174A-175A</pages><issn>0895-7061</issn><eissn>1941-7225</eissn><coden>AJHYE6</coden><abstract>To demonstrate the effects of obesity on renal hemodynamics and the role of renal kallikrein (rKal) and nitric oxide (NO) on renal response to oral protein load (renal reserve, RR), we studied 14 obese (BMI: 32.9 ±1.1, age: 50.5 ±0.9 yrs, SBP: 152.8 ±2.4mmHg, DBP 96.2 ±2.2mmHg, 5 males and 9 females) and 9 non obese hypertensive patients (BMI=22.9±1.1, age 50.6±2.7yrs, SBP=151.2±2.8 mmHg, DBP: 97.9±2.1mmHg, 4 males and 5 females). Hemodynamic and metabolic evaluations were conducted at basal conditions and after protein challenge moment (1g/kg of weight). Glomerular filtration rate (GFR) was estimated by clearance of inulin, and renal plasma flow (RPF) was calculated by the clearance of 131 orthoiodohippurate. We measured the levels of serum NO by the Griess reaction modified, and the urinary excretion of Kallikrein (Kal) by chromogenic substrate. After protein load there were significant increases of urinary Kal /Creat in both obese individuals (0.12±0.04 vs 0.29±0.06, p=0.002) and lean subjects (0.052±0.008 vs 0.22±0.02, p<0.05) with no differences in response between groups. RPF significantly increased in both groups (374.2±25.5 vs 438.8±27.2 ml/min, p=0.02 in obese, and 496.1±19.9 vs 637.1±40.4 ml/min p= 0.001 in lean subjects) accompanied by increases in GFR (130.9±3.3 vs 138.5±3.5ml/min, p<0.001 in obese and 101.4±3.6 vs 112.9±3.5ml/min, p<0.001 in lean subjects). Serum NO increased in lean subjects but not in obese individuals (19.5±1.2 vs 23.4±3.4 μM, p<0.04 and 23.2±0.9 vs 22.1±1.2 μM, respectively). The NO changes after protein challenge correlated significantly to RR (r=0.51, p <0.03). The mean RR was lower in obese (7.1±0.9) compared to lean hypertensive individuals (11.3±0.8, p=0.005). In our group of obese hypertensive individuals renal reserve is deteriorated compared to lean hypertensive individuals, which appears to be related to differences on vasodilator capacity of renal vasculature after protein load. This effect may be mediated by renal kallikrein and NO, pointing out a deleterious role of obesity on renal reserve.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><doi>10.1016/S0895-7061(02)02749-8</doi></addata></record> |
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| title | P-398: Loss of renal reserve in obese hypertensive patients |
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