Mechanism of impaired urinary concentration in chronic primary glomerulonephritis
Mechanism of impaired urinary concentration in chronic primary glomerulonephritis. To define the role of medullary damage and the influence of solute load and blood pressure (BP) in impairing urinary concentration, patients with chronic glomerulonephritis were investigated by histological and functi...
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Veröffentlicht in: | Kidney international 1985-05, Vol.27 (5), p.792-798 |
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description | Mechanism of impaired urinary concentration in chronic primary glomerulonephritis. To define the role of medullary damage and the influence of solute load and blood pressure (BP) in impairing urinary concentration, patients with chronic glomerulonephritis were investigated by histological and functional studies. In 59 biopsy specimens, the degree of medullary fibrosis was correlated inversely with urinary specific gravity and was significantly greater in hypertensive than in normotensive subjects. The following clearance studies were carried out in patients with a GFR of 15 to 40ml/min in maximal antidiuresis: (1) Eight patients were studied while receiving a high sodium and protein diet and then after 1 week of low sodium, low protein diet; (2) ten patients were loaded with hypertonic saline (3%) to increase urine volume up to 25 to 30% of GFR; (3) the concentrating ability was compared in 15 normotensives and 15 hypertensives with comparable GFR; (4) the concentrating ability was studied in nine hypertensive patients before and after drug-induced normalization of BP. In (1) no change occurred in maximal urine osmolality (UOsm) even if fractional sodium excretion and filtered load of urea were reduced. In (2), values of UOsm fell below those of plasma osmolality. In (3), UOsm and negative free-water generation were lower in hypertensive than in normotensive subjects. In (4), normalization of BP was not associated with any change in UOsm These results indicate that osmotic diuresis does not play a critical role in reducing urinary concentration. This defect is better accounted for by an intrinsic medullary damage, enhanced in hypertensive patients, which may impair the permeability of collecting ducts to water.
Mécanisme de l'altération de la concentration urinaire au cours des glomérulonéphrites chroniques primitives. Afin de définir le rôle des altérations médullaires et de l'influence de la charge en solutés et de la pression sanguine (BP) dans le défaut de concentration urinaire, des malades atteints de glomérulonéphrite chronique ont été explorés par des études histologiques et fonctionnelles. Dans 59 biopsies, le degré de fibrose médullaire était inversement corrélé à la densité spécifique urinaire, et était significativement plus important chez les hypertendus que chez les normaux tendus. Les études de clearance suivantes ont été entreprises chez des malades dont GFR était de 15–40ml/min en antidiurèse maximale: (1) huit malades ont été étudiés alor |
doi_str_mv | 10.1038/ki.1985.82 |
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Mécanisme de l'altération de la concentration urinaire au cours des glomérulonéphrites chroniques primitives. Afin de définir le rôle des altérations médullaires et de l'influence de la charge en solutés et de la pression sanguine (BP) dans le défaut de concentration urinaire, des malades atteints de glomérulonéphrite chronique ont été explorés par des études histologiques et fonctionnelles. Dans 59 biopsies, le degré de fibrose médullaire était inversement corrélé à la densité spécifique urinaire, et était significativement plus important chez les hypertendus que chez les normaux tendus. Les études de clearance suivantes ont été entreprises chez des malades dont GFR était de 15–40ml/min en antidiurèse maximale: (1) huit malades ont été étudiés alors qu'ils recevaient un régime riche en sodium et en protides, puis après une semaine de régime pauvre en sodium et pauvre en protides; (2) dix malades ont reçu une surcharge de soluté salé hypertonique; (3) la capacité de concentration a été comparée chez 15 normotendus et 15 hypertendus à GFR comparable; (4) la capacité de concentration a été étudiée chez 9 hypertendus avant et après normalisation médicamenteuse de la BP. Chez (1), aucune modification de l'osmolalité urinaire maximale (Uosm) ne s'est produite, même si l'excrétion fractionnelle du sodium et la charge uréique filtrée étaient réduites. Chez (2), les valeurs de Uosm ont chuté en dessous de celles de l'osmolalité plasmatique. Chez (3), Uosm et la génération d'eau libre négative étaient moindres chez les hypertendus que chez les normotendus. Chez (4), la normalisation de BP n'était associée à aucune modification de Uosm. Ces résultats indiquent qu'une diurèse osmotique ne joue pas de rôle critique dans la réduction de la concentration urinaire. Ce défaut est mieux expliqué par une perturbation médullaire intrinsèque, accrue chez les hypertendus, qui pourrait altérer la perméabilité des canaux collecteurs à l'eau.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/ki.1985.82</identifier><identifier>PMID: 4021313</identifier><identifier>CODEN: KDYIA5</identifier><language>eng</language><publisher>New York, NY: Elsevier Inc</publisher><subject>Adolescent ; Adult ; Aged ; Biological and medical sciences ; Female ; Glomerulonephritis ; Humans ; Kidney Concentrating Ability ; Kidney Failure, Chronic - physiopathology ; Kidney Function Tests ; Male ; Medical sciences ; Middle Aged ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure</subject><ispartof>Kidney international, 1985-05, Vol.27 (5), p.792-798</ispartof><rights>1985 International Society of Nephrology</rights><rights>1986 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c392t-da49908d9272989286ada38ba5ab44c9eb10bc0c4cd25885a52a4471725492473</citedby><cites>FETCH-LOGICAL-c392t-da49908d9272989286ada38ba5ab44c9eb10bc0c4cd25885a52a4471725492473</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=8452210$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/4021313$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Conte, Giuseppe</creatorcontrib><creatorcontrib>Canton, Antonio Dal</creatorcontrib><creatorcontrib>Fuiano, Giorgio</creatorcontrib><creatorcontrib>Terribile, Maurizio</creatorcontrib><creatorcontrib>Sabbatini, Massimo</creatorcontrib><creatorcontrib>Balletta, Mario</creatorcontrib><creatorcontrib>Stanziale, Pasquale</creatorcontrib><creatorcontrib>Andreucci, Vittorio E.</creatorcontrib><title>Mechanism of impaired urinary concentration in chronic primary glomerulonephritis</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Mechanism of impaired urinary concentration in chronic primary glomerulonephritis. To define the role of medullary damage and the influence of solute load and blood pressure (BP) in impairing urinary concentration, patients with chronic glomerulonephritis were investigated by histological and functional studies. In 59 biopsy specimens, the degree of medullary fibrosis was correlated inversely with urinary specific gravity and was significantly greater in hypertensive than in normotensive subjects. The following clearance studies were carried out in patients with a GFR of 15 to 40ml/min in maximal antidiuresis: (1) Eight patients were studied while receiving a high sodium and protein diet and then after 1 week of low sodium, low protein diet; (2) ten patients were loaded with hypertonic saline (3%) to increase urine volume up to 25 to 30% of GFR; (3) the concentrating ability was compared in 15 normotensives and 15 hypertensives with comparable GFR; (4) the concentrating ability was studied in nine hypertensive patients before and after drug-induced normalization of BP. In (1) no change occurred in maximal urine osmolality (UOsm) even if fractional sodium excretion and filtered load of urea were reduced. In (2), values of UOsm fell below those of plasma osmolality. In (3), UOsm and negative free-water generation were lower in hypertensive than in normotensive subjects. In (4), normalization of BP was not associated with any change in UOsm These results indicate that osmotic diuresis does not play a critical role in reducing urinary concentration. This defect is better accounted for by an intrinsic medullary damage, enhanced in hypertensive patients, which may impair the permeability of collecting ducts to water.
Mécanisme de l'altération de la concentration urinaire au cours des glomérulonéphrites chroniques primitives. Afin de définir le rôle des altérations médullaires et de l'influence de la charge en solutés et de la pression sanguine (BP) dans le défaut de concentration urinaire, des malades atteints de glomérulonéphrite chronique ont été explorés par des études histologiques et fonctionnelles. Dans 59 biopsies, le degré de fibrose médullaire était inversement corrélé à la densité spécifique urinaire, et était significativement plus important chez les hypertendus que chez les normaux tendus. Les études de clearance suivantes ont été entreprises chez des malades dont GFR était de 15–40ml/min en antidiurèse maximale: (1) huit malades ont été étudiés alors qu'ils recevaient un régime riche en sodium et en protides, puis après une semaine de régime pauvre en sodium et pauvre en protides; (2) dix malades ont reçu une surcharge de soluté salé hypertonique; (3) la capacité de concentration a été comparée chez 15 normotendus et 15 hypertendus à GFR comparable; (4) la capacité de concentration a été étudiée chez 9 hypertendus avant et après normalisation médicamenteuse de la BP. Chez (1), aucune modification de l'osmolalité urinaire maximale (Uosm) ne s'est produite, même si l'excrétion fractionnelle du sodium et la charge uréique filtrée étaient réduites. Chez (2), les valeurs de Uosm ont chuté en dessous de celles de l'osmolalité plasmatique. Chez (3), Uosm et la génération d'eau libre négative étaient moindres chez les hypertendus que chez les normotendus. Chez (4), la normalisation de BP n'était associée à aucune modification de Uosm. Ces résultats indiquent qu'une diurèse osmotique ne joue pas de rôle critique dans la réduction de la concentration urinaire. Ce défaut est mieux expliqué par une perturbation médullaire intrinsèque, accrue chez les hypertendus, qui pourrait altérer la perméabilité des canaux collecteurs à l'eau.</description><subject>Adolescent</subject><subject>Adult</subject><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Female</subject><subject>Glomerulonephritis</subject><subject>Humans</subject><subject>Kidney Concentrating Ability</subject><subject>Kidney Failure, Chronic - physiopathology</subject><subject>Kidney Function Tests</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1985</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNptkE1L7DAUhoMoOo5u7l7oQlwIHZOTxCbLy-AXKCLoOqRpxjnXNpmbtIL_3g5TXLk6HN6H9xweQv4wumCUq6sPXDCt5ELBHpkxCbxklZT7ZEapkiVIro7Icc7_6LhrTg_JoaDAOOMz8vLk3doGzF0RVwV2G4vJN8WQMNj0VbgYnA99sj3GUGAo3DrFgK7YJOy2wHsbO5-GNga_WSfsMZ-Qg5Vtsz-d5py83d68Lu_Lx-e7h-Xfx9JxDX3ZWKE1VY2GCrTSoK5tY7mqrbS1EE77mtHaUSdcA1IpaSVYISpWgRQaRMXn5GLXu0nx_-BzbzrMzretDT4O2VTXAJQJPoKXO9ClmHPyKzM9bxg1W3_mA83Wn1EwwmdT61B3vvlBJ2Fjfj7lNjvbrpINDvMPpoQEGDvnROwwPxr4RJ9MduhHl82o1_Wmifjb9W9-4Yny</recordid><startdate>198505</startdate><enddate>198505</enddate><creator>Conte, Giuseppe</creator><creator>Canton, Antonio Dal</creator><creator>Fuiano, Giorgio</creator><creator>Terribile, Maurizio</creator><creator>Sabbatini, Massimo</creator><creator>Balletta, Mario</creator><creator>Stanziale, Pasquale</creator><creator>Andreucci, Vittorio E.</creator><general>Elsevier Inc</general><general>Nature Publishing</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>7X8</scope></search><sort><creationdate>198505</creationdate><title>Mechanism of impaired urinary concentration in chronic primary glomerulonephritis</title><author>Conte, Giuseppe ; Canton, Antonio Dal ; Fuiano, Giorgio ; Terribile, Maurizio ; Sabbatini, Massimo ; Balletta, Mario ; Stanziale, Pasquale ; Andreucci, Vittorio E.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c392t-da49908d9272989286ada38ba5ab44c9eb10bc0c4cd25885a52a4471725492473</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1985</creationdate><topic>Adolescent</topic><topic>Adult</topic><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Female</topic><topic>Glomerulonephritis</topic><topic>Humans</topic><topic>Kidney Concentrating Ability</topic><topic>Kidney Failure, Chronic - physiopathology</topic><topic>Kidney Function Tests</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Conte, Giuseppe</creatorcontrib><creatorcontrib>Canton, Antonio Dal</creatorcontrib><creatorcontrib>Fuiano, Giorgio</creatorcontrib><creatorcontrib>Terribile, Maurizio</creatorcontrib><creatorcontrib>Sabbatini, Massimo</creatorcontrib><creatorcontrib>Balletta, Mario</creatorcontrib><creatorcontrib>Stanziale, Pasquale</creatorcontrib><creatorcontrib>Andreucci, Vittorio 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>MEDLINE - Academic</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Conte, Giuseppe</au><au>Canton, Antonio Dal</au><au>Fuiano, Giorgio</au><au>Terribile, Maurizio</au><au>Sabbatini, Massimo</au><au>Balletta, Mario</au><au>Stanziale, Pasquale</au><au>Andreucci, Vittorio E.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Mechanism of impaired urinary concentration in chronic primary glomerulonephritis</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>1985-05</date><risdate>1985</risdate><volume>27</volume><issue>5</issue><spage>792</spage><epage>798</epage><pages>792-798</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><coden>KDYIA5</coden><abstract>Mechanism of impaired urinary concentration in chronic primary glomerulonephritis. To define the role of medullary damage and the influence of solute load and blood pressure (BP) in impairing urinary concentration, patients with chronic glomerulonephritis were investigated by histological and functional studies. In 59 biopsy specimens, the degree of medullary fibrosis was correlated inversely with urinary specific gravity and was significantly greater in hypertensive than in normotensive subjects. The following clearance studies were carried out in patients with a GFR of 15 to 40ml/min in maximal antidiuresis: (1) Eight patients were studied while receiving a high sodium and protein diet and then after 1 week of low sodium, low protein diet; (2) ten patients were loaded with hypertonic saline (3%) to increase urine volume up to 25 to 30% of GFR; (3) the concentrating ability was compared in 15 normotensives and 15 hypertensives with comparable GFR; (4) the concentrating ability was studied in nine hypertensive patients before and after drug-induced normalization of BP. In (1) no change occurred in maximal urine osmolality (UOsm) even if fractional sodium excretion and filtered load of urea were reduced. In (2), values of UOsm fell below those of plasma osmolality. In (3), UOsm and negative free-water generation were lower in hypertensive than in normotensive subjects. In (4), normalization of BP was not associated with any change in UOsm These results indicate that osmotic diuresis does not play a critical role in reducing urinary concentration. This defect is better accounted for by an intrinsic medullary damage, enhanced in hypertensive patients, which may impair the permeability of collecting ducts to water.
Mécanisme de l'altération de la concentration urinaire au cours des glomérulonéphrites chroniques primitives. Afin de définir le rôle des altérations médullaires et de l'influence de la charge en solutés et de la pression sanguine (BP) dans le défaut de concentration urinaire, des malades atteints de glomérulonéphrite chronique ont été explorés par des études histologiques et fonctionnelles. Dans 59 biopsies, le degré de fibrose médullaire était inversement corrélé à la densité spécifique urinaire, et était significativement plus important chez les hypertendus que chez les normaux tendus. Les études de clearance suivantes ont été entreprises chez des malades dont GFR était de 15–40ml/min en antidiurèse maximale: (1) huit malades ont été étudiés alors qu'ils recevaient un régime riche en sodium et en protides, puis après une semaine de régime pauvre en sodium et pauvre en protides; (2) dix malades ont reçu une surcharge de soluté salé hypertonique; (3) la capacité de concentration a été comparée chez 15 normotendus et 15 hypertendus à GFR comparable; (4) la capacité de concentration a été étudiée chez 9 hypertendus avant et après normalisation médicamenteuse de la BP. Chez (1), aucune modification de l'osmolalité urinaire maximale (Uosm) ne s'est produite, même si l'excrétion fractionnelle du sodium et la charge uréique filtrée étaient réduites. Chez (2), les valeurs de Uosm ont chuté en dessous de celles de l'osmolalité plasmatique. Chez (3), Uosm et la génération d'eau libre négative étaient moindres chez les hypertendus que chez les normotendus. Chez (4), la normalisation de BP n'était associée à aucune modification de Uosm. Ces résultats indiquent qu'une diurèse osmotique ne joue pas de rôle critique dans la réduction de la concentration urinaire. Ce défaut est mieux expliqué par une perturbation médullaire intrinsèque, accrue chez les hypertendus, qui pourrait altérer la perméabilité des canaux collecteurs à l'eau.</abstract><cop>New York, NY</cop><pub>Elsevier Inc</pub><pmid>4021313</pmid><doi>10.1038/ki.1985.82</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Adolescent Adult Aged Biological and medical sciences Female Glomerulonephritis Humans Kidney Concentrating Ability Kidney Failure, Chronic - physiopathology Kidney Function Tests Male Medical sciences Middle Aged Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure |
title | Mechanism of impaired urinary concentration in chronic primary glomerulonephritis |
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