An analysis of renal tubular acidosis by the Stewart method
Renal tubular acidosis (RTA) comprises a group of disorders characterized by a low capacity for net acid excretion and persistent hyperchloremic, metabolic acidosis. To investigate the role of chloride, we performed hypotonic (0.45%) saline-loading experiments in 12 children with alkali-treated dist...
Gespeichert in:
| Veröffentlicht in: | Pediatric nephrology (Berlin, West) West), 2006-02, Vol.21 (2), p.206-211 |
|---|---|
| Hauptverfasser: | , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 211 |
|---|---|
| container_issue | 2 |
| container_start_page | 206 |
| container_title | Pediatric nephrology (Berlin, West) |
| container_volume | 21 |
| creator | Corey, Howard E Vallo, Alfredo Rodríguez-Soriano, Juan |
| description | Renal tubular acidosis (RTA) comprises a group of disorders characterized by a low capacity for net acid excretion and persistent hyperchloremic, metabolic acidosis. To investigate the role of chloride, we performed hypotonic (0.45%) saline-loading experiments in 12 children with alkali-treated distal RTA (dRTA) and compared the results with data obtained from 17 healthy control subjects. In patients, but not in controls, saline loading induced both hyperchloremia and metabolic acidosis. Hyperchloremia was associated with high total and high distal fractional reabsorption of chloride [C(H20)/(C(H20)+C(Cl))]. The increase in plasma chloride varied inversely with the fractional excretion of chloride (C(Cl)) and correlated with the decrease in blood pH. However, the urinary excretion of bicarbonate did not correlate with either changes in blood pH or plasma bicarbonate concentration. Our findings suggest that the mechanism of hyperchloremia was enhanced Cl(-)/HCO(3) (-) exchange by the distal tubule. The resulting metabolic acidosis is better explained by changes in the strong ion difference (the Stewart theory) than by changes in the urine bicarbonate excretion (the traditional theory). |
| doi_str_mv | 10.1007/s00467-005-2081-8 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_proqu</sourceid><recordid>TN_cdi_proquest_miscellaneous_70694108</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A152922968</galeid><sourcerecordid>A152922968</sourcerecordid><originalsourceid>FETCH-LOGICAL-c357t-481f8d33f93a65ce51ba77d09255ab41ef0447333f8bc208f88a6106ab2ffb1d3</originalsourceid><addsrcrecordid>eNpdkN9LwzAQx4Mobk7_AF-k-OBb9a5J0xSfxvAXDHxQYW8hbRPb0S4zSZH997ZsMDAvR7jPfbn7EHKNcI8A2YMHYDyLAdI4AYGxOCFTZDSJMRerUzKFnGIMDFcTcuH9GgBEKvg5mSCnPKE5nZLH-SZSG9XufOMjayKnh08U-qJvlYtU2VR27BS7KNQ6-gj6V7kQdTrUtrokZ0a1Xl8d6ox8PT99Ll7j5fvL22K-jEuaZiFmAo2oKDU5VTwtdYqFyrIK8iRNVcFQG2AsowMginK4wwihOAJXRWJMgRWdkbt97tbZn177ILvGl7pt1Ubb3ssMeM4QxADe_gPXtnfDQV4mw8spMDimfatWy1qrNtTetn1o7MbLOaZJPqB8TMM9WDrrvdNGbl3TKbeTCHL0L_f-5eBfjv7lOHNz2KAvOl0dJw7C6R88gn4o</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>222293040</pqid></control><display><type>article</type><title>An analysis of renal tubular acidosis by the Stewart method</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Corey, Howard E ; Vallo, Alfredo ; Rodríguez-Soriano, Juan</creator><creatorcontrib>Corey, Howard E ; Vallo, Alfredo ; Rodríguez-Soriano, Juan</creatorcontrib><description>Renal tubular acidosis (RTA) comprises a group of disorders characterized by a low capacity for net acid excretion and persistent hyperchloremic, metabolic acidosis. To investigate the role of chloride, we performed hypotonic (0.45%) saline-loading experiments in 12 children with alkali-treated distal RTA (dRTA) and compared the results with data obtained from 17 healthy control subjects. In patients, but not in controls, saline loading induced both hyperchloremia and metabolic acidosis. Hyperchloremia was associated with high total and high distal fractional reabsorption of chloride [C(H20)/(C(H20)+C(Cl))]. The increase in plasma chloride varied inversely with the fractional excretion of chloride (C(Cl)) and correlated with the decrease in blood pH. However, the urinary excretion of bicarbonate did not correlate with either changes in blood pH or plasma bicarbonate concentration. Our findings suggest that the mechanism of hyperchloremia was enhanced Cl(-)/HCO(3) (-) exchange by the distal tubule. The resulting metabolic acidosis is better explained by changes in the strong ion difference (the Stewart theory) than by changes in the urine bicarbonate excretion (the traditional theory).</description><identifier>ISSN: 0931-041X</identifier><identifier>EISSN: 1432-198X</identifier><identifier>DOI: 10.1007/s00467-005-2081-8</identifier><identifier>PMID: 16362393</identifier><language>eng</language><publisher>Germany: Springer</publisher><subject>Acid-Base Imbalance - etiology ; Acidosis ; Acidosis, Renal Tubular - complications ; Acidosis, Renal Tubular - metabolism ; Carrier proteins ; Child ; Child, Preschool ; Chloride ; Chlorides - metabolism ; Electrolytes ; Female ; Health aspects ; Humans ; Hydrogen ; Hypotonic Solutions ; Infant ; Male ; Metabolism ; Mutation ; Plasma ; Proteins ; Protons ; Sodium Chloride ; Urine</subject><ispartof>Pediatric nephrology (Berlin, West), 2006-02, Vol.21 (2), p.206-211</ispartof><rights>COPYRIGHT 2006 Springer</rights><rights>IPNA 2006</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c357t-481f8d33f93a65ce51ba77d09255ab41ef0447333f8bc208f88a6106ab2ffb1d3</citedby><cites>FETCH-LOGICAL-c357t-481f8d33f93a65ce51ba77d09255ab41ef0447333f8bc208f88a6106ab2ffb1d3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27923,27924</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/16362393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Corey, Howard E</creatorcontrib><creatorcontrib>Vallo, Alfredo</creatorcontrib><creatorcontrib>Rodríguez-Soriano, Juan</creatorcontrib><title>An analysis of renal tubular acidosis by the Stewart method</title><title>Pediatric nephrology (Berlin, West)</title><addtitle>Pediatr Nephrol</addtitle><description>Renal tubular acidosis (RTA) comprises a group of disorders characterized by a low capacity for net acid excretion and persistent hyperchloremic, metabolic acidosis. To investigate the role of chloride, we performed hypotonic (0.45%) saline-loading experiments in 12 children with alkali-treated distal RTA (dRTA) and compared the results with data obtained from 17 healthy control subjects. In patients, but not in controls, saline loading induced both hyperchloremia and metabolic acidosis. Hyperchloremia was associated with high total and high distal fractional reabsorption of chloride [C(H20)/(C(H20)+C(Cl))]. The increase in plasma chloride varied inversely with the fractional excretion of chloride (C(Cl)) and correlated with the decrease in blood pH. However, the urinary excretion of bicarbonate did not correlate with either changes in blood pH or plasma bicarbonate concentration. Our findings suggest that the mechanism of hyperchloremia was enhanced Cl(-)/HCO(3) (-) exchange by the distal tubule. The resulting metabolic acidosis is better explained by changes in the strong ion difference (the Stewart theory) than by changes in the urine bicarbonate excretion (the traditional theory).</description><subject>Acid-Base Imbalance - etiology</subject><subject>Acidosis</subject><subject>Acidosis, Renal Tubular - complications</subject><subject>Acidosis, Renal Tubular - metabolism</subject><subject>Carrier proteins</subject><subject>Child</subject><subject>Child, Preschool</subject><subject>Chloride</subject><subject>Chlorides - metabolism</subject><subject>Electrolytes</subject><subject>Female</subject><subject>Health aspects</subject><subject>Humans</subject><subject>Hydrogen</subject><subject>Hypotonic Solutions</subject><subject>Infant</subject><subject>Male</subject><subject>Metabolism</subject><subject>Mutation</subject><subject>Plasma</subject><subject>Proteins</subject><subject>Protons</subject><subject>Sodium Chloride</subject><subject>Urine</subject><issn>0931-041X</issn><issn>1432-198X</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2006</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNpdkN9LwzAQx4Mobk7_AF-k-OBb9a5J0xSfxvAXDHxQYW8hbRPb0S4zSZH997ZsMDAvR7jPfbn7EHKNcI8A2YMHYDyLAdI4AYGxOCFTZDSJMRerUzKFnGIMDFcTcuH9GgBEKvg5mSCnPKE5nZLH-SZSG9XufOMjayKnh08U-qJvlYtU2VR27BS7KNQ6-gj6V7kQdTrUtrokZ0a1Xl8d6ox8PT99Ll7j5fvL22K-jEuaZiFmAo2oKDU5VTwtdYqFyrIK8iRNVcFQG2AsowMginK4wwihOAJXRWJMgRWdkbt97tbZn177ILvGl7pt1Ubb3ssMeM4QxADe_gPXtnfDQV4mw8spMDimfatWy1qrNtTetn1o7MbLOaZJPqB8TMM9WDrrvdNGbl3TKbeTCHL0L_f-5eBfjv7lOHNz2KAvOl0dJw7C6R88gn4o</recordid><startdate>200602</startdate><enddate>200602</enddate><creator>Corey, Howard E</creator><creator>Vallo, Alfredo</creator><creator>Rodríguez-Soriano, Juan</creator><general>Springer</general><general>Springer Nature B.V</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>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>AZQEC</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9-</scope><scope>K9.</scope><scope>KB0</scope><scope>M0R</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>200602</creationdate><title>An analysis of renal tubular acidosis by the Stewart method</title><author>Corey, Howard E ; Vallo, Alfredo ; Rodríguez-Soriano, Juan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c357t-481f8d33f93a65ce51ba77d09255ab41ef0447333f8bc208f88a6106ab2ffb1d3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2006</creationdate><topic>Acid-Base Imbalance - etiology</topic><topic>Acidosis</topic><topic>Acidosis, Renal Tubular - complications</topic><topic>Acidosis, Renal Tubular - metabolism</topic><topic>Carrier proteins</topic><topic>Child</topic><topic>Child, Preschool</topic><topic>Chloride</topic><topic>Chlorides - metabolism</topic><topic>Electrolytes</topic><topic>Female</topic><topic>Health aspects</topic><topic>Humans</topic><topic>Hydrogen</topic><topic>Hypotonic Solutions</topic><topic>Infant</topic><topic>Male</topic><topic>Metabolism</topic><topic>Mutation</topic><topic>Plasma</topic><topic>Proteins</topic><topic>Protons</topic><topic>Sodium Chloride</topic><topic>Urine</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Corey, Howard E</creatorcontrib><creatorcontrib>Vallo, Alfredo</creatorcontrib><creatorcontrib>Rodríguez-Soriano, Juan</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>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 Essentials</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>Consumer Health Database (Alumni Edition)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Database (Alumni Edition)</collection><collection>Consumer Health Database</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>Pediatric nephrology (Berlin, West)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Corey, Howard E</au><au>Vallo, Alfredo</au><au>Rodríguez-Soriano, Juan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>An analysis of renal tubular acidosis by the Stewart method</atitle><jtitle>Pediatric nephrology (Berlin, West)</jtitle><addtitle>Pediatr Nephrol</addtitle><date>2006-02</date><risdate>2006</risdate><volume>21</volume><issue>2</issue><spage>206</spage><epage>211</epage><pages>206-211</pages><issn>0931-041X</issn><eissn>1432-198X</eissn><abstract>Renal tubular acidosis (RTA) comprises a group of disorders characterized by a low capacity for net acid excretion and persistent hyperchloremic, metabolic acidosis. To investigate the role of chloride, we performed hypotonic (0.45%) saline-loading experiments in 12 children with alkali-treated distal RTA (dRTA) and compared the results with data obtained from 17 healthy control subjects. In patients, but not in controls, saline loading induced both hyperchloremia and metabolic acidosis. Hyperchloremia was associated with high total and high distal fractional reabsorption of chloride [C(H20)/(C(H20)+C(Cl))]. The increase in plasma chloride varied inversely with the fractional excretion of chloride (C(Cl)) and correlated with the decrease in blood pH. However, the urinary excretion of bicarbonate did not correlate with either changes in blood pH or plasma bicarbonate concentration. Our findings suggest that the mechanism of hyperchloremia was enhanced Cl(-)/HCO(3) (-) exchange by the distal tubule. The resulting metabolic acidosis is better explained by changes in the strong ion difference (the Stewart theory) than by changes in the urine bicarbonate excretion (the traditional theory).</abstract><cop>Germany</cop><pub>Springer</pub><pmid>16362393</pmid><doi>10.1007/s00467-005-2081-8</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0931-041X |
| ispartof | Pediatric nephrology (Berlin, West), 2006-02, Vol.21 (2), p.206-211 |
| issn | 0931-041X 1432-198X |
| language | eng |
| recordid | cdi_proquest_miscellaneous_70694108 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Acid-Base Imbalance - etiology Acidosis Acidosis, Renal Tubular - complications Acidosis, Renal Tubular - metabolism Carrier proteins Child Child, Preschool Chloride Chlorides - metabolism Electrolytes Female Health aspects Humans Hydrogen Hypotonic Solutions Infant Male Metabolism Mutation Plasma Proteins Protons Sodium Chloride Urine |
| title | An analysis of renal tubular acidosis by the Stewart method |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-09T07%3A17%3A53IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_proqu&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=An%20analysis%20of%20renal%20tubular%20acidosis%20by%20the%20Stewart%20method&rft.jtitle=Pediatric%20nephrology%20(Berlin,%20West)&rft.au=Corey,%20Howard%20E&rft.date=2006-02&rft.volume=21&rft.issue=2&rft.spage=206&rft.epage=211&rft.pages=206-211&rft.issn=0931-041X&rft.eissn=1432-198X&rft_id=info:doi/10.1007/s00467-005-2081-8&rft_dat=%3Cgale_proqu%3EA152922968%3C/gale_proqu%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=222293040&rft_id=info:pmid/16362393&rft_galeid=A152922968&rfr_iscdi=true |