Correction of metabolic acidosis improves thyroid and growth hormone axes in haemodialysis patients
Background. Chronic metabolic acidosis (CMA) in normal adults results in complex endocrine and metabolic alterations including growth hormone (GH) insensitivity, hypothyroidism, hyperglucocorticoidism, hypoalbuminaemia and loss of protein stores. Similar alterations occur in chronic renal failure, a...
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description | Background. Chronic metabolic acidosis (CMA) in normal adults results in complex endocrine and metabolic alterations including growth hormone (GH) insensitivity, hypothyroidism, hyperglucocorticoidism, hypoalbuminaemia and loss of protein stores. Similar alterations occur in chronic renal failure, a prototypical state of CMA. We evaluated whether metabolic acidosis contributes to the endocrine and metabolic alterations characteristic of end-stage renal disease. Methods. We treated 14 chronic haemodialysis patients with daily oral Na-citrate for 4 weeks, yielding a steady-state pre-dialytic plasma bicarbonate concentration of 26.7 mmol/l, followed by 4 weeks of equimolar Na-chloride, yielding a steady-state pre-dialytic plasma bicarbonate of 20.2 mmol/l. Results. Blood pressure, body weight and dialysis adequacy were equivalent in the two protocols. Na-citrate treatment corrected CMA, improved GH insensitivity, increased and normalized plasma free T3 concentration, and improved plasma albumin. Correction of CMA had no significant effect on measured cytokines (interleukin-1β and -6, tumour necrosis factor-α) or acute phase reactants (C-reactive protein, serum amyloid A, α2-macroglobulin). Conclusion. CMA contributes to the derangements of the growth and thyroid hormone axes and to hypoalbuminaemia, but is not a modulator of systemic inflammation in dialysis patients. Correcting CMA may improve nutritional and metabolic parameters and thus lower morbidity and mortality. |
doi_str_mv | 10.1093/ndt/gfh096 |
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Chronic metabolic acidosis (CMA) in normal adults results in complex endocrine and metabolic alterations including growth hormone (GH) insensitivity, hypothyroidism, hyperglucocorticoidism, hypoalbuminaemia and loss of protein stores. Similar alterations occur in chronic renal failure, a prototypical state of CMA. We evaluated whether metabolic acidosis contributes to the endocrine and metabolic alterations characteristic of end-stage renal disease. Methods. We treated 14 chronic haemodialysis patients with daily oral Na-citrate for 4 weeks, yielding a steady-state pre-dialytic plasma bicarbonate concentration of 26.7 mmol/l, followed by 4 weeks of equimolar Na-chloride, yielding a steady-state pre-dialytic plasma bicarbonate of 20.2 mmol/l. Results. Blood pressure, body weight and dialysis adequacy were equivalent in the two protocols. Na-citrate treatment corrected CMA, improved GH insensitivity, increased and normalized plasma free T3 concentration, and improved plasma albumin. Correction of CMA had no significant effect on measured cytokines (interleukin-1β and -6, tumour necrosis factor-α) or acute phase reactants (C-reactive protein, serum amyloid A, α2-macroglobulin). Conclusion. CMA contributes to the derangements of the growth and thyroid hormone axes and to hypoalbuminaemia, but is not a modulator of systemic inflammation in dialysis patients. Correcting CMA may improve nutritional and metabolic parameters and thus lower morbidity and mortality.</description><identifier>ISSN: 0931-0509</identifier><identifier>EISSN: 1460-2385</identifier><identifier>DOI: 10.1093/ndt/gfh096</identifier><identifier>PMID: 14993483</identifier><identifier>CODEN: NDTREA</identifier><language>eng</language><publisher>Oxford: Oxford University Press</publisher><subject>Acidosis - blood ; Acidosis - therapy ; Administration, Oral ; Adult ; Aged ; albumin ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Bicarbonates - blood ; Biological and medical sciences ; Blood Gas Analysis ; Citrates - administration & dosage ; Citrates - therapeutic use ; Cytokines - blood ; dialysis ; Emergency and intensive care: renal failure. Dialysis management ; Female ; Glomerulonephritis ; growth hormone ; Human Growth Hormone - blood ; Humans ; Intensive care medicine ; Male ; Medical sciences ; metabolic acidosis ; Middle Aged ; Nephrology. Urinary tract diseases ; Nephropathies. Renovascular diseases. Renal failure ; Reference Values ; Renal Dialysis ; Renal failure ; Serum Albumin - metabolism ; Sodium - blood ; thyroid ; Triiodothyronine - blood</subject><ispartof>Nephrology, dialysis, transplantation, 2004-05, Vol.19 (5), p.1190-1197</ispartof><rights>2004 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c453t-ff7c47b9842f79d2450e0b083f75309406d45ef264c06b71fb4db6115e00ca963</citedby><cites>FETCH-LOGICAL-c453t-ff7c47b9842f79d2450e0b083f75309406d45ef264c06b71fb4db6115e00ca963</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=15749535$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/14993483$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wiederkehr, Michael R.</creatorcontrib><creatorcontrib>Kalogiros, Jris</creatorcontrib><creatorcontrib>Krapf, Reto</creatorcontrib><title>Correction of metabolic acidosis improves thyroid and growth hormone axes in haemodialysis patients</title><title>Nephrology, dialysis, transplantation</title><addtitle>Nephrol. Dial. Transplant</addtitle><description>Background. Chronic metabolic acidosis (CMA) in normal adults results in complex endocrine and metabolic alterations including growth hormone (GH) insensitivity, hypothyroidism, hyperglucocorticoidism, hypoalbuminaemia and loss of protein stores. Similar alterations occur in chronic renal failure, a prototypical state of CMA. We evaluated whether metabolic acidosis contributes to the endocrine and metabolic alterations characteristic of end-stage renal disease. Methods. We treated 14 chronic haemodialysis patients with daily oral Na-citrate for 4 weeks, yielding a steady-state pre-dialytic plasma bicarbonate concentration of 26.7 mmol/l, followed by 4 weeks of equimolar Na-chloride, yielding a steady-state pre-dialytic plasma bicarbonate of 20.2 mmol/l. Results. Blood pressure, body weight and dialysis adequacy were equivalent in the two protocols. Na-citrate treatment corrected CMA, improved GH insensitivity, increased and normalized plasma free T3 concentration, and improved plasma albumin. Correction of CMA had no significant effect on measured cytokines (interleukin-1β and -6, tumour necrosis factor-α) or acute phase reactants (C-reactive protein, serum amyloid A, α2-macroglobulin). Conclusion. CMA contributes to the derangements of the growth and thyroid hormone axes and to hypoalbuminaemia, but is not a modulator of systemic inflammation in dialysis patients. Correcting CMA may improve nutritional and metabolic parameters and thus lower morbidity and mortality.</description><subject>Acidosis - blood</subject><subject>Acidosis - therapy</subject><subject>Administration, Oral</subject><subject>Adult</subject><subject>Aged</subject><subject>albumin</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Bicarbonates - blood</subject><subject>Biological and medical sciences</subject><subject>Blood Gas Analysis</subject><subject>Citrates - administration & dosage</subject><subject>Citrates - therapeutic use</subject><subject>Cytokines - blood</subject><subject>dialysis</subject><subject>Emergency and intensive care: renal failure. Dialysis management</subject><subject>Female</subject><subject>Glomerulonephritis</subject><subject>growth hormone</subject><subject>Human Growth Hormone - blood</subject><subject>Humans</subject><subject>Intensive care medicine</subject><subject>Male</subject><subject>Medical sciences</subject><subject>metabolic acidosis</subject><subject>Middle Aged</subject><subject>Nephrology. Urinary tract diseases</subject><subject>Nephropathies. Renovascular diseases. Renal failure</subject><subject>Reference Values</subject><subject>Renal Dialysis</subject><subject>Renal failure</subject><subject>Serum Albumin - metabolism</subject><subject>Sodium - blood</subject><subject>thyroid</subject><subject>Triiodothyronine - blood</subject><issn>0931-0509</issn><issn>1460-2385</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2004</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpF0Mtu1DAUBmALgehQ2PAAyBtYIIUex7d4iUYwRarUSi0XsbEcXxpDEg-2p3TenlQzoquz-L9zdPQj9JrABwKKns2unt2GAZR4glaECWha2vGnaLWEpAEO6gS9KOUXAKhWyufohDClKOvoCtl1ytnbGtOMU8CTr6ZPY7TY2OhSiQXHaZvTnS-4DvucosNmdvg2p791wEPKU5o9NvdLHmc8GD8lF824f9jcmhr9XMtL9CyYsfhXx3mKvn7-dLM-by4uN1_WHy8ayzitTQjSMtmrjrVBKtcyDh566GiQnIJiIBzjPrSCWRC9JKFnrheEcA9gjRL0FL073F0e_rPzpeopFuvH0cw-7YqWpOMAjC7w_QHanErJPuhtjpPJe01AP1Sql0r1odIFvzle3fWTd4_02OEC3h6BKdaMIZvZxvLouGSKU7645uBiqf7-f27yby0klVyf__ipxfW3zXd1tdHX9B9iRZBq</recordid><startdate>20040501</startdate><enddate>20040501</enddate><creator>Wiederkehr, Michael R.</creator><creator>Kalogiros, Jris</creator><creator>Krapf, Reto</creator><general>Oxford University Press</general><scope>BSCLL</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>20040501</creationdate><title>Correction of metabolic acidosis improves thyroid and growth hormone axes in haemodialysis patients</title><author>Wiederkehr, Michael R. ; Kalogiros, Jris ; Krapf, Reto</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c453t-ff7c47b9842f79d2450e0b083f75309406d45ef264c06b71fb4db6115e00ca963</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2004</creationdate><topic>Acidosis - blood</topic><topic>Acidosis - therapy</topic><topic>Administration, Oral</topic><topic>Adult</topic><topic>Aged</topic><topic>albumin</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Bicarbonates - blood</topic><topic>Biological and medical sciences</topic><topic>Blood Gas Analysis</topic><topic>Citrates - administration & dosage</topic><topic>Citrates - therapeutic use</topic><topic>Cytokines - blood</topic><topic>dialysis</topic><topic>Emergency and intensive care: renal failure. Dialysis management</topic><topic>Female</topic><topic>Glomerulonephritis</topic><topic>growth hormone</topic><topic>Human Growth Hormone - blood</topic><topic>Humans</topic><topic>Intensive care medicine</topic><topic>Male</topic><topic>Medical sciences</topic><topic>metabolic acidosis</topic><topic>Middle Aged</topic><topic>Nephrology. Urinary tract diseases</topic><topic>Nephropathies. Renovascular diseases. Renal failure</topic><topic>Reference Values</topic><topic>Renal Dialysis</topic><topic>Renal failure</topic><topic>Serum Albumin - metabolism</topic><topic>Sodium - blood</topic><topic>thyroid</topic><topic>Triiodothyronine - blood</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wiederkehr, Michael R.</creatorcontrib><creatorcontrib>Kalogiros, Jris</creatorcontrib><creatorcontrib>Krapf, Reto</creatorcontrib><collection>Istex</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>Nephrology, dialysis, transplantation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wiederkehr, Michael R.</au><au>Kalogiros, Jris</au><au>Krapf, Reto</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correction of metabolic acidosis improves thyroid and growth hormone axes in haemodialysis patients</atitle><jtitle>Nephrology, dialysis, transplantation</jtitle><addtitle>Nephrol. Dial. Transplant</addtitle><date>2004-05-01</date><risdate>2004</risdate><volume>19</volume><issue>5</issue><spage>1190</spage><epage>1197</epage><pages>1190-1197</pages><issn>0931-0509</issn><eissn>1460-2385</eissn><coden>NDTREA</coden><abstract>Background. Chronic metabolic acidosis (CMA) in normal adults results in complex endocrine and metabolic alterations including growth hormone (GH) insensitivity, hypothyroidism, hyperglucocorticoidism, hypoalbuminaemia and loss of protein stores. Similar alterations occur in chronic renal failure, a prototypical state of CMA. We evaluated whether metabolic acidosis contributes to the endocrine and metabolic alterations characteristic of end-stage renal disease. Methods. We treated 14 chronic haemodialysis patients with daily oral Na-citrate for 4 weeks, yielding a steady-state pre-dialytic plasma bicarbonate concentration of 26.7 mmol/l, followed by 4 weeks of equimolar Na-chloride, yielding a steady-state pre-dialytic plasma bicarbonate of 20.2 mmol/l. Results. Blood pressure, body weight and dialysis adequacy were equivalent in the two protocols. Na-citrate treatment corrected CMA, improved GH insensitivity, increased and normalized plasma free T3 concentration, and improved plasma albumin. Correction of CMA had no significant effect on measured cytokines (interleukin-1β and -6, tumour necrosis factor-α) or acute phase reactants (C-reactive protein, serum amyloid A, α2-macroglobulin). Conclusion. CMA contributes to the derangements of the growth and thyroid hormone axes and to hypoalbuminaemia, but is not a modulator of systemic inflammation in dialysis patients. Correcting CMA may improve nutritional and metabolic parameters and thus lower morbidity and mortality.</abstract><cop>Oxford</cop><pub>Oxford University Press</pub><pmid>14993483</pmid><doi>10.1093/ndt/gfh096</doi><tpages>8</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Acidosis - blood Acidosis - therapy Administration, Oral Adult Aged albumin Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Bicarbonates - blood Biological and medical sciences Blood Gas Analysis Citrates - administration & dosage Citrates - therapeutic use Cytokines - blood dialysis Emergency and intensive care: renal failure. Dialysis management Female Glomerulonephritis growth hormone Human Growth Hormone - blood Humans Intensive care medicine Male Medical sciences metabolic acidosis Middle Aged Nephrology. Urinary tract diseases Nephropathies. Renovascular diseases. Renal failure Reference Values Renal Dialysis Renal failure Serum Albumin - metabolism Sodium - blood thyroid Triiodothyronine - blood |
title | Correction of metabolic acidosis improves thyroid and growth hormone axes in haemodialysis patients |
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