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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Veröffentlicht in:Nephrology, dialysis, transplantation dialysis, transplantation, 2004-05, Vol.19 (5), p.1190-1197
Hauptverfasser: Wiederkehr, Michael R., Kalogiros, Jris, Krapf, Reto
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creator Wiederkehr, Michael R.
Kalogiros, Jris
Krapf, Reto
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.
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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. 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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 &amp; 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 &amp; 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. 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source Oxford University Press Journals All Titles (1996-Current); MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection
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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