Vascular calcification: Contribution of parathyroid hormone in renal failure
Hyperphosphatemia is a driving force in the pathogenesis of vascular calcification (VC) and secondary hyperparathyroidism associated with renal failure. To test for the possible contribution of parathyroid hormone (PTH) to cardiovascular calcification, we removed the parathyroid glands from rats but...
Gespeichert in:
| Veröffentlicht in: | Kidney international 2007-06, Vol.71 (12), p.1262-1270 |
|---|---|
| Hauptverfasser: | , , , , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 1270 |
|---|---|
| container_issue | 12 |
| container_start_page | 1262 |
| container_title | Kidney international |
| container_volume | 71 |
| creator | Neves, K.-R. Graciolli, F.-G. dos Reis, L.-M. Graciolli, R.-G. Neves, C.-L. Magalhães, A.-O. Custódio, M.-R. Batista, D.-G. Jorgetti, V. Moysés, R.M.A. |
| description | Hyperphosphatemia is a driving force in the pathogenesis of vascular calcification (VC) and secondary hyperparathyroidism associated with renal failure. To test for the possible contribution of parathyroid hormone (PTH) to cardiovascular calcification, we removed the parathyroid glands from rats but infused synthetic hormone at a supraphysiologic rate. All rats were pair-fed low, normal, or high phosphorus diets and subjected to a sham or 5/6 nephrectomy (remnant kidney). Control rats were given a normal diet and underwent both sham parathyroidectomy and 5/6 nephrectomy. Heart weight/body weight ratios and serum creatinine levels were higher in remnant kidney rats than in the sham-operated rats. Remnant kidney rats on the high phosphorus diet and PTH replacement developed hyperphosphatemia and hypocalcemia along with low bone trabecular volume. Remnant kidney rats on the low phosphorus diet or intact kidney rats on a normal phosphorus diet, each with hormone replacement, developed hypercalcemia. All rats on PTH replacement developed intense aortic medial calcification, and some animals presented coronary calcification. We suggest that high PTH levels induce high bone turnover and medial calcification resembling Mömckeberg's sclerosis independent of uremia. This model may be useful in defining mechanisms underlying VC. |
| doi_str_mv | 10.1038/sj.ki.5002241 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_755133440</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><els_id>S0085253815523016</els_id><sourcerecordid>755133440</sourcerecordid><originalsourceid>FETCH-LOGICAL-c437t-74062bdff162a9f9fe69a0824ce7c895f1df88b37dd2fd3b5e3b45fe3d8e049c3</originalsourceid><addsrcrecordid>eNp90UtLAzEUBeAgitbH0q0MLnQ1Nc9Oxp0UX1Bwo25DJrmhaaeTmswI_fdGWhAEJYtw4ePAPRehc4LHBDN5kxbjpR8LjCnlZA-NiKCsJJUQ-2iEsRQlFUweoeOUFjjPNcOH6IhUnOD8Rmj2rpMZWh0Lo1vjnTe696G7Laah66Nvhu-pCK5Y66j7-SYGb4t5iKvQQeG7IkKn28Jp3w4RTtGB022Cs91_gt4e7l-nT-Xs5fF5ejcrDWdVX1YcT2hjnSMTqmtXO5jUGkvKDVRG1sIR66RsWGUtdZY1AljDhQNmJWBeG3aCrre56xg-Bki9WvlkoG11B2FIKm9PGOMcZ3n1v8SipkySDC9_wUUYYt4tKZqLIlJillG5RSaGlCI4tY5-peNGEay-r6HSQi292l0j-4td6NCswP7oXf0ZVFsAua1PD1El46EzYH0E0ysb_B_RX_GQmMQ</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>210118803</pqid></control><display><type>article</type><title>Vascular calcification: Contribution of parathyroid hormone in renal failure</title><source>MEDLINE</source><source>Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals</source><source>Alma/SFX Local Collection</source><creator>Neves, K.-R. ; Graciolli, F.-G. ; dos Reis, L.-M. ; Graciolli, R.-G. ; Neves, C.-L. ; Magalhães, A.-O. ; Custódio, M.-R. ; Batista, D.-G. ; Jorgetti, V. ; Moysés, R.M.A.</creator><creatorcontrib>Neves, K.-R. ; Graciolli, F.-G. ; dos Reis, L.-M. ; Graciolli, R.-G. ; Neves, C.-L. ; Magalhães, A.-O. ; Custódio, M.-R. ; Batista, D.-G. ; Jorgetti, V. ; Moysés, R.M.A.</creatorcontrib><description>Hyperphosphatemia is a driving force in the pathogenesis of vascular calcification (VC) and secondary hyperparathyroidism associated with renal failure. To test for the possible contribution of parathyroid hormone (PTH) to cardiovascular calcification, we removed the parathyroid glands from rats but infused synthetic hormone at a supraphysiologic rate. All rats were pair-fed low, normal, or high phosphorus diets and subjected to a sham or 5/6 nephrectomy (remnant kidney). Control rats were given a normal diet and underwent both sham parathyroidectomy and 5/6 nephrectomy. Heart weight/body weight ratios and serum creatinine levels were higher in remnant kidney rats than in the sham-operated rats. Remnant kidney rats on the high phosphorus diet and PTH replacement developed hyperphosphatemia and hypocalcemia along with low bone trabecular volume. Remnant kidney rats on the low phosphorus diet or intact kidney rats on a normal phosphorus diet, each with hormone replacement, developed hypercalcemia. All rats on PTH replacement developed intense aortic medial calcification, and some animals presented coronary calcification. We suggest that high PTH levels induce high bone turnover and medial calcification resembling Mömckeberg's sclerosis independent of uremia. This model may be useful in defining mechanisms underlying VC.</description><identifier>ISSN: 0085-2538</identifier><identifier>EISSN: 1523-1755</identifier><identifier>DOI: 10.1038/sj.ki.5002241</identifier><identifier>PMID: 17410101</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Animals ; Aorta - pathology ; Body Weight - drug effects ; Bone Remodeling ; Calcinosis - complications ; Calcinosis - metabolism ; Calcinosis - pathology ; Cardiovascular Diseases - complications ; Cardiovascular Diseases - metabolism ; Cardiovascular Diseases - pathology ; chronic ; Coronary Vessels - pathology ; Disease Models, Animal ; Eating - drug effects ; Hypercalcemia - etiology ; kidney failure ; Male ; parathyroid hormone ; Parathyroid Hormone - pharmacology ; Parathyroid Hormone - physiology ; phosphorus ; Plethysmography ; Rats ; Rats, Wistar ; Renal Insufficiency - etiology ; renal osteodystrophy ; vascular calcification</subject><ispartof>Kidney international, 2007-06, Vol.71 (12), p.1262-1270</ispartof><rights>2007 International Society of Nephrology</rights><rights>Copyright Nature Publishing Group Jun 2007</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c437t-74062bdff162a9f9fe69a0824ce7c895f1df88b37dd2fd3b5e3b45fe3d8e049c3</citedby><cites>FETCH-LOGICAL-c437t-74062bdff162a9f9fe69a0824ce7c895f1df88b37dd2fd3b5e3b45fe3d8e049c3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/17410101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Neves, K.-R.</creatorcontrib><creatorcontrib>Graciolli, F.-G.</creatorcontrib><creatorcontrib>dos Reis, L.-M.</creatorcontrib><creatorcontrib>Graciolli, R.-G.</creatorcontrib><creatorcontrib>Neves, C.-L.</creatorcontrib><creatorcontrib>Magalhães, A.-O.</creatorcontrib><creatorcontrib>Custódio, M.-R.</creatorcontrib><creatorcontrib>Batista, D.-G.</creatorcontrib><creatorcontrib>Jorgetti, V.</creatorcontrib><creatorcontrib>Moysés, R.M.A.</creatorcontrib><title>Vascular calcification: Contribution of parathyroid hormone in renal failure</title><title>Kidney international</title><addtitle>Kidney Int</addtitle><description>Hyperphosphatemia is a driving force in the pathogenesis of vascular calcification (VC) and secondary hyperparathyroidism associated with renal failure. To test for the possible contribution of parathyroid hormone (PTH) to cardiovascular calcification, we removed the parathyroid glands from rats but infused synthetic hormone at a supraphysiologic rate. All rats were pair-fed low, normal, or high phosphorus diets and subjected to a sham or 5/6 nephrectomy (remnant kidney). Control rats were given a normal diet and underwent both sham parathyroidectomy and 5/6 nephrectomy. Heart weight/body weight ratios and serum creatinine levels were higher in remnant kidney rats than in the sham-operated rats. Remnant kidney rats on the high phosphorus diet and PTH replacement developed hyperphosphatemia and hypocalcemia along with low bone trabecular volume. Remnant kidney rats on the low phosphorus diet or intact kidney rats on a normal phosphorus diet, each with hormone replacement, developed hypercalcemia. All rats on PTH replacement developed intense aortic medial calcification, and some animals presented coronary calcification. We suggest that high PTH levels induce high bone turnover and medial calcification resembling Mömckeberg's sclerosis independent of uremia. This model may be useful in defining mechanisms underlying VC.</description><subject>Animals</subject><subject>Aorta - pathology</subject><subject>Body Weight - drug effects</subject><subject>Bone Remodeling</subject><subject>Calcinosis - complications</subject><subject>Calcinosis - metabolism</subject><subject>Calcinosis - pathology</subject><subject>Cardiovascular Diseases - complications</subject><subject>Cardiovascular Diseases - metabolism</subject><subject>Cardiovascular Diseases - pathology</subject><subject>chronic</subject><subject>Coronary Vessels - pathology</subject><subject>Disease Models, Animal</subject><subject>Eating - drug effects</subject><subject>Hypercalcemia - etiology</subject><subject>kidney failure</subject><subject>Male</subject><subject>parathyroid hormone</subject><subject>Parathyroid Hormone - pharmacology</subject><subject>Parathyroid Hormone - physiology</subject><subject>phosphorus</subject><subject>Plethysmography</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Renal Insufficiency - etiology</subject><subject>renal osteodystrophy</subject><subject>vascular calcification</subject><issn>0085-2538</issn><issn>1523-1755</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2007</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp90UtLAzEUBeAgitbH0q0MLnQ1Nc9Oxp0UX1Bwo25DJrmhaaeTmswI_fdGWhAEJYtw4ePAPRehc4LHBDN5kxbjpR8LjCnlZA-NiKCsJJUQ-2iEsRQlFUweoeOUFjjPNcOH6IhUnOD8Rmj2rpMZWh0Lo1vjnTe696G7Laah66Nvhu-pCK5Y66j7-SYGb4t5iKvQQeG7IkKn28Jp3w4RTtGB022Cs91_gt4e7l-nT-Xs5fF5ejcrDWdVX1YcT2hjnSMTqmtXO5jUGkvKDVRG1sIR66RsWGUtdZY1AljDhQNmJWBeG3aCrre56xg-Bki9WvlkoG11B2FIKm9PGOMcZ3n1v8SipkySDC9_wUUYYt4tKZqLIlJillG5RSaGlCI4tY5-peNGEay-r6HSQi292l0j-4td6NCswP7oXf0ZVFsAua1PD1El46EzYH0E0ysb_B_RX_GQmMQ</recordid><startdate>20070601</startdate><enddate>20070601</enddate><creator>Neves, K.-R.</creator><creator>Graciolli, F.-G.</creator><creator>dos Reis, L.-M.</creator><creator>Graciolli, R.-G.</creator><creator>Neves, C.-L.</creator><creator>Magalhães, A.-O.</creator><creator>Custódio, M.-R.</creator><creator>Batista, D.-G.</creator><creator>Jorgetti, V.</creator><creator>Moysés, R.M.A.</creator><general>Elsevier Inc</general><general>Elsevier Limited</general><scope>6I.</scope><scope>AAFTH</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>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>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</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><scope>7QR</scope><scope>8FD</scope><scope>FR3</scope><scope>P64</scope></search><sort><creationdate>20070601</creationdate><title>Vascular calcification: Contribution of parathyroid hormone in renal failure</title><author>Neves, K.-R. ; Graciolli, F.-G. ; dos Reis, L.-M. ; Graciolli, R.-G. ; Neves, C.-L. ; Magalhães, A.-O. ; Custódio, M.-R. ; Batista, D.-G. ; Jorgetti, V. ; Moysés, R.M.A.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c437t-74062bdff162a9f9fe69a0824ce7c895f1df88b37dd2fd3b5e3b45fe3d8e049c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2007</creationdate><topic>Animals</topic><topic>Aorta - pathology</topic><topic>Body Weight - drug effects</topic><topic>Bone Remodeling</topic><topic>Calcinosis - complications</topic><topic>Calcinosis - metabolism</topic><topic>Calcinosis - pathology</topic><topic>Cardiovascular Diseases - complications</topic><topic>Cardiovascular Diseases - metabolism</topic><topic>Cardiovascular Diseases - pathology</topic><topic>chronic</topic><topic>Coronary Vessels - pathology</topic><topic>Disease Models, Animal</topic><topic>Eating - drug effects</topic><topic>Hypercalcemia - etiology</topic><topic>kidney failure</topic><topic>Male</topic><topic>parathyroid hormone</topic><topic>Parathyroid Hormone - pharmacology</topic><topic>Parathyroid Hormone - physiology</topic><topic>phosphorus</topic><topic>Plethysmography</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Renal Insufficiency - etiology</topic><topic>renal osteodystrophy</topic><topic>vascular calcification</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Neves, K.-R.</creatorcontrib><creatorcontrib>Graciolli, F.-G.</creatorcontrib><creatorcontrib>dos Reis, L.-M.</creatorcontrib><creatorcontrib>Graciolli, R.-G.</creatorcontrib><creatorcontrib>Neves, C.-L.</creatorcontrib><creatorcontrib>Magalhães, A.-O.</creatorcontrib><creatorcontrib>Custódio, M.-R.</creatorcontrib><creatorcontrib>Batista, D.-G.</creatorcontrib><creatorcontrib>Jorgetti, V.</creatorcontrib><creatorcontrib>Moysés, R.M.A.</creatorcontrib><collection>ScienceDirect Open Access Titles</collection><collection>Elsevier:ScienceDirect:Open Access</collection><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</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>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><collection>Chemoreception Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>Biotechnology and BioEngineering Abstracts</collection><jtitle>Kidney international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Neves, K.-R.</au><au>Graciolli, F.-G.</au><au>dos Reis, L.-M.</au><au>Graciolli, R.-G.</au><au>Neves, C.-L.</au><au>Magalhães, A.-O.</au><au>Custódio, M.-R.</au><au>Batista, D.-G.</au><au>Jorgetti, V.</au><au>Moysés, R.M.A.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Vascular calcification: Contribution of parathyroid hormone in renal failure</atitle><jtitle>Kidney international</jtitle><addtitle>Kidney Int</addtitle><date>2007-06-01</date><risdate>2007</risdate><volume>71</volume><issue>12</issue><spage>1262</spage><epage>1270</epage><pages>1262-1270</pages><issn>0085-2538</issn><eissn>1523-1755</eissn><abstract>Hyperphosphatemia is a driving force in the pathogenesis of vascular calcification (VC) and secondary hyperparathyroidism associated with renal failure. To test for the possible contribution of parathyroid hormone (PTH) to cardiovascular calcification, we removed the parathyroid glands from rats but infused synthetic hormone at a supraphysiologic rate. All rats were pair-fed low, normal, or high phosphorus diets and subjected to a sham or 5/6 nephrectomy (remnant kidney). Control rats were given a normal diet and underwent both sham parathyroidectomy and 5/6 nephrectomy. Heart weight/body weight ratios and serum creatinine levels were higher in remnant kidney rats than in the sham-operated rats. Remnant kidney rats on the high phosphorus diet and PTH replacement developed hyperphosphatemia and hypocalcemia along with low bone trabecular volume. Remnant kidney rats on the low phosphorus diet or intact kidney rats on a normal phosphorus diet, each with hormone replacement, developed hypercalcemia. All rats on PTH replacement developed intense aortic medial calcification, and some animals presented coronary calcification. We suggest that high PTH levels induce high bone turnover and medial calcification resembling Mömckeberg's sclerosis independent of uremia. This model may be useful in defining mechanisms underlying VC.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>17410101</pmid><doi>10.1038/sj.ki.5002241</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0085-2538 |
| ispartof | Kidney international, 2007-06, Vol.71 (12), p.1262-1270 |
| issn | 0085-2538 1523-1755 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_755133440 |
| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Animals Aorta - pathology Body Weight - drug effects Bone Remodeling Calcinosis - complications Calcinosis - metabolism Calcinosis - pathology Cardiovascular Diseases - complications Cardiovascular Diseases - metabolism Cardiovascular Diseases - pathology chronic Coronary Vessels - pathology Disease Models, Animal Eating - drug effects Hypercalcemia - etiology kidney failure Male parathyroid hormone Parathyroid Hormone - pharmacology Parathyroid Hormone - physiology phosphorus Plethysmography Rats Rats, Wistar Renal Insufficiency - etiology renal osteodystrophy vascular calcification |
| title | Vascular calcification: Contribution of parathyroid hormone in renal failure |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-03T06%3A15%3A47IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Vascular%20calcification:%20Contribution%20of%20parathyroid%20hormone%20in%20renal%20failure&rft.jtitle=Kidney%20international&rft.au=Neves,%20K.-R.&rft.date=2007-06-01&rft.volume=71&rft.issue=12&rft.spage=1262&rft.epage=1270&rft.pages=1262-1270&rft.issn=0085-2538&rft.eissn=1523-1755&rft_id=info:doi/10.1038/sj.ki.5002241&rft_dat=%3Cproquest_cross%3E755133440%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=210118803&rft_id=info:pmid/17410101&rft_els_id=S0085253815523016&rfr_iscdi=true |