Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients
Background After kidney transplantation, fibroblast growth factor-23 (FGF-23) normally returns to baseline within 1 year whereas hyperparathyroidism persists in most kidney transplant (KT) recipients. As a result, serum phosphate remains relatively low in association with increased serum calcium and...
Gespeichert in:
| Veröffentlicht in: | Clinical and experimental nephrology 2017-10, Vol.21 (5), p.926-931 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 931 |
|---|---|
| container_issue | 5 |
| container_start_page | 926 |
| container_title | Clinical and experimental nephrology |
| container_volume | 21 |
| creator | Prakobsuk, Sumanee Sirilak, Supinda Vipattawat, Kotcharat Taweesedt, Pahnwat T. Sumethkul, Vasant Kantachuvesiri, Surasak Disthabanchong, Sinee |
| description | Background
After kidney transplantation, fibroblast growth factor-23 (FGF-23) normally returns to baseline within 1 year whereas hyperparathyroidism persists in most kidney transplant (KT) recipients. As a result, serum phosphate remains relatively low in association with increased serum calcium and urinary phosphate excretion when compared to chronic kidney disease patients. The relationship between mineral metabolism and outcomes in long-term KT recipients has not been extensively studied. This study investigated whether the alteration in mineral metabolism influenced graft survival in long-term KT recipients.
Methods
This study included 273 KT recipients after 1 year of transplantation. Mineral parameters were obtained at the time of enrolment and patients were followed prospectively for an average of 71 months.
Results
Graft loss (death-censored) occurred in 41 (15%) patients. In univariate analysis, deceased donor transplantation, decreased serum albumin and estimated glomerular filtration rate, increased serum phosphate, parathyroid hormone (PTH), FGF-23 and fractional excretion of phosphate (FePi) predicted future allograft loss. After adjustments for cardiovascular disease risk factors, donor type, dialysis vintage, serum albumin and allograft function, only increased PTH and FePi remained associated with the outcome. Relationships between increased serum phosphate and FGF-23 with graft survival were lost after adjustments. Adjusted survival curves revealed the association between PTH > 90 pg/mL and FePi > 20% with worse graft survival.
Conclusions
Hyperparathyroidism and increased FePi predicted allograft loss in long-term KT recipients. |
| doi_str_mv | 10.1007/s10157-016-1370-9 |
| format | Article |
| fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1852687386</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1953099431</sourcerecordid><originalsourceid>FETCH-LOGICAL-c451t-6c79e866e17a71064ab1432413087cf67afa04791b128cc127d45ce550e2850a3</originalsourceid><addsrcrecordid>eNp1kcFuFDEMhiNERUvhAbigSFy4hMaTySQ5oqpQpEpcyjnKZjy7KTOTkGQl9s6DN6stCCFxsuV8_h37J-QN8A_AuboqwEEqxmFgIBRn5hm5gF4oppQxz1su-o6BknBOXpbywDnXRpoX5LxTRoMw4oL8uj0kzMllV3eHHMMYykLdOtKw-oyu4Ein7HwNcXUzxZ-teMxpnGjaxZJ2riJNGcfgK3XzHLfZTZXOsZQm0eK6ZRXzQr-HccUDrdmtJc1urTSjDyngWssrcja5ueDrp3hJvn26ub--ZXdfP3-5_njHfC-hssErg3oYEJRTwIfebdq2XQ-Ca-WnQbnJ8V4Z2ECnvYdOjb30KCXHTkvuxCV5f9JNOf7YY6l2CcXj3L6DcV8saNkNWgk9NPTdP-hD3Od2g0YZKbgxvYBGwYnyuS2ccbIph8XlgwVujxbZk0W2WWSPFlnTet4-Ke83C45_On570oDuBJT2tG4x_zX6v6qPDsSd_A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1953099431</pqid></control><display><type>article</type><title>Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients</title><source>MEDLINE</source><source>SpringerLink Journals - AutoHoldings</source><creator>Prakobsuk, Sumanee ; Sirilak, Supinda ; Vipattawat, Kotcharat ; Taweesedt, Pahnwat T. ; Sumethkul, Vasant ; Kantachuvesiri, Surasak ; Disthabanchong, Sinee</creator><creatorcontrib>Prakobsuk, Sumanee ; Sirilak, Supinda ; Vipattawat, Kotcharat ; Taweesedt, Pahnwat T. ; Sumethkul, Vasant ; Kantachuvesiri, Surasak ; Disthabanchong, Sinee</creatorcontrib><description>Background
After kidney transplantation, fibroblast growth factor-23 (FGF-23) normally returns to baseline within 1 year whereas hyperparathyroidism persists in most kidney transplant (KT) recipients. As a result, serum phosphate remains relatively low in association with increased serum calcium and urinary phosphate excretion when compared to chronic kidney disease patients. The relationship between mineral metabolism and outcomes in long-term KT recipients has not been extensively studied. This study investigated whether the alteration in mineral metabolism influenced graft survival in long-term KT recipients.
Methods
This study included 273 KT recipients after 1 year of transplantation. Mineral parameters were obtained at the time of enrolment and patients were followed prospectively for an average of 71 months.
Results
Graft loss (death-censored) occurred in 41 (15%) patients. In univariate analysis, deceased donor transplantation, decreased serum albumin and estimated glomerular filtration rate, increased serum phosphate, parathyroid hormone (PTH), FGF-23 and fractional excretion of phosphate (FePi) predicted future allograft loss. After adjustments for cardiovascular disease risk factors, donor type, dialysis vintage, serum albumin and allograft function, only increased PTH and FePi remained associated with the outcome. Relationships between increased serum phosphate and FGF-23 with graft survival were lost after adjustments. Adjusted survival curves revealed the association between PTH > 90 pg/mL and FePi > 20% with worse graft survival.
Conclusions
Hyperparathyroidism and increased FePi predicted allograft loss in long-term KT recipients.</description><identifier>ISSN: 1342-1751</identifier><identifier>EISSN: 1437-7799</identifier><identifier>DOI: 10.1007/s10157-016-1370-9</identifier><identifier>PMID: 27981393</identifier><language>eng</language><publisher>Tokyo: Springer Japan</publisher><subject>Adult ; Albumin ; Allografts ; Calcium (blood) ; Calcium (urinary) ; Calcium phosphates ; Cardiovascular diseases ; Dialysis ; Excretion ; Female ; Fibroblast growth factor 23 ; Glomerular Filtration Rate ; Graft Survival ; Humans ; Hyperparathyroidism ; Hyperparathyroidism - blood ; Hyperparathyroidism - diagnosis ; Hyperparathyroidism - etiology ; Hyperparathyroidism - physiopathology ; Hypophosphatemia - blood ; Hypophosphatemia - diagnosis ; Hypophosphatemia - etiology ; Hypophosphatemia - physiopathology ; Hypophosphatemia, Familial - diagnosis ; Hypophosphatemia, Familial - etiology ; Hypophosphatemia, Familial - physiopathology ; Hypophosphatemia, Familial - urine ; Kidney - physiopathology ; Kidney transplantation ; Kidney Transplantation - adverse effects ; Kidney transplants ; Male ; Medicine ; Medicine & Public Health ; Metabolism ; Middle Aged ; Nephrology ; Original Article ; Parathyroid ; Parathyroid hormone ; Phosphate ; Phosphates - blood ; Phosphates - urine ; Prospective Studies ; Renal Dialysis ; Renal Elimination ; Risk Factors ; Survival ; Time Factors ; Transplantation ; Transplants & implants ; Treatment Outcome ; Urology ; Vitamin D</subject><ispartof>Clinical and experimental nephrology, 2017-10, Vol.21 (5), p.926-931</ispartof><rights>Japanese Society of Nephrology 2016</rights><rights>Clinical and Experimental Nephrology is a copyright of Springer, 2017.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c451t-6c79e866e17a71064ab1432413087cf67afa04791b128cc127d45ce550e2850a3</citedby><cites>FETCH-LOGICAL-c451t-6c79e866e17a71064ab1432413087cf67afa04791b128cc127d45ce550e2850a3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s10157-016-1370-9$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10157-016-1370-9$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27901,27902,41464,42533,51294</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27981393$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Prakobsuk, Sumanee</creatorcontrib><creatorcontrib>Sirilak, Supinda</creatorcontrib><creatorcontrib>Vipattawat, Kotcharat</creatorcontrib><creatorcontrib>Taweesedt, Pahnwat T.</creatorcontrib><creatorcontrib>Sumethkul, Vasant</creatorcontrib><creatorcontrib>Kantachuvesiri, Surasak</creatorcontrib><creatorcontrib>Disthabanchong, Sinee</creatorcontrib><title>Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients</title><title>Clinical and experimental nephrology</title><addtitle>Clin Exp Nephrol</addtitle><addtitle>Clin Exp Nephrol</addtitle><description>Background
After kidney transplantation, fibroblast growth factor-23 (FGF-23) normally returns to baseline within 1 year whereas hyperparathyroidism persists in most kidney transplant (KT) recipients. As a result, serum phosphate remains relatively low in association with increased serum calcium and urinary phosphate excretion when compared to chronic kidney disease patients. The relationship between mineral metabolism and outcomes in long-term KT recipients has not been extensively studied. This study investigated whether the alteration in mineral metabolism influenced graft survival in long-term KT recipients.
Methods
This study included 273 KT recipients after 1 year of transplantation. Mineral parameters were obtained at the time of enrolment and patients were followed prospectively for an average of 71 months.
Results
Graft loss (death-censored) occurred in 41 (15%) patients. In univariate analysis, deceased donor transplantation, decreased serum albumin and estimated glomerular filtration rate, increased serum phosphate, parathyroid hormone (PTH), FGF-23 and fractional excretion of phosphate (FePi) predicted future allograft loss. After adjustments for cardiovascular disease risk factors, donor type, dialysis vintage, serum albumin and allograft function, only increased PTH and FePi remained associated with the outcome. Relationships between increased serum phosphate and FGF-23 with graft survival were lost after adjustments. Adjusted survival curves revealed the association between PTH > 90 pg/mL and FePi > 20% with worse graft survival.
Conclusions
Hyperparathyroidism and increased FePi predicted allograft loss in long-term KT recipients.</description><subject>Adult</subject><subject>Albumin</subject><subject>Allografts</subject><subject>Calcium (blood)</subject><subject>Calcium (urinary)</subject><subject>Calcium phosphates</subject><subject>Cardiovascular diseases</subject><subject>Dialysis</subject><subject>Excretion</subject><subject>Female</subject><subject>Fibroblast growth factor 23</subject><subject>Glomerular Filtration Rate</subject><subject>Graft Survival</subject><subject>Humans</subject><subject>Hyperparathyroidism</subject><subject>Hyperparathyroidism - blood</subject><subject>Hyperparathyroidism - diagnosis</subject><subject>Hyperparathyroidism - etiology</subject><subject>Hyperparathyroidism - physiopathology</subject><subject>Hypophosphatemia - blood</subject><subject>Hypophosphatemia - diagnosis</subject><subject>Hypophosphatemia - etiology</subject><subject>Hypophosphatemia - physiopathology</subject><subject>Hypophosphatemia, Familial - diagnosis</subject><subject>Hypophosphatemia, Familial - etiology</subject><subject>Hypophosphatemia, Familial - physiopathology</subject><subject>Hypophosphatemia, Familial - urine</subject><subject>Kidney - physiopathology</subject><subject>Kidney transplantation</subject><subject>Kidney Transplantation - adverse effects</subject><subject>Kidney transplants</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Metabolism</subject><subject>Middle Aged</subject><subject>Nephrology</subject><subject>Original Article</subject><subject>Parathyroid</subject><subject>Parathyroid hormone</subject><subject>Phosphate</subject><subject>Phosphates - blood</subject><subject>Phosphates - urine</subject><subject>Prospective Studies</subject><subject>Renal Dialysis</subject><subject>Renal Elimination</subject><subject>Risk Factors</subject><subject>Survival</subject><subject>Time Factors</subject><subject>Transplantation</subject><subject>Transplants & implants</subject><subject>Treatment Outcome</subject><subject>Urology</subject><subject>Vitamin D</subject><issn>1342-1751</issn><issn>1437-7799</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp1kcFuFDEMhiNERUvhAbigSFy4hMaTySQ5oqpQpEpcyjnKZjy7KTOTkGQl9s6DN6stCCFxsuV8_h37J-QN8A_AuboqwEEqxmFgIBRn5hm5gF4oppQxz1su-o6BknBOXpbywDnXRpoX5LxTRoMw4oL8uj0kzMllV3eHHMMYykLdOtKw-oyu4Ein7HwNcXUzxZ-teMxpnGjaxZJ2riJNGcfgK3XzHLfZTZXOsZQm0eK6ZRXzQr-HccUDrdmtJc1urTSjDyngWssrcja5ueDrp3hJvn26ub--ZXdfP3-5_njHfC-hssErg3oYEJRTwIfebdq2XQ-Ca-WnQbnJ8V4Z2ECnvYdOjb30KCXHTkvuxCV5f9JNOf7YY6l2CcXj3L6DcV8saNkNWgk9NPTdP-hD3Od2g0YZKbgxvYBGwYnyuS2ccbIph8XlgwVujxbZk0W2WWSPFlnTet4-Ke83C45_On570oDuBJT2tG4x_zX6v6qPDsSd_A</recordid><startdate>20171001</startdate><enddate>20171001</enddate><creator>Prakobsuk, Sumanee</creator><creator>Sirilak, Supinda</creator><creator>Vipattawat, Kotcharat</creator><creator>Taweesedt, Pahnwat T.</creator><creator>Sumethkul, Vasant</creator><creator>Kantachuvesiri, Surasak</creator><creator>Disthabanchong, Sinee</creator><general>Springer Japan</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>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>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope></search><sort><creationdate>20171001</creationdate><title>Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients</title><author>Prakobsuk, Sumanee ; Sirilak, Supinda ; Vipattawat, Kotcharat ; Taweesedt, Pahnwat T. ; Sumethkul, Vasant ; Kantachuvesiri, Surasak ; Disthabanchong, Sinee</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c451t-6c79e866e17a71064ab1432413087cf67afa04791b128cc127d45ce550e2850a3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Adult</topic><topic>Albumin</topic><topic>Allografts</topic><topic>Calcium (blood)</topic><topic>Calcium (urinary)</topic><topic>Calcium phosphates</topic><topic>Cardiovascular diseases</topic><topic>Dialysis</topic><topic>Excretion</topic><topic>Female</topic><topic>Fibroblast growth factor 23</topic><topic>Glomerular Filtration Rate</topic><topic>Graft Survival</topic><topic>Humans</topic><topic>Hyperparathyroidism</topic><topic>Hyperparathyroidism - blood</topic><topic>Hyperparathyroidism - diagnosis</topic><topic>Hyperparathyroidism - etiology</topic><topic>Hyperparathyroidism - physiopathology</topic><topic>Hypophosphatemia - blood</topic><topic>Hypophosphatemia - diagnosis</topic><topic>Hypophosphatemia - etiology</topic><topic>Hypophosphatemia - physiopathology</topic><topic>Hypophosphatemia, Familial - diagnosis</topic><topic>Hypophosphatemia, Familial - etiology</topic><topic>Hypophosphatemia, Familial - physiopathology</topic><topic>Hypophosphatemia, Familial - urine</topic><topic>Kidney - physiopathology</topic><topic>Kidney transplantation</topic><topic>Kidney Transplantation - adverse effects</topic><topic>Kidney transplants</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Metabolism</topic><topic>Middle Aged</topic><topic>Nephrology</topic><topic>Original Article</topic><topic>Parathyroid</topic><topic>Parathyroid hormone</topic><topic>Phosphate</topic><topic>Phosphates - blood</topic><topic>Phosphates - urine</topic><topic>Prospective Studies</topic><topic>Renal Dialysis</topic><topic>Renal Elimination</topic><topic>Risk Factors</topic><topic>Survival</topic><topic>Time Factors</topic><topic>Transplantation</topic><topic>Transplants & implants</topic><topic>Treatment Outcome</topic><topic>Urology</topic><topic>Vitamin D</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Prakobsuk, Sumanee</creatorcontrib><creatorcontrib>Sirilak, Supinda</creatorcontrib><creatorcontrib>Vipattawat, Kotcharat</creatorcontrib><creatorcontrib>Taweesedt, Pahnwat T.</creatorcontrib><creatorcontrib>Sumethkul, Vasant</creatorcontrib><creatorcontrib>Kantachuvesiri, Surasak</creatorcontrib><creatorcontrib>Disthabanchong, Sinee</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>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>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>Clinical and experimental nephrology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Prakobsuk, Sumanee</au><au>Sirilak, Supinda</au><au>Vipattawat, Kotcharat</au><au>Taweesedt, Pahnwat T.</au><au>Sumethkul, Vasant</au><au>Kantachuvesiri, Surasak</au><au>Disthabanchong, Sinee</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients</atitle><jtitle>Clinical and experimental nephrology</jtitle><stitle>Clin Exp Nephrol</stitle><addtitle>Clin Exp Nephrol</addtitle><date>2017-10-01</date><risdate>2017</risdate><volume>21</volume><issue>5</issue><spage>926</spage><epage>931</epage><pages>926-931</pages><issn>1342-1751</issn><eissn>1437-7799</eissn><abstract>Background
After kidney transplantation, fibroblast growth factor-23 (FGF-23) normally returns to baseline within 1 year whereas hyperparathyroidism persists in most kidney transplant (KT) recipients. As a result, serum phosphate remains relatively low in association with increased serum calcium and urinary phosphate excretion when compared to chronic kidney disease patients. The relationship between mineral metabolism and outcomes in long-term KT recipients has not been extensively studied. This study investigated whether the alteration in mineral metabolism influenced graft survival in long-term KT recipients.
Methods
This study included 273 KT recipients after 1 year of transplantation. Mineral parameters were obtained at the time of enrolment and patients were followed prospectively for an average of 71 months.
Results
Graft loss (death-censored) occurred in 41 (15%) patients. In univariate analysis, deceased donor transplantation, decreased serum albumin and estimated glomerular filtration rate, increased serum phosphate, parathyroid hormone (PTH), FGF-23 and fractional excretion of phosphate (FePi) predicted future allograft loss. After adjustments for cardiovascular disease risk factors, donor type, dialysis vintage, serum albumin and allograft function, only increased PTH and FePi remained associated with the outcome. Relationships between increased serum phosphate and FGF-23 with graft survival were lost after adjustments. Adjusted survival curves revealed the association between PTH > 90 pg/mL and FePi > 20% with worse graft survival.
Conclusions
Hyperparathyroidism and increased FePi predicted allograft loss in long-term KT recipients.</abstract><cop>Tokyo</cop><pub>Springer Japan</pub><pmid>27981393</pmid><doi>10.1007/s10157-016-1370-9</doi><tpages>6</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1342-1751 |
| ispartof | Clinical and experimental nephrology, 2017-10, Vol.21 (5), p.926-931 |
| issn | 1342-1751 1437-7799 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_1852687386 |
| source | MEDLINE; SpringerLink Journals - AutoHoldings |
| subjects | Adult Albumin Allografts Calcium (blood) Calcium (urinary) Calcium phosphates Cardiovascular diseases Dialysis Excretion Female Fibroblast growth factor 23 Glomerular Filtration Rate Graft Survival Humans Hyperparathyroidism Hyperparathyroidism - blood Hyperparathyroidism - diagnosis Hyperparathyroidism - etiology Hyperparathyroidism - physiopathology Hypophosphatemia - blood Hypophosphatemia - diagnosis Hypophosphatemia - etiology Hypophosphatemia - physiopathology Hypophosphatemia, Familial - diagnosis Hypophosphatemia, Familial - etiology Hypophosphatemia, Familial - physiopathology Hypophosphatemia, Familial - urine Kidney - physiopathology Kidney transplantation Kidney Transplantation - adverse effects Kidney transplants Male Medicine Medicine & Public Health Metabolism Middle Aged Nephrology Original Article Parathyroid Parathyroid hormone Phosphate Phosphates - blood Phosphates - urine Prospective Studies Renal Dialysis Renal Elimination Risk Factors Survival Time Factors Transplantation Transplants & implants Treatment Outcome Urology Vitamin D |
| title | Hyperparathyroidism and increased fractional excretion of phosphate predict allograft loss in long-term kidney transplant recipients |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-02-08T12%3A17%3A32IST&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=Hyperparathyroidism%20and%20increased%20fractional%20excretion%20of%20phosphate%20predict%20allograft%20loss%20in%20long-term%20kidney%20transplant%20recipients&rft.jtitle=Clinical%20and%20experimental%20nephrology&rft.au=Prakobsuk,%20Sumanee&rft.date=2017-10-01&rft.volume=21&rft.issue=5&rft.spage=926&rft.epage=931&rft.pages=926-931&rft.issn=1342-1751&rft.eissn=1437-7799&rft_id=info:doi/10.1007/s10157-016-1370-9&rft_dat=%3Cproquest_cross%3E1953099431%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=1953099431&rft_id=info:pmid/27981393&rfr_iscdi=true |