{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,7]],"date-time":"2026-07-07T13:20:52Z","timestamp":1783430452329,"version":"3.54.6"},"reference-count":32,"publisher":"Oxford University Press (OUP)","issue":"3","license":[{"start":{"date-parts":[[2019,4,21]],"date-time":"2019-04-21T00:00:00Z","timestamp":1555804800000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/journals\/pages\/open_access\/funder_policies\/chorus\/standard_publication_model"}],"funder":[{"DOI":"10.13039\/100002429","name":"Amgen","doi-asserted-by":"publisher","id":[{"id":"10.13039\/100002429","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2020,3,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:sec>\n                  <jats:title>Background<\/jats:title>\n                  <jats:p>There is little information in haemodialysis (HD) patients on whether temporal changes in serum calcium, phosphate or intact parathyroid hormone (iPTH) are associated with mortality.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Methods<\/jats:title>\n                  <jats:p>We analysed associations of phosphate, total calcium and iPTH with all-cause and cardiovascular mortality in 8817 incident HD patients from the European second Analyzing Data, Recognizing Excellence and Optimizing Outcomes (AROii) cohort enrolled in 2007\u201309, which were prospectively followed for a median of 3\u2009years, using time-dependent Cox proportional hazards models. We evaluated changes in risk over time depending on changes in phosphate, calcium or iPTH.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Results<\/jats:title>\n                  <jats:p>The association of phosphate and iPTH with all-cause mortality was U-shaped, with the lowest risk ranges between 1.20 and 1.89\u2009mmol\/L for phosphate and between 239 and 710\u2009ng\/L for iPTH. For total calcium, the associations were J-shaped, with an increased risk for all-cause mortality at levels &amp;gt;2.36\u2009mmol\/L. Lowest risk ranges for cardiovascular mortality did not change markedly for all three parameters. If iPTH was below the lowest risk range at baseline (iPTH\u2009&amp;lt;239\u2009ng\/L), a subsequent increase in levels was associated with improved survival. For phosphate, an increase or decrease out of the lowest risk range was associated with increased mortality risk. For calcium, this was only the case when the values increased above the lowest risk range.<\/jats:p>\n               <\/jats:sec>\n               <jats:sec>\n                  <jats:title>Conclusion<\/jats:title>\n                  <jats:p>In the AROii cohort, the ranges of bone mineral biomarkers associated with the lowest mortality ranges were largely consistent with the current Kidney Disease: Improving Global Outcomes chronic kidney disease\u2013mineral and bone disorder guideline recommendations. Allowing a suppressed iPTH to increase was associated with a lower mortality, whereas shifts of phosphate or calcium outside the lowest risk range increased mortality.<\/jats:p>\n               <\/jats:sec>","DOI":"10.1093\/ndt\/gfz060","type":"journal-article","created":{"date-parts":[[2019,3,27]],"date-time":"2019-03-27T22:01:28Z","timestamp":1553724088000},"page":"478-487","source":"Crossref","is-referenced-by-count":29,"title":["Association of changes in bone mineral parameters with mortality in haemodialysis patients: insights from the ARO cohort"],"prefix":"10.1093","volume":"35","author":[{"given":"Claudia","family":"Lamina","sequence":"first","affiliation":[{"name":"Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Florian","family":"Kronenberg","sequence":"additional","affiliation":[{"name":"Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Stenvinkel","sequence":"additional","affiliation":[{"name":"Department of Renal Medicine, Karolinska University Hospital Huddinge, Stockholm, Sweden"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Marc","family":"Froissart","sequence":"additional","affiliation":[{"name":"Centre Hospitalier Universitaire Vaudois, Clinical Trial Unit, Lausanne, Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lukas","family":"Forer","sequence":"additional","affiliation":[{"name":"Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sebastian","family":"Sch\u00f6nherr","sequence":"additional","affiliation":[{"name":"Division of Genetic Epidemiology, Department of Medical Genetics, Molecular and Clinical Pharmacology, Medical University of Innsbruck, Innsbruck, Austria"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David C","family":"Wheeler","sequence":"additional","affiliation":[{"name":"Center for Nephrology, University College London, London, UK"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kai-Uwe","family":"Eckardt","sequence":"additional","affiliation":[{"name":"Department of Nephrology and Medical Intensive Care, Charit\u00e9-Universit\u00e4tsmedizin Berlin, Germany"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J\u00fcrgen","family":"Floege","sequence":"additional","affiliation":[{"name":"Department of Nephrology, Division of Nephrology and Clinical Immunology, RWTH University of 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