{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T18:21:25Z","timestamp":1790878885381,"version":"4.1.0"},"reference-count":21,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2021,9,14]],"date-time":"2021-09-14T00:00:00Z","timestamp":1631577600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"DOI":"10.13039\/501100004061","name":"Oesterreichische Nationalbank","doi-asserted-by":"publisher","award":["15366"],"award-info":[{"award-number":["15366"]}],"id":[{"id":"10.13039\/501100004061","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100004061","name":"Oesterreichische Nationalbank","doi-asserted-by":"publisher","award":["18362"],"award-info":[{"award-number":["18362"]}],"id":[{"id":"10.13039\/501100004061","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Med."],"abstract":"<jats:p><jats:bold>Background:<\/jats:bold> Personalized management of secondary hyperparathyroidism is a critical part of hemodialysis patient care. We used a mathematical model of parathyroid gland (PTG) biology to predict (1) short-term peridialytic intact PTH (iPTH) changes in response to diffusive calcium (Ca) fluxes and (2) to predict long-term iPTH levels.<\/jats:p><jats:p><jats:bold>Methods:<\/jats:bold> We dialyzed 26 maintenance hemodialysis patients on a single occasion with a dialysate Ca concentration of 1.75 mmol\/l to attain a positive dialysate-to-blood ionized Ca (iCa) gradient and thus diffusive Ca loading. Intradialytic iCa kinetics, peridialytic iPTH change, and dialysate-sided iCa mass balance (iCaMB) were assessed. Patient-specific PTG model parameters were estimated using clinical, medication, and laboratory data. We then used the personalized PTG model to predict peridialytic and long-term (6-months) iPTH levels.<\/jats:p><jats:p><jats:bold>Results:<\/jats:bold> At dialysis start, the median dialysate-to-blood iCa gradient was 0.3 mmol\/l (IQR 0.11). The intradialytic iCa gain was 488 mg (IQR 268). Median iPTH decrease was 75% (IQR 15) from pre-dialysis 277 to post-dialysis 51 pg\/ml. Neither iCa gradient nor iCaMB were significantly associated with peridialytic iPTH changes. The personalized PTG model accurately predicted both short-term, treatment-level peridialytic iPTH changes (r = 0.984, <jats:italic>p<\/jats:italic> &amp;lt; 0.001, <jats:italic>n<\/jats:italic> = 26) and patient-level 6-months iPTH levels (r = 0.848, <jats:italic>p<\/jats:italic> &amp;lt; 0.001, <jats:italic>n<\/jats:italic> = 13).<\/jats:p><jats:p><jats:bold>Conclusions:<\/jats:bold> This is the first report showing that both short-term and long-term iPTH dynamics can be predicted using a personalized mathematical model of PTG biology. Prospective studies are warranted to explore further model applications, such as patient-level prediction of iPTH response to PTH-lowering treatment.<\/jats:p>","DOI":"10.3389\/fmed.2021.704970","type":"journal-article","created":{"date-parts":[[2021,9,14]],"date-time":"2021-09-14T06:15:25Z","timestamp":1631600125000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":7,"title":["Personalized Prediction of Short- and Long-Term PTH Changes in Maintenance Hemodialysis Patients"],"prefix":"10.3389","volume":"8","author":[{"given":"Markus","family":"Pirklbauer","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David A.","family":"Bushinsky","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter","family":"Kotanko","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gudrun","family":"Schappacher-Tilp","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2021,9,14]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","first-page":"S1","DOI":"10.1038\/ki.2009.188","article-title":"KDIGO clinical practice guideline for the diagnosis, evaluation, prevention, and treatment of Chronic Kidney Disease-Mineral and Bone Disorder (CKD-MBD)","volume":"113","year":"2009","journal-title":"Kidney Int Suppl"},{"key":"B2","doi-asserted-by":"publisher","first-page":"1119","DOI":"10.1001\/jama.2011.308","article-title":"Serum levels of phosphorus, parathyroid hormone, and calcium and risks of death and cardiovascular disease in individuals with chronic kidney disease: a systematic review and meta-analysis","volume":"305","author":"Palmer","year":"2011","journal-title":"JAMA"},{"key":"B3","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1016\/j.kisu.2017.04.001","article-title":"KDIGO 2017 clinical practice guideline update for the diagnosis, evaluation, prevention, and treatment of chronic kidney disease-mineral and bone disorder (CKD-MBD)","volume":"7","year":"2017","journal-title":"Kidney Int Suppl (2011)"},{"key":"B4","doi-asserted-by":"publisher","first-page":"2","DOI":"10.1093\/ndt\/15.suppl_5.2","article-title":"Molecular mechanisms of secondary hyperparathyroidism","volume":"15","author":"Silver","year":"2000","journal-title":"Nephrol Dial Transplant"},{"key":"B5","doi-asserted-by":"publisher","first-page":"913","DOI":"10.2215\/CJN.06040710","article-title":"Secondary hyperparathyroidism: pathogenesis, disease progression, therapeutic options","volume":"6","author":"Cunningham","year":"2011","journal-title":"Clin J Am Soc Nephrol"},{"key":"B6","doi-asserted-by":"publisher","first-page":"336","DOI":"10.1097\/00041552-199607000-00008","article-title":"Molecular genetics of hyperparathyroid disease","volume":"5","author":"Tominaga","year":"1996","journal-title":"Curr Opin Nephrol Hypertens"},{"key":"B7","doi-asserted-by":"publisher","first-page":"1828","DOI":"10.1093\/ndt\/gfm177","article-title":"Can calcimimetics inhibit parathyroid hyperplasia? 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