{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,30]],"date-time":"2026-10-30T01:21:48Z","timestamp":1793323308124,"version":"4.5.0"},"reference-count":67,"publisher":"F1000 Research Ltd","license":[{"start":{"date-parts":[[2020,9,1]],"date-time":"2020-09-01T00:00:00Z","timestamp":1598918400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["f1000research.com"],"crossmark-restriction":false},"short-container-title":["F1000Res"],"abstract":"<ns4:p>Secondary hyperparathyroidism is a complex pathology that develops as chronic kidney disease progresses. The retention of phosphorus and the reductions in calcium and vitamin D levels stimulate the synthesis and secretion of parathyroid hormone as well as the proliferation rate of parathyroid cells. Parathyroid growth is initially diffuse but it becomes nodular as the disease progresses, making the gland less susceptible to be inhibited. Although the mechanisms underlying the pathophysiology of secondary hyperparathyroidism are well known, new evidence has shed light on unknown aspects of the deregulation of parathyroid function. Secondary hyperparathyroidism is an important feature of chronic kidney disease\u2013mineral and bone disorder and plays an important role in the development of bone disease and vascular calcification. Thus, part of the management of chronic kidney disease relies on maintaining acceptable levels of mineral metabolism parameters in an attempt to slow down or prevent the development of secondary hyperparathyroidism. Here, we will also review the latest evidence regarding several aspects of the clinical and surgical management of secondary hyperparathyroidism.<\/ns4:p>","DOI":"10.12688\/f1000research.22636.1","type":"journal-article","created":{"date-parts":[[2020,9,1]],"date-time":"2020-09-01T14:25:29Z","timestamp":1598970329000},"page":"1077","update-policy":"https:\/\/doi.org\/10.12688\/f1000research.crossmark-policy","source":"Crossref","is-referenced-by-count":64,"title":["Recent advances in understanding and managing secondary hyperparathyroidism in chronic kidney disease"],"prefix":"10.12688","volume":"9","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-3696-582X","authenticated-orcid":false,"given":"Mar\u00eda E.","family":"Rodr\u00edguez-Ortiz","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariano","family":"Rodr\u00edguez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"2560","published-online":{"date-parts":[[2020,9,1]]},"reference":[{"key":"ref-1","doi-asserted-by":"publisher","first-page":"913-21","DOI":"10.2215\/CJN.06040710","article-title":"Secondary hyperparathyroidism: Pathogenesis, disease progression, and therapeutic options.","volume":"6","author":"J Cunningham","year":"2011","journal-title":"Clin J Am Soc Nephrol."},{"key":"ref-2","doi-asserted-by":"publisher","first-page":"79-95","DOI":"10.1007\/s11154-017-9421-4","article-title":"Secondary Hyperparthyroidism: Pathogenesis, Diagnosis, Preventive and Therapeutic Strategies.","volume":"18","author":"M Portillo","year":"2017","journal-title":"Rev Endocr Metab Disord."},{"key":"ref-3","doi-asserted-by":"publisher","first-page":"641-9","DOI":"10.1038\/nrneph.2013.147","article-title":"FGF-23 and secondary hyperparathyroidism in chronic kidney disease.","volume":"9","author":"J Silver","year":"2013","journal-title":"Nat Rev Nephrol."},{"key":"ref-4","doi-asserted-by":"publisher","first-page":"970-6","DOI":"10.1002\/jbmr.5650110714","article-title":"Direct effect of phosphorus on PTH secretion from whole rat parathyroid glands in vitro.","volume":"11","author":"Y Almaden","year":"1996","journal-title":"J Bone Miner Res."},{"key":"ref-5","doi-asserted-by":"crossref","first-page":"1762-8","DOI":"10.1093\/oxfordjournals.ndt.a027665","article-title":"A direct effect in vitro of phosphate on PTH release from bovine parathyroid tissue slices but not from dispersed parathyroid cells.","volume":"11","author":"P Nielsen","year":"1996","journal-title":"Nephrol Dial Transplant."},{"key":"ref-6","doi-asserted-by":"publisher","first-page":"2534-40","DOI":"10.1172\/JCI118701","article-title":"Phosphorus restriction prevents parathyroid gland growth. 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