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[Frontiers in vitamin D; basic research and clinical application. Vitamin D and secondary hyperparathyroidism].
Clin Calcium. 2011 Nov; 21(11):27-34.CC

Abstract

In chronic kidney disease (CKD) , phosphate retention and low 1, 25-dihydroxyvitamin D [1, 25 (OH) ₂D] due to a decrease in the number of functioning nephrons had long been considered to contribute to the pathogenesis of secondary hyperparathyroidism (SHPT) . The discovery of fibroblast growth factor 23 (FGF23) drastically changed our understanding and provided new implication of the development of SHPT. In addition, CKD impairs the maintenance of normal 25-hydoxyvitamin D [25 (OH) D] levels which can act directly on the parathyroid glands to repress PTH synthesis. Active vitamin D therapy is widely used for the treatment of SHPT. However, the active form of vitamin D, 1, 25 (OH) ₂D and its analogs increase the calcium and phosphate levels by increasing the intestinal calcium and phosphate absorption. To suppress PTH secretion without these potential complications, several vitamin D analogs including paricalcitol, maxacalcitol and doxercalciferol are already in clinical use. A novel therapeutic concept in new vitamin D therapies are expected to improve patient outcome.

Authors+Show Affiliations

Division of Nephrology, Endocrinology and Metabolism, Tokai University School of Medicine, Japan.No affiliation info availableNo affiliation info available

Pub Type(s)

Journal Article
Review

Language

jpn

PubMed ID

22040818

Citation

Tanaka, Hisae, et al. "[Frontiers in Vitamin D; Basic Research and Clinical Application. Vitamin D and Secondary Hyperparathyroidism]." Clinical Calcium, vol. 21, no. 11, 2011, pp. 27-34.
Tanaka H, Komaba H, Fukagawa M. [Frontiers in vitamin D; basic research and clinical application. Vitamin D and secondary hyperparathyroidism]. Clin Calcium. 2011;21(11):27-34.
Tanaka, H., Komaba, H., & Fukagawa, M. (2011). [Frontiers in vitamin D; basic research and clinical application. Vitamin D and secondary hyperparathyroidism]. Clinical Calcium, 21(11), 27-34. https://doi.org/CliCa111116111618
Tanaka H, Komaba H, Fukagawa M. [Frontiers in Vitamin D; Basic Research and Clinical Application. Vitamin D and Secondary Hyperparathyroidism]. Clin Calcium. 2011;21(11):27-34. PubMed PMID: 22040818.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - [Frontiers in vitamin D; basic research and clinical application. Vitamin D and secondary hyperparathyroidism]. AU - Tanaka,Hisae, AU - Komaba,Hirotaka, AU - Fukagawa,Masafumi, PY - 2011/11/2/entrez PY - 2011/11/2/pubmed PY - 2012/2/10/medline SP - 27 EP - 34 JF - Clinical calcium JO - Clin Calcium VL - 21 IS - 11 N2 - In chronic kidney disease (CKD) , phosphate retention and low 1, 25-dihydroxyvitamin D [1, 25 (OH) ₂D] due to a decrease in the number of functioning nephrons had long been considered to contribute to the pathogenesis of secondary hyperparathyroidism (SHPT) . The discovery of fibroblast growth factor 23 (FGF23) drastically changed our understanding and provided new implication of the development of SHPT. In addition, CKD impairs the maintenance of normal 25-hydoxyvitamin D [25 (OH) D] levels which can act directly on the parathyroid glands to repress PTH synthesis. Active vitamin D therapy is widely used for the treatment of SHPT. However, the active form of vitamin D, 1, 25 (OH) ₂D and its analogs increase the calcium and phosphate levels by increasing the intestinal calcium and phosphate absorption. To suppress PTH secretion without these potential complications, several vitamin D analogs including paricalcitol, maxacalcitol and doxercalciferol are already in clinical use. A novel therapeutic concept in new vitamin D therapies are expected to improve patient outcome. SN - 0917-5857 UR - https://www.unboundmedicine.com/medline/citation/22040818/[Frontiers_in_vitamin_D L2 - https://medlineplus.gov/vitamind.html DB - PRIME DP - Unbound Medicine ER -