Abstract
In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.
Original language | English |
---|---|
Article number | 1890 |
Journal | Nutrients |
Volume | 10 |
Issue number | 12 |
DOIs | |
Publication status | Published - Dec 1 2018 |
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Keywords
- Calcimimetics
- Calcitriol
- Nutritional vitamin D
- Secondary hyperparathyroidism
ASJC Scopus subject areas
- Food Science
- Nutrition and Dietetics
Cite this
The emerging role of nutritional vitamin D in secondary hyperparathyroidism in ckd. / Lu, Chien Lin; Yeih, Dong Feng; Hou, Yi Chou; Jow, Guey Mei; Li, Zong Yu; Liu, Wen Chih; Zheng, Cai Mei; Lin, Yuh Feng; Shyu, Jia Fwu; Chen, Remy; Huang, Chung Yu; Lu, Kuo Cheng.
In: Nutrients, Vol. 10, No. 12, 1890, 01.12.2018.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - The emerging role of nutritional vitamin D in secondary hyperparathyroidism in ckd
AU - Lu, Chien Lin
AU - Yeih, Dong Feng
AU - Hou, Yi Chou
AU - Jow, Guey Mei
AU - Li, Zong Yu
AU - Liu, Wen Chih
AU - Zheng, Cai Mei
AU - Lin, Yuh Feng
AU - Shyu, Jia Fwu
AU - Chen, Remy
AU - Huang, Chung Yu
AU - Lu, Kuo Cheng
PY - 2018/12/1
Y1 - 2018/12/1
N2 - In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.
AB - In chronic kidney disease (CKD), hyperphosphatemia induces fibroblast growth factor-23 (FGF-23) expression that disturbs renal 1,25-dihydroxy vitamin D (1,25D) synthesis; thereby increasing parathyroid hormone (PTH) production. FGF-23 acts on the parathyroid gland (PTG) to increase 1α-hydroxylase activity and results in increase intra-gland 1,25D production that attenuates PTH secretion efficiently if sufficient 25D are available. Interesting, calcimimetics can further increase PTG 1α-hydroxylase activity that emphasizes the demand for nutritional vitamin D (NVD) under high PTH status. In addition, the changes in hydroxylase enzyme activity highlight the greater parathyroid 25-hydroxyvitmain D (25D) requirement in secondary hyperparathyroidism (SHPT); the higher proportion of oxyphil cells as hyperplastic parathyroid progression; lower cytosolic vitamin D binding protein (DBP) content in the oxyphil cell; and calcitriol promote vitamin D degradation are all possible reasons supports nutritional vitamin D (NVD; e.g., Cholecalciferol) supplement is crucial in SHPT. Clinically, NVD can effectively restore serum 25D concentration and prevent the further increase in PTH level. Therefore, NVD might have the benefit of alleviating the development of SHPT in early CKD and further lowering PTH in moderate to severe SHPT in dialysis patients.
KW - Calcimimetics
KW - Calcitriol
KW - Nutritional vitamin D
KW - Secondary hyperparathyroidism
UR - http://www.scopus.com/inward/record.url?scp=85058048097&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=85058048097&partnerID=8YFLogxK
U2 - 10.3390/nu10121890
DO - 10.3390/nu10121890
M3 - Article
AN - SCOPUS:85058048097
VL - 10
JO - Nutrients
JF - Nutrients
SN - 2072-6643
IS - 12
M1 - 1890
ER -