Nutritional vitamin D in CKD: Should we measure? Should we treat?

2020 ◽  
Vol 501 ◽  
pp. 186-197 ◽  
Author(s):  
Irene Capelli ◽  
Giuseppe Cianciolo ◽  
Lorenzo Gasperoni ◽  
Andrea Galassi ◽  
Paola Ciceri ◽  
...  
Keyword(s):  
Vitamin D ◽  
Nutritional Vitamin

Nutritional vitamin D: the benefits of supplementation

2008 ◽  
Vol 7 (5) ◽  
pp. 490-492
Author(s):  
David A Bushinsky ◽  
Justin Silver
Keyword(s):  
Vitamin D ◽  
Nutritional Vitamin

Role of nutritional vitamin D in osteoporosis treatment

2018 ◽  
Vol 484 ◽  
pp. 179-191 ◽  
Author(s):  
Yi-Chou Hou ◽  
Chia-Chao Wu ◽  
Min-Tser Liao ◽  
Jia-Fwu Shyu ◽  
Chi-Feng Hung ◽  
...  
Keyword(s):  
Vitamin D ◽  
Osteoporosis Treatment ◽  
Nutritional Vitamin

scholarly journals The Emerging Role of Nutritional Vitamin D in Secondary Hyperparathyroidism in CKD

Nutrients ◽  
2018 ◽  
Vol 10 (12) ◽  
pp. 1890 ◽  
Author(s):  
Chien-Lin Lu ◽  
Dong-Feng Yeih ◽  
Yi-Chou Hou ◽  
Guey-Mei Jow ◽  
Zong-Yu Li ◽  
...  
Keyword(s):  
Vitamin D ◽  
Secondary Hyperparathyroidism ◽  
Fibroblast Growth Factor 23 ◽  
Vitamin D Binding Protein ◽  
Hydroxylase Activity ◽  
Fgf 23 ◽  
Oxyphil Cell ◽  
Pth Level ◽  
Nutritional Vitamin

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.

scholarly journals Circulating 25-Hydroxyvitamin D Levels in Fully Breastfed Infants on Oral Vitamin D Supplementation

2010 ◽  
Vol 2010 ◽  
pp. 1-5 ◽  
Author(s):  
Carol L. Wagner ◽  
Cindy Howard ◽  
Thomas C. Hulsey ◽  
Ruth A. Lawrence ◽  
Sarah N. Taylor ◽  
...  
Keyword(s):  
Vitamin D ◽  
Vitamin D Supplementation ◽  
Vitamin Supplementation ◽  
Oral Vitamin ◽  
Oil Emulsion ◽  
Hydroxyvitamin D ◽  
Breastfed Infants ◽  
25 Hydroxyvitamin D ◽  
The Mean ◽  
Nutritional Vitamin

Objective. To examine the effectiveness of oral vitamin (400 IU) supplementation on the nutritional vitamin D status of breastfeeding infants.Design. As part of a larger ongoing vitamin D RCT trial of lactating women, infants of mothers assigned to control received 1 drop of 400 IU vitamin /day starting at one month of age. Infant 25(OH)D levels (mean S.D.) were measured by RIA at visits 1, 4, and 7.Results. The infant mean S.D. 25(OH)D at baseline was 16.0 9.3 ng/mL (range 1.0–40.8; ); 24 (72.7%) had baseline levels <20 ng/mL (consistent with deficiency). The mean levels increased to 43.6 14.1 (range 18.2–69.7) at 4 months and remained relatively unchanged at month 7: 42.5 12.1 ng/mL (range 18.9–67.2). The change in values between 1 and 4 months and 1 and 7 months was statistically significant , and despite a decrease in dose per kilogram, values were not significantly different between months 4 and 7 .Conclusions. Oral vitamin supplementation as an oil emulsion was associated with significant and sustained increases in 25(OH)D from baseline in fully breastfeeding infants through 7 months.

scholarly journals Nutritional Vitamin D in Renal Transplant Patients: Speculations and Reality

Nutrients ◽  
2017 ◽  
Vol 9 (6) ◽  
pp. 550 ◽  
Author(s):  
Piergiorgio Messa ◽  
Anna Regalia ◽  
Carlo Alfieri
Keyword(s):  
Vitamin D ◽  
Renal Transplant ◽  
Transplant Patients ◽  
Renal Transplant Patients ◽  
Nutritional Vitamin

scholarly journals P0891META-ANALYSIS OF NUTRITIONAL VITAMIN D FOR THE TREATMENT OF SECONDARY HYPERPARATHYROIDISM IN PATIENTS WITH NON-DIALYSIS CHRONIC KIDNEY DISEASE

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Joel Gunnarsson ◽  
Rosa Lauppe ◽  
Edelgard Kaiser ◽  
Marco Soro ◽  
Philipp Csomor
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Secondary Hyperparathyroidism ◽  
Fixed Effects ◽  
Untreated Patient ◽  
Critical Role ◽  
Vitamin D Levels ◽  
Patient Groups ◽  
Nutritional Vitamin

Abstract Background and Aims Chronic kidney disease (CKD) is commonly associated with mineral and bone disorder (CKD-MBD). Secondary hyperparathyroidism (SHPT) is a critical component of CKD-MBD characterized by excessive PTH secretion and parathyroid hyperplasia. SHPT develops in CKD because of disturbances in CKD-MBD parameters such as increases in serum phosphate and fibroblast growth factor 23, and reductions in 25-hydroxyvitamin D (25(OH)D), 1,25-dihydroxyvitamin D (1,25(OH)2D) and serum calcium. Low vitamin D levels play a critical role in the development and progression of SHPT. Nutritional vitamin D (NVD) supplements are being frequently used to address SHPT, especially in early CKD. The objective of this meta-analysis (MA) was to evaluate the effectiveness of the NVDs cholecalciferol and ergocalciferol in reducing PTH and increasing 25(OH)D in patients with non-dialysis CKD (ND-CKD). Method A systematic literature search was performed in PubMed to identify relevant randomized control trials (RCTs) to be included in the MA. All analyses were performed using both random and fixed effects models with inverted-variance weighting. Comparisons were made between the effects of NVDs relative to placebo-treated or untreated patients and between the baseline and end-of-study values of the patients treated with the NVDs, i.e. the effects in treated patients only. Results A total of 14 RCTs comprising 974 patients were included in the analyses. Overall reductions in PTH were small when compared to baseline (reduction of 10.95 pg/ml, 95 % confidence interval (CI): -15.99 to -5.91 pg/ml), while reductions in PTH were approximately three times larger when compared to placebo-treated or untreated patient groups (reduction of 34.35 pg/ml, 95 % CI:-47.47 to -21.24 pg/ml). This indicated a limited potential to actively lower PTH with NVDs as the relative effect on PTH when compared to placebo-treated or untreated patient groups was driven to a large degree by increases in PTH in the comparator arms. Treatment with NVDs tended to increase levels of 25(OH)D both when compared to placebo-treated or untreated patients (increase of 26.54 ng/ml, 95 % CI: 24.62 to 28.46 ng/ml) and when only the changes in treated patients were considered (increase of 21.49 ng/ml, 95 % CI: 20.54 to 22.44 ng/ml). However, large variations in effect sizes on levels of 25(OH)D were observed, making judgements about the size of any true treatment effect difficult. Average levels of 25(OH)D in treated patients at the end of the study period were &gt;30 ng/ml in all but two RCTs and &gt;50 ng/ml in only five of the included RCTs. No clear relationship was observed between study length (range: 4 to 144 weeks) or doses administered (range: 14 000 to 75 000 UI weekly average) and effects on 25(OH)D or PTH. Conclusion Our results suggest that treatment with NVDs is not efficacious to reliably and consistently lower PTH in ND-CKD patients with SHPT. Although treatment with NVDs can potentially be used to correct vitamin D insufficiency, our results suggest that the potential of NVD treatment to raise 25(OH)D levels to &gt;50 ng/ml, a level needed to reduce PTH, is limited.

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