scholarly journals Impact of nutritional vitamin D supplementation on parathyroid hormone and 25-hydroxyvitamin D levels in non-dialysis chronic kidney disease: a Meta-analysis

2021 ◽  
Author(s):  
Jordi Bover ◽  
Joel Gunnarsson ◽  
Philipp Csomor ◽  
Edelgard Kaiser ◽  
Giuseppe Cianciolo ◽  
...  

Abstract Background Secondary hyperparathyroidism (SHPT) is a common and major complication in chronic kidney disease (CKD), reflecting the increase of parathyroid hormone (PTH) in response to reduced Vitamin D signaling and hypocalcemia. This meta-analysis evaluated the impact of nutritional vitamin D (NVD) (cholecalciferol or ergocalciferol) on SHPT-related biomarkers. Methods A systematic literature search was performed in PubMed to identify relevant randomized control trials (RCTs) to be included in the meta-analysis. Fixed and random effects models were used to pool study level results. Effects were studied within NVD study arms and relative to control groups (placebo/no treatment); the former in order to identify the effect of actively altering biomarkers levels. Results Reductions in PTH from supplementation with NVD were small when observed within the NVD study arms (pooled reduction: 10.5 pg/ml) and larger when compared to placebo/no treatment (pooled reduction: 49.7 pg/ml). NVD supplementation increased levels of vitamin D (25(OH)D) in both analyses (increase within NVD study arm: 20.6 ng/ml, increase versus placebo/no treatment: 26.9 ng/ml). While small and statistically non-significant changes in phosphate and fibroblast growth factor 23 (FGF23) were observed, NVD supplementation caused calcium levels to increase when compared versus placebo/no treatment (increase: 0.23 mg/dl). Conclusions Our results suggest that supplementation with NVD can be used to increase 25(OH)D to a certain extent, while the potential of NVD to actively reduce PTH in ND-CKD patients with SHPT is limited.

2014 ◽  
Vol 86 (2) ◽  
pp. 407-413 ◽  
Author(s):  
Maarten W. Taal ◽  
Victoria Thurston ◽  
Natasha J. McIntyre ◽  
Richard J. Fluck ◽  
Christopher W. McIntyre

Author(s):  
Alexandra Voinescu ◽  
Nadia Wasi Iqbal ◽  
Kevin J. Martin

Chronic kidney disease is associated with the inability to control normal mineral homeostasis, resulting in abnormalities in serum levels of calcium, phosphorus, parathyroid hormone, fibroblast growth factor 23 (FGF23) and vitamin D metabolism. These disturbances lead to the development of secondary hyperparathyroidism, skeletal abnormalities, vascular calcifications, and other systemic manifestations. Traditionally, mineral and bone abnormalities seen in chronic kidney disease were included in the term ‘renal osteodystrophy’. More recently, the term chronic kidney disease-mineral and bone disorder was introduced to define the biochemical abnormalities of phosphorus, parathyroid hormone, FGF23, calcium, or vitamin D metabolism, abnormalities in bone remodelling and mineralization, and vascular or other soft tissue calcifications.


2011 ◽  
Vol 44 (1) ◽  
pp. 167-171 ◽  
Author(s):  
Chrysoula Pipili ◽  
Chrysostomos Dimitriadis ◽  
Nigar Sekercioglu ◽  
Joanne M. Bargman ◽  
Dimitrios D. Oreopoulos

Author(s):  
Marilena Christodoulou ◽  
Terence J. Aspray ◽  
Inez Schoenmakers

AbstractA large proportion of patients with chronic kidney disease (CKD) are vitamin D deficient (plasma 25-hydroxyvitamin D (25(OH)D) < 25 or 30 nmol/L per UK and US population guidelines) and this contributes to the development of CKD–mineral bone disease (CKD–MBD). Gaps in the evidence-base for the management of vitamin D status in relation to CKD–MBD are hindering the formulation of comprehensive guidelines. We conducted a systemic review of 22 RCTs with different forms of vitamin D or analogues with CKD–MBD related outcomes and meta-analyses for parathyroid hormone (PTH). We provide a comprehensive overview of current guidelines for the management of vitamin D status for pre-dialysis CKD patients. Vitamin D supplementation had an inconsistent effect on PTH concentrations and meta-analysis showed non- significant reduction (P = 0.08) whereas calcifediol, calcitriol and paricalcitol consistently reduced PTH. An increase in Fibroblast Growth Factor 23 (FGF23) with analogue administration was found in all 3 studies reporting FGF23, but was unaltered in 4 studies with vitamin D or calcifediol. Few RCTS reported markers of bone metabolism and variations in the range of markers prevented direct comparisons. Guidelines for CKD stages G1–G3a follow general population recommendations. For the correction of deficiency general or CKD-specific patient guidelines provide recommendations. Calcitriol or analogues administration is restricted to stages G3b–G5 and depends on patient characteristics. In conclusion, the effect of vitamin D supplementation in CKD patients was inconsistent between studies. Calcifediol and analogues consistently suppressed PTH, but the increase in FGF23 with calcitriol analogues warrants caution.


2013 ◽  
Vol 2013 ◽  
pp. 1-10 ◽  
Author(s):  
Andrea Galassi ◽  
Antonio Bellasi ◽  
Sara Auricchio ◽  
Sergio Papagni ◽  
Mario Cozzolino

Vitamin D is a common treatment against secondary hyperparathyroidism in renal patients. However, the rationale for the prescription of vitamin D sterols in chronic kidney disease (CKD) is rapidly increasing due to the coexistence of growing expectancies close to unsatisfactory evidences, such as (1) the lack of randomized controlled trials (RCTs) proving the superiority of any vitamin D sterol against placebo on patients centered outcomes, (2) the scanty clinical data on head to head comparisons between the multiple vitamin D sterols currently available, (3) the absence of RCTs confirming the crescent expectations on nutritional vitamin D pleiotropic effects even in CKD patients, (4) the promising effects of vitamin D receptors activators (VDRA) against proteinuria and myocardial hypertrophy in diabetic CKD cohorts, and (5) the conflicting data on the impact on mortality of VDRA versus calcimimetic centered regimens to control CKD-MBD. The present review arguments these issues focusing on the opened questions that nephrologists should consider dealing with the prescription of nutritional vitamin D or VDRA and with the choice of a VDRA versus a calcimimetic based regimen in CKD-MBD patients.


2018 ◽  
Vol 33 (12) ◽  
pp. 2208-2217 ◽  
Author(s):  
Christian Lerch ◽  
Rukshana Shroff ◽  
Mandy Wan ◽  
Lesley Rees ◽  
Helen Aitkenhead ◽  
...  

2021 ◽  
Vol 10 (9) ◽  
pp. e53310917752
Author(s):  
Letícya Thaís Mendes Viana ◽  
Larissa Lages Rodrigues ◽  
Jurandy do Nascimento Silva ◽  
Maria Márcia Dantas de Sousa ◽  
Fhanuel Silva Andrade ◽  
...  

Chronic Kidney Disease (CKD) is an injury that causes progressive impairment of exocrine and endocrine renal functions. A very common complication is anemia, caused by reduced erythropoietin production, iron deficiency and inflammation. Evidence demonstrates that vitamin D has effects on anemia of inflammation, through the increase in erythrocytes and decrease in pro-inflammatory cytokines. This study aims to review the effects of vitamin D supplementation on 25(OH)D2 concentrations, on anemia markers and on PTH levels. This is an integrative review carried out through the search and selection of original publications, in english and portuguese, indexed in PubMed, Web of Science and Science Direct databases belonging to the 2010-2020 range. The results pointed to 25(OH)D2 concentrations compatible with normality after vitamin D supplementation. In five studies, there was no change in hemoglobin and PTH levels, and in four studies there was a reduction in the dose of EPO or erythroid stimulating agent, attributing such effect on the role of calcitriol as a substrate for bone marrow erythropoietic cells. The study concluded that vitamin D supplementation had beneficial effects for correction of 25(OH)D2 deficiency, however, it reinforces the controversy about the behavior of vitamin D on the improvement of anemia markers and PTH levels in patients with DRC. Therefore, it is suggested that the beneficial effect of vitamin D on anemia in renal patients may be independent of PTH suppression.


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