scholarly journals Insight into the impact of vitamin D on cardiovascular outcomes in chronic kidney disease

Nephrology ◽  
2019 ◽  
Vol 24 (8) ◽  
pp. 781-790 ◽  
Author(s):  
Joey Junarta ◽  
Vivekanand Jha ◽  
Debasish Banerjee
2016 ◽  
Vol 2016 ◽  
pp. 1-21 ◽  
Author(s):  
José Pedraza-Chaverri ◽  
Laura G. Sánchez-Lozada ◽  
Horacio Osorio-Alonso ◽  
Edilia Tapia ◽  
Alexandra Scholze

In chronic kidney disease inflammatory processes and stimulation of immune cells result in overproduction of free radicals. In combination with a reduced antioxidant capacity this causes oxidative stress. This review focuses on current pathogenic concepts of oxidative stress for the decline of kidney function and development of cardiovascular complications. We discuss the impact of mitochondrial alterations and dysfunction, a pathogenic role for hyperuricemia, and disturbances of vitamin D metabolism and signal transduction. Recent antioxidant therapy options including the use of vitamin D and pharmacologic therapies for hyperuricemia are discussed. Finally, we review some new therapy options in diabetic nephropathy including antidiabetic agents (noninsulin dependent), plant antioxidants, and food components as alternative antioxidant therapies.


2021 ◽  
Vol 2021 ◽  
pp. 1-9
Author(s):  
Safaa Ali ◽  
Mohamed Saber ◽  
Mohamed Kassem

Objective. To evaluate the association of bone mineral biomarkers of calcium, phosphorus metabolism, and 25-hydroxy vitamin D with diastolic dysfunction of the left ventricle and left ventricle mass in predialysis chronic kidney children. Patients and Methods. A cross-sectional observational study was conducted on 60 children with chronic kidney disease and treated by conservative treatment from October 2018 to September 2019 in the Pediatric Nephrology and Cardiology Department at our University Hospital. Results. The most common causes of CKD were congenital renal anomalies accounted for 22 (36.67%) of the studied cases. The mean age of children was 7.05 ± 2.74   years , and 32 (53.33%) were males. The children who had a normal diastolic function were 32 (53.33%), while those who had diastolic dysfunction were 28 (46.67%). There was a statistically significant in serum phosphorus ( p value = 0.03), serum PTH ( p value = 0.002), and hypertension ( p value = 0.03). There was a statistically significant positive correlation between LVMI and iPTH level ( r = 0.89 , p ≤ 0.0001 ), 25(OH) cholecalciferol ( r = − 0.27 , p = 0.04 ), serum Ca ( r = − 0.37 , p = 0.004 ), and serum phosphorus ( r = − 0.45 , p = 0.0003 ). Conclusion. Our results revealed that hyperparathyroidism, hyperphosphatemia, and hypertension were significantly associated with diastolic dysfunction while hypovitaminosis D was not significantly associated. Vitamin D deficiency was prevalent in all children with CKD. Biomarkers of mineral bone density were significantly associated with left ventricular hypertrophy and increased left ventricular mass index.


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.


2020 ◽  
Vol 29 ◽  
pp. S150-S151
Author(s):  
A. Bhat ◽  
S. Karthikeyan ◽  
M. Denniss ◽  
M. Kayes ◽  
A. Gupta ◽  
...  

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.


2014 ◽  
Vol 8 (1) ◽  
pp. 41-48 ◽  
Author(s):  
M. C. Mann ◽  
A. J. Hobbs ◽  
B. R. Hemmelgarn ◽  
D. J. Roberts ◽  
S. B. Ahmed ◽  
...  

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

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