Sclerostin as a new key factor in vascular calcification in chronic kidney disease stages 3 and 4

2016 ◽  
Vol 48 (12) ◽  
pp. 2043-2050 ◽  
Author(s):  
Wei Lv ◽  
Lina Guan ◽  
Yan Zhang ◽  
Shengqiang Yu ◽  
Bofeng Cao ◽  
...  
2019 ◽  
pp. 78-85
Author(s):  
S. A. Martynov ◽  
M. Sh. Shamkhalova

Hyperphosphatemia in renal pathology is a key factor for developing mineral and bone disorders. It can develop even in the early stages of renal function decline and predict the formation of vascular calcification and an increased risk for developing cardiovascular complications in patients with chronic kidney disease, especially in those, who receive program hemodialysis. The use of calcium-free phosphate-binding agents that are not associated with the risk for developing hypercalcemia can slow the development of vascular calcification, reduce the incidence of adverse cardiovascular events and mortality in patients with chronic kidney disease.


2015 ◽  
Vol 125 (9) ◽  
pp. 631-640 ◽  
Author(s):  
Ilona Kurnatowska ◽  
Piotr Grzelak ◽  
Anna Masajtis-Zagajewska ◽  
Magdalena Kaczmarska ◽  
Ludomir Stefańczyk ◽  
...  

2020 ◽  
Author(s):  
Maria L Mace ◽  
Eva Gravesen ◽  
Anders Nordholm ◽  
Soeren Egstrand ◽  
Marya Morevati ◽  
...  

Author(s):  
Adhi Permana ◽  
Ian Effendi ◽  
Taufik Indrajaya

Chronic kidney disease is associated with a high mortality rate, especially cardiovascular disease associated with mineral and bone disorders. Sclerostin is an inhibitor of Wnt signaling which has the effect of increasing the occurrence of vascular calcification in patients with chronic kidney disease. There are several studies that show different results. Carotid intima media thickness ultrasound examination is a tool to identify atherosclerosis which is part of vascular calcification. The aim of this study is to look at the correlation of sclerostin with carotid intima media thickness (CIMT) in patients with chronic kidney disease undergoing hemodialysis. In this cross section, the concentration of sclerostin was measured by examination of enzymed linked immunosorbent assay. CIMT measurement by ultrasound mode B examination. There were 40 patients in this study. The mean sclerostin level was 256.68 ± 127.76 pg / ml. Sclerostin levels are declared high if above 162 pg / ml there are 30 people. CIMT thickening was present in 11 patients. There was no significant correlation of serum sclerostin with CIMT in patients with chronic kidney disease undergoing hemodialysis (r-0.32 p0,847). In multivariate linear regression, hemodialysis duration is an independent factor that is significantly significant with CIMT. There was no significant correlation of serum sclerostin with CIMT in patients with chronic kidney disease undergoing hemodialysis.


2019 ◽  
Vol 20 (4) ◽  
pp. 421-430
Author(s):  
Zar Chi Thent ◽  
Gabriele R.A. Froemming ◽  
Suhaila Abd Muid

Increasing interest in vascular pseudo-ossification has alarmed the modern atherosclerotic society. High phosphate is one of the key factors in vascular pseudo ossification, also known as vascular calcification. The active process of deposition of the phosphate crystals in vascular tissues results in arterial stiffness. High phosphate condition is mainly observed in chronic kidney disease patients. However, prolonged exposure with high phosphate enriched foods such as canned drinks, dietary foods, etc. can be considered as modifiable risk factors for vascular complication in a population regardless of chronic kidney disease. High intake of vitamin K regulates the vascular calcification by exerting its anti-calcification effect. The changes in serum phosphate and vitamin K levels in a normal individual with high phosphate intake are not well investigated. This review summarised the underlying mechanisms of high phosphate induced vascular pseudo ossification such as vascular transdifferentiation, vascular apoptosis and phosphate uptake by sodium-dependent co-transporters. Pubmed, Science Direct, Scopus, ISI Web of Knowledge and Google Scholar were searched using the terms ‘vitamin K’, ‘vascular calcification, ‘phosphate’, ‘transdifferentiation’ and ‘vascular pseudoossification’. Vitamin K certainly activates the matrix GIA protein and inhibits vascular transition and apoptosis in vascular pseudo-ossification. The present view highlighted the possible therapeutic linkage between vitamin K and the disease. Understanding the role of vitamin K will be considered as potent prophylaxis agent against the vascular disease in near future.


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