scholarly journals Effects of sevelamer carbonate versus calcium acetate on vascular calcification, inflammation, and endothelial dysfunction in chronic kidney disease

2021 ◽  
Author(s):  
Darius L. Mason ◽  
Kavitha Godugu ◽  
Daryl Nnani ◽  
Shaker A. Mousa
Keyword(s):  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Calcium Acetate ◽  
Sevelamer Carbonate

scholarly journals Effects of Sevelamer Carbonate versus Calcium Acetate on Vascular Calcification, Inflammation, and Endothelial Dysfunction in Chronic Kidney Disease

2021 ◽  
Author(s):  
Darius Mason ◽  
Kavitha Godugu ◽  
Daryl Nnani ◽  
Shaker A. Mousa
Keyword(s):  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Hdl Cholesterol ◽  
Calcium Acetate ◽  
Phosphate Binders ◽  
Sevelamer Carbonate ◽  
Stage Renal Disease ◽  
End Stage

Rationale & Objective: Hyperphosphatemia is present in most patients with end-stage renal disease (ESRD) and has been associated with increased cardiovascular mortality. Phosphate binders (calcium-based and calcium free) are the mainstay pharmacologic treatment to lower phosphorus levels in patients with ESRD. Study Design: We evaluated biochemical markers of vascular calcification, inflammation, and endothelial dysfunction in patients with Chronic Kidney Disease (CKD) treated with sevelamer carbonate versus calcium acetate. Setting & Participants: We enrolled 50 CKD patients (stages 3 and 4) and treated them with sevelamer carbonate and calcium acetate for 12 weeks. Outcomes: At the end of the study the biomarkers of vascular calcification, inflammation, and endothelial dysfunction were analyzed. Results: A significant increase in HDL-cholesterol was observed with sevelamer carbonate but not with calcium acetate. Treatment with sevelamer carbonate reduced serum phosphate, calcium phosphate, and FGF-23 levels and there was no change with calcium acetate treatment. The inflammatory markers IL-8, IFN-γ, and TNFα decreased with response to both treatments. The levels of IL-6 significantly increased with calcium acetate treatment and no change was observed in the sevelamer carbonate treatment group. Conclusion: Sevelamer carbonate showed favorable effects on anti-inflammatory and vascular calcification biomarkers compared to calcium acetate treatment. Funding: Funding was received from Sanofi/Genzyme. Trial Registration: Registered at trial.com, registration number NCT01277497.

scholarly journals Reversal of the Adynamic Bone Disorder and Decreased Vascular Calcification in Chronic Kidney Disease by Sevelamer Carbonate Therapy

2006 ◽  
Vol 18 (1) ◽  
pp. 122-130 ◽  
Author(s):  
Suresh Mathew ◽  
Richard J. Lund ◽  
Frank Strebeck ◽  
Kimberly S. Tustison ◽  
Theresa Geurs ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Sevelamer Carbonate ◽  
Bone Disorder ◽  
Adynamic Bone

Author response for "Chronic Kidney Disease–Induced Vascular Calcification Impairs Bone Metabolism"

2020 ◽  
Author(s):  
Maria L Mace ◽  
Eva Gravesen ◽  
Anders Nordholm ◽  
Soeren Egstrand ◽  
Marya Morevati ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Metabolism ◽  
Vascular Calcification ◽  
Author Response

Correlation of Serum Sclerostin Levels with Carotid Intima Media Thickness in Chronic Kidney Disease Hemodialysis

2020 ◽  
Vol 6 (1) ◽  
pp. 18-26
Author(s):  
Adhi Permana ◽  
Ian Effendi ◽  
Taufik Indrajaya
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Ultrasound Examination ◽  
Intima Media Thickness ◽  
Carotid Intima Media Thickness ◽  
Media Thickness ◽  
The Mean ◽  
Sclerostin Level ◽  
Hemodialysis Duration

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.

Does Vitamin K Intake Influence High Phosphate Induced Vascular Pseudo-ossification: An Underappreciated Therapeutic Prospect in General Population?

2019 ◽  
Vol 20 (4) ◽  
pp. 421-430
Author(s):  
Zar Chi Thent ◽  
Gabriele R.A. Froemming ◽  
Suhaila Abd Muid
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Prolonged Exposure ◽  
Vascular Complication ◽  
Key Factors ◽  
The Matrix ◽  
Underlying Mechanisms ◽  
High Phosphate

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.

scholarly journals Role of crosstalk between endothelial cells and smooth muscle cells in vascular calcification in chronic kidney disease

2021 ◽  
Author(s):  
Yu‐Xia Zhang ◽  
Ri‐Ning Tang ◽  
Li‐Ting Wang ◽  
Bi‐Cheng Liu
Keyword(s):  
Chronic Kidney Disease ◽  
Endothelial Cells ◽  
Smooth Muscle ◽  
Kidney Disease ◽  
Smooth Muscle Cells ◽  
Vascular Calcification ◽  
Muscle Cells

scholarly journals POS-272 DIFFERENTIAL EFFECTS OF ENDOTHELIN ETA RECEPTOR BLOCKADE ON VASCULAR CALCIFICATION AND RENAL INJURY IN RATS WITH CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 6 (4) ◽  
pp. S115
Author(s):  
R. Lariviere ◽  
R.V. Ung ◽  
S. Picard ◽  
D. Richard ◽  
M. Agharazii ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Renal Injury ◽  
Receptor Blockade ◽  
Differential Effects ◽  
Eta Receptor
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