scholarly journals Effects of repetitive diet-induced fluctuations in plasma phosphorus on vascular calcification and inflammation in rats with early-stage chronic kidney disease

2020 ◽  
Vol 66 (2) ◽  
pp. 139-145 ◽  
Author(s):  
Mariko Tani ◽  
Sarasa Tanaka ◽  
Kana Takamiya ◽  
Motoyoshi Sakaue ◽  
Mikiko Ito
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Early Stage ◽  
Plasma Phosphorus

Vascular Calcification in Patients with Early-Stage Chronic Kidney Disease: The Pivotal Role of Estimated Glomerular Filtration Rate

2021 ◽  
Vol 104 (6) ◽  
pp. 989-997
Keyword(s):  
Chronic Kidney Disease ◽  
Glomerular Filtration Rate ◽  
Kidney Disease ◽  
Glomerular Filtration ◽  
Vascular Calcification ◽  
Filtration Rate ◽  
Estimated Glomerular Filtration Rate ◽  
Early Stage ◽  
Abdominal Aortic Calcification ◽  
Abdominal Aortic

Background: Vascular calcification in advanced chronic kidney disease (CKD) is correlated with uremic toxins and severely impaired calciumphosphate- parathyroid metabolism. The association factors of vascular calcification in early-stage CKD are still unestablished. Objective: To identify the risk factors for vascular calcification in the early-stage CKD, which was the non-target population, different from other previous studies that explored this association in advanced stage CKD. Materials and Methods: The present study was a longitudinal study conducted to examine the risk factors of vascular calcification in CKD stage G2 and G3 patients who had no previous cardiovascular diseases. All parameters including coronary artery calcification (CAC) and abdominal aortic calcification (AAC) at baseline and after twelve months were evaluated. Results: Twenty-two patients without established cardiovascular diseases were included and completed the follow-up period. Mean baseline LDL was 99 mg/dL and no patient received statin. At 12-month, the median CAC score was significantly increased to 266 (126 to 956) versus 282 (198 to 846), (p=0.024]. By multivariable analysis in generalized estimating equations, only estimated glomerular filtration rate (eGFR) was associated with CAC score greater than 400 (aOR 0.92, p=0.041), and AAC score greater than 5 (aOR 0.90, p=0.023). Conclusion: In early-stage CKD, eGFR was associated with vascular calcification. Further studies should explore the potential benefits of delaying CKD progression on vascular calcification in the early-stage CKD patients. Keywords: Chronic kidney disease; Vascular calcification; Coronary artery calcification; Abdominal aortic calcification; Glomerular filtration rate; Renal function

scholarly journals Vascular Calcification and Renal Bone Disorders

2014 ◽  
Vol 2014 ◽  
pp. 1-20 ◽  
Author(s):  
Kuo-Cheng Lu ◽  
Chia-Chao Wu ◽  
Jen-Fen Yen ◽  
Wen-Chih Liu
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Bone Turnover ◽  
Vascular Calcification ◽  
Serum Calcium ◽  
Mineral Metabolism ◽  
Early Stage ◽  
Mineral Bone Disorder ◽  
High Bone ◽  
The Individual

At the early stage of chronic kidney disease (CKD), the systemic mineral metabolism and bone composition start to change. This alteration is known as chronic kidney disease-mineral bone disorder (CKD-MBD). It is well known that the bone turnover disorder is the most common complication of CKD-MBD. Besides, CKD patients usually suffer from vascular calcification (VC), which is highly associated with mortality. Many factors regulate the VC mechanism, which include imbalances in serum calcium and phosphate, systemic inflammation, RANK/RANKL/OPG triad, aldosterone, microRNAs, osteogenic transdifferentiation, and effects of vitamins. These factors have roles in both promoting and inhibiting VC. Patients with CKD usually have bone turnover problems. Patients with high bone turnover have increase of calcium and phosphate release from the bone. By contrast, when bone turnover is low, serum calcium and phosphate levels are frequently maintained at high levels because the reservoir functions of bone decrease. Both of these conditions will increase the possibility of VC. In addition, the calcified vessel may secrete FGF23 and Wnt inhibitors such as sclerostin, DKK-1, and secreted frizzled-related protein to prevent further VC. However, all of them may fight back the inhibition of bone formation resulting in fragile bone. There are several ways to treat VC depending on the bone turnover status of the individual. The main goals of therapy are to maintain normal bone turnover and protect against VC.

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.

ASSESSMENT OF KIDNEY FUNCTIONAL RESERVE ON THE BACKGROUND OF ANTI-AGGREGATE THERAPY IN CHRONIC KIDNEY DISEASE II-III STAGE

2020 ◽  
Vol 6 (1) ◽  
pp. 49-54
Author(s):  
Khabib Barnoev ◽  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Comparative Study ◽  
Early Stage ◽  
Raw Material ◽  
Functional Reserve ◽  
Functional Reserves ◽  
Term Administration ◽  
Antiaggregant Therapy

The article presents the results of a study to assess the functional reserve of the kidneys against the background of a comparative study of antiaggregant therapy dipyridamole and allthrombosepin in 50 patients with a relatively early stage of chronic kidney disease. Studies have shown that long-term administration of allthrombosepin to patients has resulted in better maintenance of kidney functional reserves. Therefore, our research has once again confirmed that diphtheridamol, which is widely used as an antiaggregant drug in chronic kidney disease, does not lag behind the domestic raw material allthrombosepin

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.

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