Role of vascular calcification inhibitors in preventing vascular dysfunction and mortality in hemodialysis patients

2017 ◽  
Vol 31 (1) ◽  
pp. 72-81 ◽  
Author(s):  
Ozkan Gungor ◽  
Ismail Kocyigit ◽  
Mahmut Ilker Yilmaz ◽  
Siren Sezer
Keyword(s):  
Vascular Calcification ◽  
Vascular Dysfunction ◽  
Hemodialysis Patients ◽  
Calcification Inhibitors

scholarly journals Circulating microRNAs and vascular calcification in hemodialysis patients

2019 ◽  
Vol 47 (7) ◽  
pp. 2929-2939 ◽  
Author(s):  
Chien-Te Lee ◽  
Yueh-Ting Lee ◽  
You-Lin Tain ◽  
Hwee-Yeong Ng ◽  
Wei-Hung Kuo
Keyword(s):  
Vascular Calcification ◽  
Fibroblast Growth Factor 23 ◽  
High Sensitivity ◽  
Hemodialysis Patients ◽  
Blood Levels ◽  
Circulating Micrornas ◽  
Reactive Protein ◽  
Calcification Score ◽  
Circulating Levels

Objective Vascular calcification is common in chronic dialysis patients and is associated with increased morbidity and mortality. However, the role of circulating microRNAs (miRs) in vascular calcification has rarely been investigated. We aimed to determine circulating levels of miRs in hemodialysis patients, and analyzed their relationship with vascular calcification. Methods Sixty-one stable hemodialysis patients were enrolled, including 31 with vascular calcification and 30 without. Demographic and biochemical data were collected and reviewed. The presence and severity of vascular calcification were determined by lumber spine X-ray. Blood levels of miR29a/b, miR223, miR9, and miR21 were determined. Results Patients with vascular calcification were older (65.6 ± 9.0 vs. 59.1 ± 7.1 years) with a higher proportion of vascular disease (55% vs. 23%) than those without vascular calcification. Additionally, high-sensitivity C-reactive protein (3.90 vs 2.09 mg/dL) and fibroblast growth factor 23 (17311 vs. 6306 pg/mL) were significantly higher. Patients with vascular calcification also had higher levels of miR29a/b and miR223. Regression analysis indicated that age and miR29a were significant associates of the calcification score. Conclusions Hemodialysis patients with vascular calcification had higher levels of miR 29a/b and miR223 than those without vascular calcification, and circulating miR29a was associated with calcification severity.

scholarly journals Lanthionine, a Novel Uremic Toxin, in the Vascular Calcification of Chronic Kidney Disease: The Role of Proinflammatory Cytokines

2021 ◽  
Vol 22 (13) ◽  
pp. 6875
Author(s):  
Alessandra Fortunata Perna ◽  
Luigi Russo ◽  
Vittoria D’Esposito ◽  
Pietro Formisano ◽  
Dario Bruzzese ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Hemodialysis Patient ◽  
Calcium Score ◽  
Hemodialysis Patients ◽  
Agatston Score ◽  
Uremic Toxin ◽  
Total Calcium

Vascular calcification (VC) is a risk factor for cardiovascular events and mortality in chronic kidney disease (CKD). Several components influence the occurrence of VC, among which inflammation. A novel uremic toxin, lanthionine, was shown to increase intracellular calcium in endothelial cells and may have a role in VC. A group of CKD patients was selected and divided into patients with a glomerular filtration rate (GFR) of <45 mL/min/1.73 m2 and ≥45 mL/min/1.73 m2. Total Calcium Score (TCS), based on the Agatston score, was assessed as circulating lanthionine and a panel of different cytokines. A hemodialysis patient group was also considered. Lanthionine was elevated in CKD patients, and levels increased significantly in hemodialysis patients with respect to the two CKD groups; in addition, lanthionine increased along with the increase in TCS, starting from one up to three. Interleukin IL-6, IL-8, and Eotaxin were significantly increased in patients with GFR < 45 mL/min/1.73 m2 with respect to those with GFR ≥ 45 mL/min/1.73 m2. IL-1b, IL-7, IL-8, IL-12, Eotaxin, and VEGF increased in calcified patients with respect to the non-calcified. IL-8 and Eotaxin were elevated both in the low GFR group and in the calcified group. We propose that lanthionine, but also IL-8 and Eotaxin, in particular, are a key feature of VC of CKD, with possible marker significance.

scholarly journals Association between KLOTHO Gene G395A Polymorphism and Carotid Artery Calcification in regular Hemodialysis Patients

2020 ◽  
Vol 8 (A) ◽  
pp. 208-213
Author(s):  
Herwindo Ahmad ◽  
Riri Andri Muzasti ◽  
Syafrizal Nasution
Keyword(s):  
Carotid Artery ◽  
Vascular Calcification ◽  
Vascular Dysfunction ◽  
Venous Blood ◽  
Hemodialysis Patients ◽  
Cross Sectional ◽  
Klotho Gene ◽  
Asian Populations ◽  
Carotid Artery Calcification ◽  
Regular Hemodialysis

BACKGROUND: The vascular calcification process in chronic kidney disease (CKD) is a complication caused by mineral and bone abnormalities and becomes the risk of cardiovascular disease and mortality in CKD patients. KLOTHO is an inhibitor of calcification and its expression has been observed to decrease in CKD patients. The KLOTHO gene G395A polymorphism is a genetic variation that is common in Asian populations and is associated with vascular dysfunction in hemodialysis patients. OBJECTIVE: The objective of the study was to determine the association between the KLOTHO gene G395A polymorphism and carotid artery calcification in regular hemodialysis patients. METHODS: This study was an analytical study with a cross-sectional design and was carried out at Rasyida Kidney Hospital Medan. Venous blood sample was taken from the patients who met the inclusion criteria for examination of the KLOTHO gene -395 polymorphism and carotid ultrasonography was assessed to evaluate the thickness of the tunica media-intima as a marker of vascular calcification. RESULTS: The majority of the study subjects were men, as many as 35 patients (50.7%). From the results of the KLOTHO gene -395 polymorphism, it was found that the majority of subjects had GG genotypes as many as 36 people (52.2%) followed by GA genotypes as many as 30 people (43,5%) and AA genotypes as many as 3 (4,3%). There was a statistically significant of the association between KLOTHO gene -395 polymorphism and the incidence of carotid artery calcification (p = 0,015). CONCLUSION: There was an association between the KLOTHO gene G395A polymorphism and carotid artery calcification in regular hemodialysis patients.

scholarly journals Role of calcification inhibitors in the pathogenesis of vascular calcification in chronic kidney disease (CKD)

2005 ◽  
Vol 67 (6) ◽  
pp. 2295-2304 ◽  
Author(s):  
Sharon M. Moe ◽  
Martina Reslerova ◽  
Markus Ketteler ◽  
Kalisha O'Neill ◽  
Danxia Duan ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Calcification Inhibitors

Progressive Vascular Calcification With Necrosis of Extremities in Hemodialysis Patients: A Possible Role of Iron Overload

1986 ◽  
Vol 7 (2) ◽  
pp. 125-129 ◽  
Author(s):  
D. Rubinger ◽  
Michael M. Friedlaender ◽  
J. Silver ◽  
Y. Kopolovic ◽  
Walter J. Czaczkes ◽  
...  
Keyword(s):  
Iron Overload ◽  
Vascular Calcification ◽  
Hemodialysis Patients

Role of Methylglyoxal in Diabetic Cardiovascular and Kidney Diseases: Insights from Basic Science for Application into Clinical Practice

2018 ◽  
Vol 24 (26) ◽  
pp. 3072-3083 ◽  
Author(s):  
Sowndramalingam Sankaralingam ◽  
Angham Ibrahim ◽  
MD Mizanur Rahman ◽  
Ali H. Eid ◽  
Shankar Munusamy
Keyword(s):  
Therapeutic Strategy ◽  
Kidney Diseases ◽  
Vascular Dysfunction ◽  
Dicarbonyl Compound ◽  
Renal Complications ◽  
Lysine Residues ◽  
Patients With Diabetes ◽  
Prevalence Of Diabetes Mellitus

Background: The incidence and prevalence of diabetes mellitus are increasing globally at alarming rates. Cardiovascular and renal complications are the major cause of morbidity and mortality in patients with diabetes. Methylglyoxal (MG) - a highly reactive dicarbonyl compound – is increased in patients with diabetes and has been implicated to play a detrimental role in the etiology of cardiovascular and renal complications. Derived from glucose, MG binds to arginine and lysine residues in proteins, and the resultant end products serve as surrogate markers of MG generation in vivo. Under normal conditions, MG is detoxified by the enzyme glyoxalase 1 (Glo1), using reduced glutathione as a co-factor. Elevated levels of MG is known to cause endothelial and vascular dysfunction, oxidative stress and atherosclerosis; all of which are risk factors for cardiovascular diseases. Moreover, MG has also been shown to cause pathologic structural alterations and impair kidney function. Conversely, MG scavengers (such as N-acetylcysteine, aminoguanidine or metformin) or Nrf2/Glo1 activators (such as trans-resveratrol / hesperetin) are shown to be useful in preventing MG-induced cardiovascular and renal complications in diabetes. However, clinical evidence supporting the MG lowering properties of these agents are limited and hence, need further investigation. Conclusion: Reducing MG levels directly using scavengers or indirectly via activation of Nrf2/Glo1 may serve as a novel and potent therapeutic strategy to counter the deleterious effects of MG in diabetic complications.

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