scholarly journals MO055CIRCULATING CALCIPROTEIN PARTICLES AND EXTRACELLULAR VESICLES AS NOVEL PLAYERS IN CHRONIC KIDNEY DISEASE VASCULAR CALCIFICATION. A ROLE FOR GLA-RICH PROTEIN

2017 ◽  
Vol 32 (suppl_3) ◽  
pp. iii67-iii68
Author(s):  
Carla Viegas ◽  
Lúcia Santos ◽  
Anjos Macedo ◽  
Rute Morais ◽  
Ana Silva ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Extracellular Vesicles ◽  
Vascular Calcification ◽  
Calciprotein Particles

scholarly journals Chronic Kidney Disease Circulating Calciprotein Particles and Extracellular Vesicles Promote Vascular Calcification

2018 ◽  
Vol 38 (3) ◽  
pp. 575-587 ◽  
Author(s):  
Carla S.B. Viegas ◽  
Lúcia Santos ◽  
Anjos L. Macedo ◽  
António A. Matos ◽  
Ana P. Silva ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Extracellular Vesicles ◽  
Vascular Calcification ◽  
Calciprotein Particles

scholarly journals Calciprotein particle inhibition explains magnesium-mediated protection against vascular calcification

2019 ◽  
Vol 35 (5) ◽  
pp. 765-773 ◽  
Author(s):  
Anique D ter Braake ◽  
Coby Eelderink ◽  
Lara W Zeper ◽  
Andreas Pasch ◽  
Stephan J L Bakker ◽  
...  
Keyword(s):  
Electron Microscopy ◽  
Chronic Kidney Disease ◽  
Smooth Muscle ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Healthy Controls ◽  
Gene And Protein Expression ◽  
Calciprotein Particles

Abstract Background Phosphate (Pi) toxicity is a strong determinant of vascular calcification development in chronic kidney disease (CKD). Magnesium (Mg2+) may improve cardiovascular risk via vascular calcification. The mechanism by which Mg2+ counteracts vascular calcification remains incompletely described. Here we investigated the effects of Mg2+ on Pi and secondary crystalline calciprotein particles (CPP2)-induced calcification and crystal maturation. Methods Vascular smooth muscle cells (VSMCs) were treated with high Pi or CPP2 and supplemented with Mg2+ to study cellular calcification. The effect of Mg2+ on CPP maturation, morphology and composition was studied by medium absorbance, electron microscopy and energy dispersive spectroscopy. To translate our findings to CKD patients, the effects of Mg2+ on calcification propensity (T50) were measured in sera from CKD patients and healthy controls. Results Mg2+ supplementation prevented Pi-induced calcification in VSMCs. Mg2+ dose-dependently delayed the maturation of primary CPP1 to CPP2 in vitro. Mg2+ did not prevent calcification and associated gene and protein expression when added to already formed CPP2. Confirmatory experiments in human serum demonstrated that the addition of 0.2 mmol/L Mg2+ increased T50 from healthy controls by 51 ± 15 min (P < 0.05) and CKD patients by 44 ± 13 min (P < 0.05). Each further 0.2 mmol/L addition of Mg2+ led to further increases in both groups. Conclusions Our results demonstrate that crystalline CPP2 mediates Pi-induced calcification in VSMCs. In vitro, Mg2+ delays crystalline CPP2 formation and thereby prevents Pi-induced calcification.

scholarly journals Emerging Role of Vitamins D and K in Modulating Uremic Vascular Calcification: The Aspect of Passive Calcification

Nutrients ◽  
2019 ◽  
Vol 11 (1) ◽  
pp. 152 ◽  
Author(s):  
Yi-Chou Hou ◽  
Chien-Lin Lu ◽  
Cai-Mei Zheng ◽  
Ruei-Ming Chen ◽  
Yuh-Feng Lin ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Vitamin K ◽  
Matrix Vesicles ◽  
Vital Role ◽  
Matrix Gla Protein ◽  
Protein Receptor ◽  
Calciprotein Particles

Vascular calcification is a critical complication in patients with chronic kidney disease (CKD) because it is predictive of cardiovascular events and mortality. In addition to the traditional mechanisms associated with endothelial dysfunction and the osteoblastic transformation of vascular smooth muscle cells (VSMCs), the regulation of calcification inhibitors, such as calciprotein particles (CPPs) and matrix vesicles plays a vital role in uremic vascular calcification in CKD patients because of the high prevalence of vitamin K deficiency. Vitamin K governs the gamma-carboxylation of matrix Gla protein (MGP) for inhibiting vascular calcification, and the vitamin D binding protein receptor is related to vitamin K gene expression. For patients with chronic kidney disease, adequate use of vitamin D supplements may play a role in vascular calcification through modulation of the calciprotein particles and matrix vesicles (MVs).

scholarly journals Calciprotein particles are a sensitive marker predicting vascular calcification in patients with chronic kidney disease

2020 ◽  
Author(s):  
Hidekazu Moriya ◽  
Yasuhiro Mochida ◽  
Kunihiro Ishioka ◽  
Machiko Oka ◽  
Kyoko Maesato ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Colloidal Particles ◽  
Lower Extremities ◽  
Rate Of Change ◽  
Arterial Calcification ◽  
Calciprotein Particles ◽  
One Year ◽  
Sensitive Marker

Abstract Background: In chronic kidney disease (CKD) patients, vascular calcification occurs in the early stage of CKD, before the titer of existing CKD mineral bone disorder (CKD-MBD)-related markers exceed the threshold. Calciprotein particles (CPPs) are crystals in which excessive phosphorus and calcium in the blood form colloidal particles and are associated with vascular calcification. However, it is unknown whether CPPs are a more sensitive marker for detecting calcification than others. Methods: In a prospective cohort study of 58 patients with CKD we examined CKD-MBD markers, including CPPs. Vascular arterial calcification score (ACS) of the lower extremities was measured with the Agatston score. One year later, the markers and ACS were reevaluated, and the relationship between the degree of progression of vascular calcification and CKD-MBD markers was evaluated. Results: The CPP titer was significantly correlated with that of serum phosphate and corrected calcium. However, the CPP titer showed no correlation with eGFR or ACS in the lower extremities. After one year, the basic titers of serum creatinine, eGFR, FGF-23, intact-PHT, 1.25-dihydroxyvitamin D3 and CPP were not significantly correlated with ACS changes in the lower extremities. There was a significant correlation between the rate of change in ACS and that in CPP (r = 0.292, p = 0.0258). CPP was an independent risk factor for the progression of calcification in the lower extremities in a multivariate analysis (p = 0.0144). Conclusions: CPP is a more sensitive marker of arterial calcification than other CKD-MBD markers in patients with CKD. Key words: Calciprotein particle, Chronic kidney disease, Vascular calcification

scholarly journals A current understanding of vascular calcification in CKD

2014 ◽  
Vol 307 (8) ◽  
pp. F891-F900 ◽  
Author(s):  
Neil J. Paloian ◽  
Cecilia M. Giachelli
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
End Stage Renal Disease ◽  
Normal Bone ◽  
Cardiovascular Morbidity And Mortality ◽  
Calciprotein Particles ◽  
Stage Renal Disease ◽  
End Stage ◽  
A Current

Patients with chronic kidney disease (CKD) and end-stage renal disease (ESRD) have significant cardiovascular morbidity and mortality that is in part due to the development of vascular calcification. Vascular calcification is an active, highly regulated process that shares many similarities with normal bone formation. New discoveries related to extracellular vesicles, microRNAs, and calciprotein particles continue to reveal the mechanisms that are involved in the initiation and progression of vascular calcification in CKD. Further innovations in these fields are critical for the development of biomarkers and therapeutic options for patients with CKD and ESRD.

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.

Sign in / Sign up

Export Citation Format

Share Document