scholarly journals Review: Therapy for the altered mineral metabolism of chronic kidney disease: implications for vascular calcification

2007 ◽  
Vol 1 (2) ◽  
pp. 107-112 ◽  
Author(s):  
Georges Saab ◽  
Adam T. Whaley-Connell ◽  
Ramesh Khanna ◽  
James R. Sowers
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Mineral Metabolism

scholarly journals Serum magnesium and its association with vascular calcification in chronic kidney disease patients on haemodialysis

2019 ◽  
Vol 7 (7) ◽  
pp. 2665
Author(s):  
Prasanna K. B. ◽  
Sharavanan T. V. K. ◽  
Ekanthalingam S. ◽  
Kannan I.
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Tamil Nadu ◽  
Mineral Metabolism ◽  
Serum Magnesium ◽  
Cardiac Risk ◽  
Cross Sectional Study ◽  
Cross Sectional ◽  
Inpatient Ward

Background: Cardiovascular disease is one of the leading causes of death in chronic kidney disease (CKD). It has been observed that haemodialysis patients have a high prevalence of cardiac risk factors with further risk due to abnormal mineral metabolism. A study has demonstrated that a higher serum magnesium significantly decreased the mortality risk in haemodialysis patients and lower serum Mg level has been found to be associated with increased mortality in them. The aim of the study was to characterize the relationship between Mg level and vascular calcification in CKD patients.Methods: It was a cross sectional study conducted in 100 CKD patients attending outpatient and inpatient ward of Tagore Medical College and Hospital, Chennai, Tamil Nadu, India. Serum magnesium levels will be measured using Xylidyl blue method. Carotid intimal medial thickness will be measured using Doppler.Results: In the study 10 patients did not show the sign of any calcification. Among the remaining 90 patients, 42 patients showed calcification and 48 patients showed stenosis. The statistical analysis showed a spearman correlation coefficient value of 0.201 thus showing only a weak association.Conclusion: The present study showed that only a weak relationship exists between the magnesium level and vascular calcification.

scholarly journals Vascular Calcification in Chronic Kidney Disease: Role of Disordered Mineral Metabolism

2014 ◽  
Vol 20 (37) ◽  
pp. 5829-5833 ◽  
Author(s):  
Shyamal Palit ◽  
Jessica Kendrick
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Mineral Metabolism

scholarly journals The interplay between mineral metabolism, vascular calcification and inflammation in Chronic Kidney Disease (CKD): challenging old concepts with new facts

Aging ◽  
2019 ◽  
Vol 11 (12) ◽  
pp. 4274-4299 ◽  
Author(s):  
Carla Viegas ◽  
Nuna Araújo ◽  
Catarina Marreiros ◽  
Dina Simes
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Mineral Metabolism

Vascular calcification in chronic kidney disease

2010 ◽  
Vol 119 (3) ◽  
pp. 111-121 ◽  
Author(s):  
Adrian Covic ◽  
Mehmet Kanbay ◽  
Luminita Voroneanu ◽  
Faruk Turgut ◽  
Dragomir N. Serban ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Vascular Calcification ◽  
Mineral Metabolism ◽  
Left Ventricular ◽  
Arterial Calcification ◽  
Pathophysiological Mechanism ◽  
Cardiovascular Morbidity And Mortality

VC (vascular calcification) is highly prevalent in patients with CKD (chronic kidney disease), but its mechanism is multifactorial and incompletely understood. In addition to increased traditional risk factors, CKD patients also have a number of non-traditional cardiovascular risk factors, which may play a prominent role in the pathogenesis of arterial calcification, such as duration of dialysis and disorders of mineral metabolism. The transformation of vascular smooth muscle cells into chondrocytes or osteoblast-like cells seems to be a key element in VC pathogenesis, in the context of passive calcium and phosphate deposition due to abnormal bone metabolism and impaired renal excretion. The process may be favoured by the low levels of circulating and locally produced VC inhibitors. VC determines increased arterial stiffness, left ventricular hypertrophy, a decrease in coronary artery perfusion, myocardial ischaemia and increased cardiovascular morbidity and mortality. Although current therapeutic strategies focus on the correction of phosphate, calcium, parathyroid hormone or vitamin D, a better understanding of the mechanisms of abnormal tissue calcification may lead to development of new therapeutic agents, which could reduce VC and improve cardiovascular outcome in CKD patients. The present review summarizes the following aspects: (i) the pathophysiological mechanism responsible for VC and its promoters and inhibitors, (ii) the methods for detection of VC in patients with CKD, including evaluation of arterial stiffness, and (iii) the management of VC in CKD patients.

scholarly journals P0873GLA-RICH PROTEIN (GRP) AS AN EARLY AND NOVEL MARKER ASSOCIATED WITH VASCULAR CALCIFICATION AND CKD-MINERAL AND BONE DISORDER (MBD) IN DIABETIC PATIENTS WITH CKD: A PILOT COHORT STUDY

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Carla Viegas ◽  
Ana Silva ◽  
Ana Macedo ◽  
Filipa Mendes ◽  
Patrícia Guilherme ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Mineral Metabolism ◽  
Roc Curves ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Mineral And Bone Disorder ◽  
Fgf 23

Abstract Background and Aims Cardiovascular disease (CVD) is the most life-threatening complication in chronic kidney disease (CKD) patients. In addition to traditional risk factors, most patients with CKD display abnormal mineral metabolism with underlying hormonal dysregulation, defined as chronic kidney disease-mineral and bone disorder (CKD-MBD). CKD-MBD involves changes in mineral ion homeostasis, bone quality and turnover, cardiovascular and soft tissue calcifications, which highly contribute for cardiovascular complications. Vascular calcification (VC) is associated with significant morbidity and mortality and a strong predictor of cardiovascular risk in CKD patients. Early preventive measures, including new diagnostic/prognostic tools, are required to reduce the development and progression of VC, left ventricular hypertrophy and arterial stiffness, which are crucial for the prevention of CVD outcomes in CKD patients. Gla-rich protein (GRP) is a vitamin K-dependent protein with a dual capacity to function as an inhibitor of pathological calcification and anti-inflammatory agent in the cardiovascular system, whose clinical utility is unknown. Our aim with this study was to evaluate the potential of GRP as a new marker for CKD-MBD and vascular calcification, in type 2 diabetic patients with chronic kidney disease (CKD) stages 2-4. Method In an observational prospective study including all eligible type 2 diabetic patients with CKD stages 2-4 (n=80) followed in outpatient nephrology consultation from 2010 to 2017, we explored correlations between levels of GRP in serum with mineral metabolism and inflammation markers, CKD developmental stage, vascular calcification and pulse pressure (PP). Vascular calcification score (VCS) was evaluated using the plain x-ray of the hands and pelvis (Adragão score), and increased cardiovascular risk was considered for VCS≥3. Measurements of GRP in serum were performed using a recently developed sandwich ELISA assay. Descriptive statistics, ANOVA and post hoc analysis with Scheffe test were used for analysis. Forward stepwise logistic regression (likelihood ratio) analysis was applied to identify predictive factors for VCS and PP, and ROC curves were used to assess the sensitivity and specificity of GRP in relation to these exposure factors. Results Spearman’s correlation analysis revealed the strong positive correlation between levels of serum GRP and eGFR (r=0.863, p<0.0001) and α klotho (r=0.647, p<0.0001), while a negative correlation with phosphate (P) (r=-0.715, <0.0001), FGF23 (r=-0.676, <0.0001), VCS (r=-0.822, p<0.0001), PP (r=-0.533, p<0.0001), calcium x phosphate (CaxP) (r=-0.302, p=0.006) and IL-6 (r=-0.349, p=0.002). Serum GRP levels were found to progressively decreased from stage 2 to stage 4 CKD. Multivariate analysis identified low levels of eGFR and GRP, and high levels of FGF-23 as independent risk factors for both the VCS and PP. The area under the ROC curves for GRP was 0.865±0.046, 95% CI (0.776-0.955), p<0.0001 for VCS and 0.782±0.054, 95% CI (0.677-0.887), p<0.0001 for PP. Conclusion Reduced levels of GRP were associated with higher levels of vascular calcification promoters such as P, FGF-23 and CaxP, and with lower levels of the VC inhibitor α-Klotho, indicating a correlation between GRP and the dysregulation of phosphate metabolism characteristic of CKD-MBD. In addition, this pilot cohort study indicates that GRP levels might be a significant clinical predictor of vascular calcifications in diabetic patients with CKD. Funding This research was funded by the Portuguese Society of Nephrology (SPN) through project funding 2016, by the Portuguese national funds from FCT - Foundation for Science and Technology through the transitional provision DL57/2016/CP1361/CT0006 and project UID/Multi/04326/2019. Acknowledgments To SPN by the attribution of the Jacinto Simões award (2018) financed by Fresenius medical care.

Updated mechanisms of calcification of cardiovascular system and its correction in chronic kidney disease

2020 ◽  
Vol 24 (5) ◽  
pp. 18-28
Author(s):  
F. U. Dzgoeva ◽  
O. V. Remizov ◽  
V. G. Goloeva ◽  
Z. R. Ikoeva
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Mineral Metabolism ◽  
Fibroblast Growth Factor 23 ◽  
Aortic Pulse Wave Velocity ◽  
Left Ventricular ◽  
Elastic Fibers ◽  
Protein Energy Wasting ◽  
Therapeutic Goals

In chronic kidney disease (CKD), progressive decline in kidney function leads to disorders of mineral metabolism, which are usually called secondary hyperparathyroidism. An increase in the serum concentration of the parathyroid hormone is associ­ated with a decrease in the level of calcium and calcitriol and/or an increase in the level of fibroblast growth factor-23 and inorganic phosphate in serum. CKD-related disorders of mineral and bone metabolism are associated with other metabolic disorders, such as acidosis, protein-energy wasting, inflammation, and accumulation of uremic toxins. This contributes to vascular calcification, which is a consequence of an imbalance between numerous inhibitors and promoters of soft tissue min­eralization. Vascular calcification is a degenerative process characterized by the accumulation of calcium and phosphate salts in the artery wall. This is observed in almost all vascular areas and can develop in the media, intima, or both vascular layers of the arteries. Calcification of the intima usually occurs due to atherosclerosis and may be responsible for coronary ischemic events. Conversely, media calcification is non-exclusive and predominantly develops along elastic fibers. As a result, media calcification increases vascular stiffness, aortic pulse wave velocity, systolic and pulse blood pressure, contributing to the de­velopment of left ventricular hypertrophy and heart failure. This review examines the current understanding of the mechanisms that lead to the development of vascular calcification in CKD. The participation of factors such as inflammation, age glycation end products, indoxyl sulfate, and others in calcification processes is discussed. Promising therapeutic goals associated with a new understanding of the mechanisms of cardiovascular calcification in CKD are identified.

Current Approaches in the Treatment of Chronic Kidney Disease Mineral and Bone Disorder

2008 ◽  
Vol 21 (3) ◽  
pp. 196-213 ◽  
Author(s):  
Priscilla P. How ◽  
Darius L. Mason ◽  
Alan H. Lau
Keyword(s):  
Chronic Kidney Disease ◽  
Vitamin D ◽  
Kidney Disease ◽  
Vascular Calcification ◽  
Mineral Metabolism ◽  
High Morbidity ◽  
Mineral And Bone Disorder ◽  
Vitamin D Analogs ◽  
Bone Disorder ◽  
Stage Renal Disease

Patients with chronic kidney disease (CKD) develop mineral and bone disorder (MBD), a common and important complication, as a result of impaired phosphorus excretion and reduced vitamin D activation. Altered mineral metabolism is now recognized as an independent cardiovascular risk factor in end-stage renal disease patients and contributes to the risk for accelerating vascular calcification. CKD patients are at high risk for cardiovascular disease and vascular calcification which account for the high morbidity and mortality in this patient population. Pharmacotherapeutic interventions are necessary to manage and treat the condition. Multiple classes of agents including phosphorus binders, vitamin D analogs, and calcimimetics are now available to treat CKD-MBD. Recent data have shown that treatment with sevelamer and vitamin D analogs are associated with a reduction in calcification and cardiovascular mortality and improved survival. This article provides an overview of the strategies and considerations for the management of CKD-MBD, as well as their implications on clinical outcomes.

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
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