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Mean IMT and (B) mean maximum IMT of the carotid bifurcations and the common carotid arteries, CBM(max), according to number of mineral metabolism in target (3: all three in target, 2: two parameters in target, 1: only one parameter in target and 0: none in target) (P ¼ 0.04 for IMT and P ¼ 0.04 for CBM(max)).
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Abnormal mineral metabolism is associated with increased cardiovascular morbidity and mortality. The exact pathogenesis linking mineral metabolism to cardiovascular risk is unknown. This study was undertaken to investigate the association between serum phosphate and/or Ca x PO(4) product with serum levels of soluble E-selectin (sE-selectin), solubl...
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Objective
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Background:
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Citations
... In the present study, there was a significant increase in circulating levels of ICAM-1 and VCAM-1 with SC compared with CA and these results are comparable with those reported in previous studies. 33,34 In accordance with the above speculation, chronic uremia is known to be associated with Systemic inflammation has been regarded as a cardiovascular risk factor. Our study demonstrated a negative correlation between serum VCAM-1 and HDL levels and a highly significant correlation between both ICAM-1 and VCAM-1 and CRP levels; this is the first report of such a relationship in chronic hemodialysis patients. ...
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. We evaluated biochemical markers of vascular calcification, inflammation, and endothelial dysfunction in patients with chronic kidney disease (CKD) treated with sevelamer carbonate (SC) versus calcium acetate (CA). Fifty patients with CKD (stages 3 and 4) were enrolled and assigned to treatment with SC and CA for 12 weeks. At the end of the study the biomarkers of vascular calcification, inflammation, and endothelial dysfunction were analyzed. A significant increase in HDL‐cholesterol was observed with SC but not with CA in patients with CKD. Treatment with SC reduced serum phosphate, calcium phosphate, and FGF‐23 levels and there was no change with CA treatment. The inflammatory markers IL‐8, IFN‐γ, and TNFα decreased with response to both treatments. The levels of IL‐6 significantly increased with CA treatment and no change was observed in the SC treatment group. SC showed favorable effects on anti‐inflammatory and vascular calcification biomarkers compared to CA treatment in patients with CKD stages 3 and 4 with normal phosphorous values.
... 3,4 This state of mineral metabolism imbalance is independently associated with increased risk of mortality from cardiovascular disease and morbidity, such as bone disease and fractures, among patients with end-stage renal disease on maintenance hemodialysis. [5][6][7][8][9] Vitamin D replacement therapy with alfacalcidol (1α-hydroxyvitamin D3) is widely used in the treatment of secondary hyperparathyroidism in hemodialysis patients. Prior studies have shown that alfacalcidol, whether administered orally Dovepress Dovepress 26 Sawalmeh et al or intravenously, is effective in suppressing PTH secretion without significant increase in the risk of hypercalcemia and hyperphosphatemia. ...
Background
Secondary hyperparathyroidism is a common complication of chronic kidney disease and is managed using vitamin D replacement therapy. Very few studies have examined the effectiveness of pulse alfacalcidol therapy in comparison to daily oral alfacalcidol therapy in suppressing serum parathyroid hormone (PTH) levels in hemodialysis patients. The aim of this randomized controlled trial was to replicate the findings of prior studies comparing effectiveness of pulse oral alfacalcidol therapy versus daily oral alfacalcidol therapy in suppressing PTH after 13 weeks of therapy using a Palestinian sample of hemodialysis patients, and to identify demographic and biomedical characteristics of patients that are independently associated with PTH levels.
Methods
One hundred and sixty-seven patients completed the study, 88 in the daily group and 79 in the pulse group. The pulse group had more clinically significant reduction in mean PTH level by 75 pg/dL at 13 weeks than the daily group, but this was not statistically significant.
Results
The effect of alfacalcidol therapy on metabolism of phosphate and corrected calcium levels was comparable in both groups, and pulse therapy was not associated with increased risk of hypercalcemia and hyperphosphatemia. Serum PTH levels were independently and inversely associated with older age and diabetes.
Conclusion
Switching daily alfacalcidol therapy to thrice-weekly alfacalcidol pulse therapy seems safe and convenient, especially for hemodialysis patients with poor compliance with treatment. This study also highlights the importance of monitoring and preventing malnutrition in hemodialysis patients and maintaining optimal glycemic control in diabetic hemodialysis patients.
... Circulating E-selectin was found to be associated with the severity of coronary artery disease in sporadic crosssectional analyses 15 , and to predict cardiovascular events in patients with type 2 diabetes mellitus 16 , but in other studies performed so far in patients with overt CVD, no 23 and did not predict adverse outcome in such patients. 24 Circulating sCD40L does not identify subclinical atherosclerosis in the general population, 25 but it has been found to be higher in patients with unstable angina 26 and in patients with stable coronary artery disease. 27 In addition, CD40L elevation identified patients at high risk for an adverse cardiovascular event in apparently healthy people 28 or with evident CVD. ...
... The evaluation of the relationship between E-selectin and mortality has led to conflicting results both in the general population [44][45][46] and in ESRD patients. 23,24 Surprisingly, a recent study of Malatino et al. reported that patients with relatively low E-selectin had a relative risk of all-cause mortality and CV events about twice higher than that observed in patients with increased E-selectin. 47 Similarly, there are few and conflicting data on the prognostic role of serum P-selectin in the general population and none in HD patients. ...
The aim of this study was to measure P-selectin, E-selectin, and CD-4L levels over time in chronic hemodialysis (HD) patients. Thirty stable patients with end-stage renal failure undergoing chronic HD were included in the study. Blood samples were obtained before HD for measurement of P-selectin, E-selectin, and CD-40L. Measurements were performed at month 0 (T0), 3 (T2), 8 (T3), and 13 (T4). The levels of P-selectin, E-selectin, and CD40L were also analyzed according to the occurrence of cardiovascular disease (CVD) and to CVD-related mortality. The levels of CD40L and P-selectin changed significantly over time, decreasing at month 3 and 6 and returning at the T0 levels at month 13. Conversely, E-selectin levels did not. The levels of CD40L, P-selectin and E-selectin over time did not differ significantly between patients with age ≤ 65 or > 65 years, between patients with or without CVD, or between patients who died or who survived during the follow-up. In end-stage renal failure patients undergoing chronic HD, CD40L and P-selectin, but not E-selectin, showed a transient decrease over time, and the serum levels of these molecules were not associated with CVD or with CVD-related mortality.
... 50 Interestingly, in patients with end-stage renal disease (ESrD), soluble E-selectin levels were not associated with carotid atherosclerosis and even had an inverse relationship with the development of cardio vascular events. 51,52 The explanation for this counter intuitive observation remains elusive but may relate to the large inter-individual variability of the assays used in the studies, the relative small sample size of the studies, and the altered pathophysiology of cardio vascular morbidity and mortality associated with ESrD. ...
The recognition of a central role for the endothelium in the development of kidney disease or the development of vascular lesions in patients with established renal dysfunction has led to the emergence of methods to test different aspects of endothelium function, including in endothelium injury and repair. Endothelial-cell activation is associated with the shedding of components of the glycocalyx, adhesion molecules and endothelial microparticles into the circulation. This process may eventually result in the detachment of endothelial cells and recruitment of circulating myeloid and progenitor cells that are involved in vascular remodeling and repair. Circulating markers of endothelium activation may therefore represent novel markers of vessel wall injury. This Review describes the biology of these circulating markers of vessel wall injury, the methodologies used to measure them, and their possible relevance to patients with kidney disease.
... Intriguing links between mineral metabolism disturbances and inflammation have been observed. In stable haemodialysis patients, the inability to achieve NKF-KDOQI™ targets for calcium, phosphorus, or Ca × P has also been linked to the up-regulation of adhesion molecules [83]. The adhesion molecule E-selectin and soluble intercellular adhesion molecule-1 mediate adherence and transendothelial migration of circulating leucocytes to vascular endothelial cells, and elevated expression of these molecules has been implicated in the development of atherosclerotic lesions. ...
Kidney disease, especially chronic kidney disease (CKD), is a worldwide public health problem with serious adverse health consequences for affected individuals. Secondary hyperparathyroidism, a disorder characterized by elevated serum parathyroid hormone levels, and alteration of calcium and phosphorus homeostasis are common metabolic complications of CKD that may impact cardiovascular health.
Here, we systematically review published reports from recent observational studies and clinical trials that examine markers of altered mineral metabolism and clinical outcomes in patients with CKD.
Mineral metabolism disturbances begin early during the course of chronic kidney disease, and are associated with cardiovascular disease and mortality in observational studies. Vascular calcification is one plausible mechanism connecting renal-related mineral metabolism with cardiovascular risk. Individual therapies to correct mineral metabolism disturbances have been associated with clinical benefit in some observational studies; clinical trials directed at more comprehensive control of this problem are warranted.
There exists a potential to improve outcomes for patients with CKD through increased awareness of the Bone Metabolism and Disease guidelines set forth by the National Kidney Foundation-Kidney Disease Outcomes Quality Initiative. Future studies may include more aggressive therapy with a combination of agents that address vitamin D deficiency, parathyroid hormone and phosphorus excess, as well as novel agents that modulate circulating promoters and inhibitors of calcification.
Disturbances in endothelial function, adipokines, and mineral metabolism due to secondary hyperparathyroidism (SHPT) shorten the lifespan in hemodialysis (HD) patients.
The aim of the study was to evaluate the effect of SHPT treatment with cinacalcet on selected adipokines and markers of endothelial injury in HD patients.
Soluble thrombomodulin (sTM), E-selectin, leptin, and adiponectin levels were measured in patients with SHPT at baseline and at 6 months of cinacalcet treatment.
A total of 18 patients completed the study. SHPT treatment with cinacalcet decreased calcium, phosphate, and intact parathormone (iPTH) levels; however, no significant changes in sTM, E-selectin, leptin, or adiponectin were observed. iPTH levels after treatment correlated with age (r = -0.51, P = 0.031), mean cinacalcet dose (r = 0.65, P = 0.004), as well as baseline calcium (r = 0.65 P = 0.003), iPTH (r = 0.59, P = 0.01), E-selectin (r = 0.56, P = 0.016), and leptin (r = -0.49, P = 0.039).
Cinacalcet treatment does not affect the markers of endothelial function and selected adipokines. Effectiveness of treatment may be modulated by E-selectin and leptin.
E-selectin is a key adhesion molecule which plays a fundamental role in endothelial progenitor cell-dependent reparative mechanisms in experimental ischaemia and it serves to anchor leucocytes to the endothelium in inflammatory processes. Inflammation is one of the strongest risk factors for death and cardiovascular (CV) events in end-stage renal disease (ESRD).
The objective of the current study was to evaluate whether E-selectin is a useful biomarker of clinical outcome in ESRD patients. We tested the prediction power of circulating E-selectin for mortality and CV events in a cohort of 265 ESRD patients.
During the follow-up, 59 patients died and 58 had CV events. All-cause mortality was inversely related to serum E-selectin, the risk of death being the lowest in patients in the third E-selectin tertile (HR: 1, reference group), intermediate in those in the second tertile (HR: 1.30) and the highest in patients in the first tertile (HR: 2.02, P = 0.01). Similarly, the risk of fatal and nonfatal CV events followed an inverse pattern being lowest in the third tertile (reference group) and highest in the first tertile (HR: 1.73, P = 0.03). The prediction power of E-selectin for death and CV events was confirmed in a Cox regression analysis where E-selectin emerged as an inverse predictor of these outcomes, particularly so in patients with severe inflammation.
These data are in keeping with the hypothesis that in systemic inflammation altered E-selectin shedding may play a role in arterial damage and implicates this adhesion molecule in atherosclerotic complications in a high-risk condition like ESRD.
