Inflammation and Endothelial Dysfunction in the Initiation and Propagation of Cardiovascular Disease in Patients with Chronic Kidney Disease

2014 ◽  
Vol 4 (13) ◽  
pp. 2568-2580 ◽  
Author(s):  
Sofia Zyga
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Initiation And Propagation

Endothelial dysfunction and cardiovascular disease in early-stage chronic kidney disease: Cause or association?

2012 ◽  
Vol 223 (1) ◽  
pp. 86-94 ◽  
Author(s):  
William E. Moody ◽  
Nicola C. Edwards ◽  
Melanie Madhani ◽  
Colin D. Chue ◽  
Richard P. Steeds ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Early Stage

scholarly journals Most exposed: the endothelium in chronic kidney disease

2019 ◽  
Vol 35 (9) ◽  
pp. 1478-1487 ◽  
Author(s):  
Marc Vila Cuenca ◽  
Peter L Hordijk ◽  
Marc G Vervloet
Keyword(s):  
Risk Factors ◽  
Reactive Oxygen Species ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Oxygen Species ◽  
Pathological Changes ◽  
Endothelial Lining ◽  
Traditional Risk Factors

Abstract Accumulating evidence indicates that the pathological changes of the endothelium may contribute to the development of cardiovascular complications in chronic kidney disease (CKD). Non-traditional risk factors related to CKD are associated with the incidence of cardiovascular disease, but their role in uraemic endothelial dysfunction has often been disregarded. In this context, soluble α-Klotho and vitamin D are of importance to maintain endothelial integrity, but their concentrations decline in CKD, thereby contributing to the dysfunction of the endothelial lining. These hormonal disturbances are accompanied by an increment of circulating fibroblast growth factor-23 and phosphate, both exacerbating endothelial toxicities. Furthermore, impaired renal function leads to an increment of inflammatory mediators, reactive oxygen species and uraemic toxins that further aggravate the endothelial abnormalities and in turn also inhibit the regeneration of disrupted endothelial lining. Here, we highlight the distinct endothelial alterations mediated by the abovementioned non-traditional risk factors as demonstrated in experimental studies and connect these to pathological changes in CKD patients, which are driven by endothelial disturbances, other than atherosclerosis. In addition, we describe therapeutic strategies that may promote restoration of endothelial abnormalities by modulating imbalanced mineral homoeostasis and attenuate the impact of uraemic retention molecules, inflammatory mediators and reactive oxygen species. A clinical perspective on endothelial dysfunction in CKD may translate into reduced structural and functional abnormalities of the vessel wall in CKD, and ultimately improved cardiovascular disease.

P3493Uremic toxin induced endothelial dysfunction can be restored by inhibition of the aryl hydrocarbon receptor: implications for cardiovascular disease treatment in chronic kidney disease patients

2019 ◽  
Vol 40 (Supplement_1) ◽  
Author(s):  
A Kompa ◽  
C Nguyen ◽  
A J Edgley ◽  
D J Kelly
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Endothelial Function ◽  
Aryl Hydrocarbon Receptor ◽  
Uremic Toxin ◽  
Aryl Hydrocarbon ◽  
Endothelium Dependent Relaxation

Abstract Introduction Cardiovascular disease (CVD) mortality is significantly higher in chronic kidney disease (CKD) patients, with vascular calcification and atherosclerosis proving to be major contributors. Endothelial dysfunction is an early marker of atherosclerosis, triggered by oxidative stress and reduced nitric oxide production. The uremic toxin indoxyl sulphate (IS), a protein-bound non-dialyzable molecule derived from dietary tryptophan that accumulates in the blood of CKD patients, activates the aryl hydrocarbon receptor (AhR) promoting downstream cytochrome P450 1A1 (CYP1A1) expression mediating oxidative stress and potentially endothelial dysfunction. Targeting IS-induced AhR activation in the endothelium has not previously been examined and may represent a novel approach in targeting endothelial dysfunction. Purpose To assess the ability of the AhR antagonist, CH223191, to inhibit IS-mediated impairment of endothelial function and disruption of redox balance. Methods To assess endothelium-dependent relaxation, the thoracic aorta from adult male Sprague Dawley rats (N=10) were used in ex vivo experiments. Rings (5mm) from the aorta were exposed to IS (300μM) in the presence and absence of the AhR antagonist CH223191 (1 and 10μM), prior to pre-constriction of the vessel with phenylephrine (30μM) followed by relaxation with acetylcholine (ACh; 1nM-30μM). Control rings were not exposed to IS or CH223191 to determine normal endothelial responses to ACh. Responses were recorded with isometric force transducers connected to a PowerLab using Chart Software. Tissue sections from these rings were stained for superoxide using dihydroethidium. To examine key AhR-mediated oxidative stress pathways, separate aortic rings were exposed to IS and CH223191, under the above conditions, for 4 hours prior to RNA extraction and real-time PCR analysis. Results IS reduced the maximum level of endothelium-dependent relaxation (Rmax) to 50.17±2.71% (P<0.001) compared to control (86.00±3.93%). In the presence of IS, CH223191 restored Rmax to 77.74±3.14% (1μM) and 81.63±3.27% (10μM) (Figure, P<0.001). The potency of ACh, known as the pEC50 (negative logarithm of the effective concentration of ACh to produce a relaxation response of 50%), in control tissues (−7.08±0.07) was increased 100-fold following exposure of IS (−5.10±0.13; P<0.001). CH223191 restored pEC50 back to control values (1μM, −6.62±0.09; 10μM, −6.83±0.08; P<0.05). IS-exposed rings increased superoxide expression (P<0.001) and CYP1A1 gene expression (P<0.001), CH223191 restored expression of both superoxide (P<0.001) and CYP1A1 (P<0.001) back to control levels. CH223191 restores endothelial function Conclusion Our findings demonstrate the adverse impact of IS-mediated AhR activation on the vascular endothelium, where oxidative stress may play a critical role inducing endothelial dysfunction in the vasculature of the heart and kidneys. AhR inhibition may provide a novel therapy for CVD in the CKD setting. Acknowledgement/Funding National Health and Medical Research Council of Australia Program Grant

scholarly journals Impact of Continuous Erythropoietin Receptor Activator on Selected Biomarkers of Cardiovascular Disease and Left Ventricle Structure and Function in Chronic Kidney Disease

2016 ◽  
Vol 2016 ◽  
pp. 1-9
Author(s):  
Piotr Bartnicki ◽  
Jacek Rysz ◽  
Beata Franczyk ◽  
Zbigniew Baj ◽  
Ewa Majewska
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Endothelial Dysfunction ◽  
Kidney Disease ◽  
Left Ventricle ◽  
Structure And Function ◽  
Erythropoietin Receptor ◽  
Receptor Activator ◽  
Continuous Erythropoietin Receptor Activator ◽  
And Function

Background. Cardiovascular morbidity and mortality are very high in patients with chronic kidney disease (CKD). The purpose of this study is to evaluate the impact of continuous erythropoietin receptor activator (CERA) on selected biomarkers of cardiovascular disease, left ventricle structure, and function in CKD.Material and Methods. Peripheral blood was collected from 25 CKD patients before and after CERA treatment and 20 healthy subjects. In serum samples, we assessed inflammatory markers (IL-1β, TNF-RI, TNF-RII, sFas, sFasL, MMP-9, TIMP-1, and TGF-β1), endothelial dysfunction markers (sE-selectin, sICAM-1, and sVCAM-1), and volume-related marker (NT-proBNP). All subjects underwent echocardiography and were evaluated for selected biochemical parameters (Hb, creatinine, and CRP).Results. Evaluated biomarkers and echocardiographic parameters of left ventricle structure were significantly increased but left ventricle EF was significantly decreased in CKD patients compared to controls. After CERA treatment, we observed a significant increase of Hb and left ventricle EF and a significant decrease of NT-proBNP and MMP-9. There was a significant negative correlation between Hb and TNF-RI, sICAM-1, and IL-1β.Conclusions. Our results indicate that selected biomarkers related to cardiovascular risk are significantly increased in CKD patients compared to controls. CERA treatment has anti-inflammatory action, diminishes endothelial dysfunction, and improves left ventricle function in these patients.

Stentul JJ ureteral - care este optiunea mai buna? New Considerations Regarding Chronic Kidney Disease, Cardiovascular Disease and Dyslipidemia in Diabetic Patients

2018 ◽  
Vol 69 (8) ◽  
pp. 2064-2066
Author(s):  
Mircea Munteanu ◽  
Adrian Apostol ◽  
Viviana Ivan
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Total Cholesterol ◽  
Total Cholesterol Level ◽  
Vascular Complications ◽  
Hdl Cholesterol ◽  
Controlled Study ◽  
Diabetic Patients ◽  
Artery Disease

The aim of the present study is to investigate the prevalance of chronic kidney disease (CKD), of cardiovascular disease (CVD) and dyslipidemia in patients with diabetes mellitus (DM). We conducted a prospective, controlled study involving 420 diabetic patients (120 T1DM, 300 T2DM) and investigate the following aspects: the presence of vascular complications (stroke, coronary artery disease, peripheral artery disease), lipid profile (total cholesterol, LDL-cholesterol, HDL-cholesterol, triglycerides), kidney function (glomerular filtration rate, albuminuria), blood pressure, HbA1C. The results that in diabetic patients with CKD there is an increased prevalence of CVD and of dislipidemia. Also we noticed a negative correlation between total cholesterol level and decease in eGFR in all patients, with or without CKD.

Sign in / Sign up

Export Citation Format

Share Document