Risk Factors for Carotid Artery Disease and Chronic Kidney Disease: Same or Unique?

2018 ◽  
Vol 22 (4) ◽  
pp. 410-411 ◽  
Author(s):  
Marijan Bosevski ◽  
Lily Stojanovska
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Carotid Artery ◽  
Carotid Artery Disease ◽  
Artery Disease

scholarly journals Biomarker Profiling of Neurovascular Diseases in Patients with Stage 5 Chronic Kidney Disease

2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 248S-254S
Author(s):  
Justin Lee ◽  
Jack Bontekoe ◽  
Brandon Trac ◽  
Vinod Bansal ◽  
José Biller ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Carotid Artery Disease ◽  
Vascular Dysfunction ◽  
Enzyme Linked Immunosorbent Assay ◽  
Neurocognitive Deficits ◽  
Intracranial Atherosclerotic Disease ◽  
Artery Disease ◽  
D Dimer ◽  
Neurovascular Diseases

Patients with stage 5 chronic kidney disease (CKD5D) have a higher risk of developing neurocognitive deficits. Stroke, cervical carotid artery disease (CCAD), and intracranial atherosclerotic disease (ICAD) are causes of such deficits in CKD5D. Chronic inflammation from renal failure elevates risk for these diseases through oxidative stress and vascular dysfunction. The adverse impact on the carotid and intracranial vasculatures contributes to the multifactorial pathophysiology of stroke. Eleven plasma biomarker levels in patients with CKD5D (n = 97) and healthy controls (n = 17-50) were measured using sandwich enzyme-linked immunosorbent assay (ELISA) method. Of the 97 patients with CKD5D, 24 had CCAD, 19 had ICAD, and 23 had acute stroke. Elevations in NACHT, LRR, and PYD domains-containing protein 3 (NALP3) levels in patients with CKD5D (+)CCAD (1.80 ± 0.11 ng/mL) compared to patients with (−)CCAD (1.55 ± 0.08 ng/mL) were statistically significant ( P = .0299). Differences in D-dimer levels were also found to be statistically significant ( P = .0258) between CKD5D (+)stroke (1.83 ± 0.42 μg/mL) and (−)stroke (0.89 ± 0.13 μg/mL) groups. The ages of the (+) neurovascular disease groups were found to be significantly elevated compared to the (−) neurovascular disease groups ( P = .0002 carotid AD; P < .0001 ICAD; P = .0157 stroke). D-dimer levels were positively correlated with age in CKD5D ( P = .0375). With the possible exception of NALP3 for CCAD, profiling levels of specific biomarkers for risk stratification of neurovascular diseases in the CKD5D population warrants further investigation.

scholarly journals Circulating Biomarker Levels in Patients With Stage 5 Chronic Kidney Disease With Respect to Neurovascular Diseases

2018 ◽  
Vol 24 (9_suppl) ◽  
pp. 314S-322S
Author(s):  
Justin Lee ◽  
Ryan McMillan ◽  
Leonidas Skiadopoulos ◽  
Vinod Bansal ◽  
José Biller ◽  
...  
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Carotid Artery Disease ◽  
Kidney Injury ◽  
Assay Method ◽  
Neurocognitive Deficits ◽  
Neutrophil Gelatinase Associated Lipocalin ◽  
Intracranial Atherosclerotic Disease ◽  
Artery Disease ◽  
Kidney Injury Molecule 1

The prevalence of neurocognitive deficits remains high in patients with stage 5 chronic kidney disease (CKD5D). Major contributors to such deficits include stroke, cervical carotid artery disease (CCAD), and intracranial atherosclerotic disease (ICAD). The risk of developing these dysfunctional vascular processes is facilitated by the chronic inflammation associated with renal failure. Plasma levels of 10 circulating biomarkers in patients with CKD5D (n = 78-90) were quantified using the sandwich enzyme linked immune sorbent assay method. Biomarkers for this study included kidney injury molecule-1, N-terminal prohormone of brain natriuretic peptide (NT-proBNP), neutrophil gelatinase-associated lipocalin, interleukin-18, endothelin 1, calcifediol, parathyroid hormone, platelet-derived growth factor, microparticles-expressing tissue factor, and lipoprotein(a) (Lp(a)). Of the 90 patients with CKD5D, 30 had CCAD, 24 had ICAD, and 22 had stroke. Lp(a) level was significantly elevated in patients with CKD5D with comorbid ICAD compared to those without (125.70 ± 10.03 ng/mL vs 97.16 ± 5.97 ng/mL; P = .0065). NT-proBNP level was also significantly elevated in patients with CKD5D with comorbid stroke diagnosis compared to those without stroke history, once patients with a diagnosis of heart failure (HF) were excluded (14.84 ± 2.80 ng/mL vs 9.06 ± 1.27 ng/mL; P = .0283). Profiling levels of Lp(a) and NT-ProBNP could thus be useful in the risk stratification of ICAD and stroke, respectively, in the CKD5D population.

Abstract 15645: Carotid Artery Stenting and Endarterectomy in Patients With Stage 5 Chronic Kidney Disease: Insights of the Healthcare Cost and Utilization Project’s National Inpatient Sample

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Fabio V Lima ◽  
Tzyy Y Yen ◽  
Luis Gruberg
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Carotid Artery ◽  
Healthcare Cost ◽  
Carotid Artery Stenting ◽  
Hospital Admissions ◽  
Multivariable Analysis ◽  
Hospital Death ◽  
National Inpatient Sample ◽  
Artery Disease

Background: Carotid artery stenting (CAS) has evolved into a viable alternative for the treatment of symptomatic and asymptomatic high-grade carotid artery stenosis, particularly in patients considered to be at a high surgical risk for carotid endarterectomy (CEA). Hypothesis: There is limited data on the outcomes of patients with stage 5 chronic kidney disease (CKD) (GFR<15 mL/min/1.73 m 2 or dialysis) undergoing CEA or CAS. Methods: The Healthcare Cost and Utilization Project’s National Inpatient Sample was screened for hospital admissions of patients undergoing CAS and CEA from 2003-2012. Baseline clinical characteristics and outcomes were identified in patients with stage 5 CKD. The primary outcome was major adverse cardiac and cerebrovascular events (MACCE), defined as the composite of in-hospital death, acute myocardial infarction and acute cerebrovascular accident (CVA). Results: Our study population consisted of 1,723 patients that underwent CEA and 544 patients that underwent CAS. Patients undergoing CAS were younger and had significantly lower rates of coronary artery disease, hypertension and hyperlipidemia. CAS patients experienced significantly higher rates of MACCE compared with patients that underwent CEA, mainly driven by a higher rate of in-hospital strokes (Fig. 1). In a multivariable analysis, CAS (OR 1.53, 95% CI 1.19-1.98) was an independent predictor of MACCE. Conclusions: In patients with stage 5 CKD (GFR<15 mL/min/1.73 m 2 or dialysis ) undergoing internal carotid artery revascularization, CAS was associated with higher rates of in-hospital MACCE, driven by higher mortality and stroke rates when compared with CEA.

Prevalence and risk factors for chronic kidney disease in patients with coronary artery disease

2012 ◽  
Vol 28 (3) ◽  
pp. 379-384 ◽  
Author(s):  
Yu-Shi Bao ◽  
Shi-Ping Na ◽  
Xi-Bei Jia ◽  
Rui-Chan Liu ◽  
Ming-Ao Wang ◽  
...  
Keyword(s):  
Risk Factors ◽  
Coronary Artery Disease ◽  
Chronic Kidney Disease ◽  
Coronary Artery ◽  
Kidney Disease ◽  
Artery Disease

scholarly journals Framing Cause-Effect Relationship of Acute Coronary Syndrome in Patients with Chronic Kidney Disease

Diagnostics ◽  
2021 ◽  
Vol 11 (8) ◽  
pp. 1518
Author(s):  
Mădălina Ioana Moisi ◽  
Simona Gabriela Bungau ◽  
Cosmin Mihai Vesa ◽  
Camelia Cristina Diaconu ◽  
Tapan Behl ◽  
...  
Keyword(s):  
Risk Factors ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Approach ◽  
Coronary Syndrome ◽  
Inflammatory Status ◽  
Ischemic Coronary Artery Disease ◽  
Improper Use ◽  
Traditional Risk Factors ◽  
Artery Disease

The main causes of death in patients with chronic kidney disease (CKD) are of cardiovascular nature. The interaction between traditional cardiovascular risk factors (CVRF) and non-traditional risk factors (RF) triggers various complex pathophysiological mechanisms that will lead to accelerated atherosclerosis in the context of decreased renal function. In terms of mortality, CKD should be considered equivalent to ischemic coronary artery disease (CAD) and properly monitored. Vascular calcification, endothelial dysfunction, oxidative stress, anemia, and inflammatory syndrome represents the main uremic RF triggered by accumulation of the uremic toxins in CKD subjects. Proteinuria that appears due to kidney function decline may initiate an inflammatory status and alteration of the coagulation – fibrinolysis systems, favorizing acute coronary syndromes (ACS) occurrence. All these factors represent potential targets for future therapy that may improve CKD patient’s survival and prevention of CV events. Once installed, the CAD in CKD population is associated with negative outcome and increased mortality rate, that is the reason why discovering the complex pathophysiological connections between the two conditions and a proper control of the uremic RF are crucial and may represent the solutions for influencing the prognostic. Exclusion of CKD subjects from the important trials dealing with ACS and improper use of the therapeutical options because of the declined kidney functioned are issues that need to be surpassed. New ongoing trials with CKD subjects and platelets reactivity studies offers new perspectives for a better clinical approach and the expected results will clarify many aspects.

scholarly journals Toll-like receptor 2 and 4 stimulation elicits an enhanced inflammatory response in human obese patients with atherosclerosis

2011 ◽  
Vol 121 (5) ◽  
pp. 205-214 ◽  
Author(s):  
Vincent P.W. Scholtes ◽  
Dik Versteeg ◽  
Jean-Paul P.M. de Vries ◽  
Imo E. Hoefer ◽  
Arjan H. Schoneveld ◽  
...  
Keyword(s):  
Risk Factors ◽  
Cardiovascular Risk ◽  
Carotid Artery ◽  
Cardiovascular Risk Factors ◽  
Carotid Artery Disease ◽  
Innate Immune ◽  
Obese Patients ◽  
Cd11b Expression ◽  
Activation Marker ◽  
Artery Disease

The innate immune response elicited by activation of TLRs (Toll-like receptors) plays an important role in the pathogenesis of atherosclerosis. We hypothesized that cardiovascular risk factors are associated with the activation status of the innate immune system. We therefore assessed the responsiveness of TLRs on circulating cells in two groups of patients with established atherosclerosis and related this to the presence of cardiovascular risk factors. TNF (tumour necrosis factor)-α release induced by TLR2 and TLR4 activation was measured in patients with established coronary [PCI (percutaneous coronary intervention) study, n=78] or carotid artery disease [CEA (carotid endarterectomy) study, n=104], by stimulating whole blood samples with lipopolysaccharide (TLR4 ligand) and Pam3CSK4 [tripalmitoylcysteinylseryl-(lysyl)4; TLR2 ligand]. As an early activation marker, CD11b expression was measured by flow cytometry on CD14+ cells. Obesity was the ‘only’ risk factor that correlated with the TLR response. In both studies, obese patients had significantly higher TNF-α levels after stimulation of TLR2 compared with non-obese patients [16.9 (7.7–49.4) compared with 7.5 (1.5–19.2) pg/ml (P=0.008) in coronary artery disease and 14.6 (8.1–28.4) compared with 9.5 (6.1–15.7) pg/ml (P=0.015) in carotid artery disease; values are medians (interquartile range)]. Similar results were obtained following TLR4 stimulation. The enhanced inflammatory state in obese patients was also confirmed by a significant increased expression of the activation marker CD11b on circulating monocytes. In conclusion, obesity is associated with an enhanced TLR response in patients suffering from established atherosclerotic disease.

Sign in / Sign up

Export Citation Format

Share Document