The risk of atherosclerosis in patients with chronic kidney disease

Olechnowicz-Tietz, Sylwia; Gluba, Anna; Paradowska, Anna; Banach, Maciej; Rysz, Jacek

doi:10.1007/s11255-013-0407-1

Cited by 86 publications

(65 citation statements)

References 24 publications

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“…Histological research has shown the existence of sub epidermal capillary micro-angiopathy in patients suffering from renal insufficiency, which is evidenced among other things by the presence of activation and an apoptosis of endothelial cells. This initial endothelial lesion leads to vasoconstriction followed by diffuse platelet aggregation, and the occlusion of vascular light by fibrinous thrombins [43,44].…”

Section: Endothelial Dysfunction and Crimentioning

confidence: 99%

Chronic Inflammatory Diseases and Endothelial Dysfunction

Castellon¹,

Bogdanova²

2016

Aging and disease

155

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Chronic inflammatory diseases are associated with increases in cardiovascular diseases (CVD) and subclinical atherosclerosis as well as early-stage endothelial dysfunction screening using the FMD method (Flow Mediated Dilation). This phenomenon, referred to as accelerated pathological remodeling of arterial wall, could be attributed to traditional risk factors associated with atherosclerosis. Several new non-invasive techniques have been used to study arterial wall's structural and functional alterations.These techniques (based of Radio Frequency, RF) allow for an assessment of artery age through calculations of intima-media thickness (RF-QIMT), pulse wave rate (RF-QAS) and endothelial dysfunction degree (FMD). The inflammatory and autoimmune diseases should now be considered as new cardiovascular risk factors, result of the major consequences of oxidative stress and RAS (Renin Angiotensin System) imbalance associated with the deleterious effect of known risk factors that lead to the alteration of the arterial wall. Inflammation plays a key role in all stages of the formation of vascular lesions maintained and exacerbated by the risk factors. The consequence of chronic inflammation is endothelial dysfunction that sets in and we can define it as an integrated marker of the damage to arterial walls by classic risk factors. The atherosclerosis, which develops among these patients, is the main cause for cardiovascular morbi-mortality and uncontrolled chronic biological inflammation, which quickly favors endothelial dysfunction. These inflammatory and autoimmune diseases should now be considered as new cardiovascular risk factors.

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Section: Endothelial Dysfunction and Crimentioning

confidence: 99%

Chronic Inflammatory Diseases and Endothelial Dysfunction

Castellon¹,

Bogdanova²

2016

Aging and disease

155

View full text Add to dashboard Cite

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“…Recently, baseline data from the National Observatory of Atherosclerosis in Nephrology (NEFRONA) (16) Study have shown that patients in early CKD stages already have a higher prevalence of atheromatous plaques than those without CKD (17,18), and as previously shown, this prevalence is even higher in advanced stages of CKD (19)(20)(21). However, it is uncertain what the velocity of atheromatosis progression in CKD is (22,23), and little is known about the predictors of plaque progression in patients with CKD.…”

Section: Introductionmentioning

confidence: 99%

Predictors of Subclinical Atheromatosis Progression over 2 Years in Patients with Different Stages of CKD

Gracia

Betriu

Martínez-Alonso

et al. 2016

Clinical Journal of the American Society of Nephrology

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Background and objectives Ultrasonographic detection of subclinical atheromatosis is a noninvasive method predicting cardiovascular events. Risk factors predicting atheromatosis progression in CKD are unknown. Predictors of atheromatosis progression were evaluated in patients with CKD.Design, setting, participants, & measurements Our multicenter, prospective, observational study included 1553 patients with CKD (2009CKD ( -2011. Carotid and femoral ultrasounds were performed at baseline and after 24 months. A subgroup of 476 patients with CKD was also randomized to undergo ultrasound examination at 12 months. Progression of atheromatosis was defined as an increase in the number of plaque territories analyzed by multivariate logistic regression.Results Prevalence of atheromatosis was 68.7% and progressed in 59.8% of patients after 24 months. CKD progression was associated with atheromatosis progression, suggesting a close association between pathologies. Variables significantly predicting atheromatosis progression, independent from CKD stages, were diabetes and two interactions of age with ferritin and plaque at baseline. Given that multiple interactions were found between CKD stage and age, phosphate, smoking, dyslipidemia, body mass index, systolic BP (SBP), carotid intima-media thickness, plaque at baseline, uric acid, cholesterol, 25-hydroxy vitamin D (25OH vitamin D), and antiplatelet and phosphate binders use, the analysis was stratified by CKD stages. In stage 3, two interactions (age with phosphate and plaque at baseline) were found, and smoking, diabetes, SBP, low levels of 25OH vitamin D, and no treatment with phosphate binders were positively associated with atheromatosis progression. In stages 4 and 5, three interactions (age with ferritin and plaque and plaque with smoking) were found, and SBP was positively associated with atheromatosis progression. In dialysis, an interaction between body mass index and 25OH vitamin D was found, and age, dyslipidemia, carotid intima-media thickness, low cholesterol, ferritin, and uric acid were positively associated with atheromatosis progression.Conclusions Atheromatosis progression affects more than one half of patients with CKD, and predictive factors differ depending on CKD stage.

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“…1 It is well established that CKD patients exhibit a disproportionate burden of atherosclerosis as compared with individuals having normal kidney function. [2][3][4][5] Furthermore, a higher prevalence of traditional risk factors for the development of atherosclerosis, such as hypertension, diabetes and hyperlipidemia, only partially accounts for the accelerated atherosclerosis in CKD patients, leading to the hypothesis that unique risk factors must be present in this population. 6,7 …”

Section: Introductionmentioning

confidence: 99%

Serum Trimethylamine-N-Oxide is Elevated in CKD and Correlates with Coronary Atherosclerosis Burden

Stubbs

House

Ocque

et al. 2016

Journal of the American Society of Nephrology

364

334

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Trimethlyamine-N-oxide (TMAO) was recently identified as a promoter of atherosclerosis. Patients with CKD exhibit accelerated development of atherosclerosis; however, no studies have explored the relationship between TMAO and atherosclerosis formation in this group. This study measured serum concentrations and urinary excretion of TMAO in a CKD cohort (n=104), identified the effect of renal transplant on serum TMAO concentration in a subset of these patients (n=6), and explored the cross-sectional relationship between serum TMAO and coronary atherosclerosis burden in a separate CKD cohort (n=220) undergoing coronary angiography. Additional exploratory analyses examined the relationship between baseline serum TMAO and long-term survival after coronary angiography. Serum TMAO concentrations demonstrated a strong inverse association with eGFR (r 2 =0.31, P,0.001). TMAO concentrations were markedly higher in patients receiving dialysis (median [interquartile range], 94.4 mM [54.8-133.0 mM] for dialysis-dependent patients versus 3.3 mM [3.1-6.0 mM] for healthy controls; P,0.001); whereas renal transplantation resulted in substantial reductions in TMAO concentrations (median [min-max] 71.2 mM [29.2-189.7 mM] pretransplant versus 11.4 mM [8.9-20.2 mM] posttransplant; P=0.03). TMAO concentration was an independent predictor for coronary atherosclerosis burden (P=0.02) and predicted long-term mortality independent of traditional cardiac risk factors (hazard ratio, 1.26 per 10 mM increment in TMAO concentration; 95% confidence interval, 1.13 to 1.40; P,0.001). In conclusion, serum TMAO concentrations substantially increase with decrements in kidney function, and this effect is reversed by renal transplantation. Increased TMAO concentrations correlate with coronary atherosclerosis burden and may associate with long-term mortality in patients with CKD undergoing coronary angiography. Patients with CKD have a high prevalence of cardiovascular comorbidities, which primarily contributes to the exceedingly high mortality in this group. 1,2 For example, the 5-year survival for ESRD patients receiving dialysis is approximately 35%, with .50% of the mortality in this group resulting directly from cardiovascular causes. 1 It is well established that CKD patients exhibit a disproportionate burden of atherosclerosis as compared with individuals having normal kidney function. [2][3][4][5] Furthermore, a higher prevalence of traditional risk factors for the development of atherosclerosis, such as hypertension, diabetes and hyperlipidemia, only partially accounts for the accelerated atherosclerosis in CKD patients, leading to the hypothesis that unique risk factors must be present in this population. 6,7

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The risk of atherosclerosis in patients with chronic kidney disease

Cited by 86 publications

References 24 publications

Chronic Inflammatory Diseases and Endothelial Dysfunction

Chronic Inflammatory Diseases and Endothelial Dysfunction

Predictors of Subclinical Atheromatosis Progression over 2 Years in Patients with Different Stages of CKD

Serum Trimethylamine-N-Oxide is Elevated in CKD and Correlates with Coronary Atherosclerosis Burden

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