scholarly journals Cardiovascular Disease Risk in Children With Chronic Kidney Disease: Impact of Apolipoprotein C-II and Apolipoprotein C-III

2021 ◽  
Vol 9 ◽  
Author(s):  
Wei-Ling Chen ◽  
You-Lin Tain ◽  
Hung-En Chen ◽  
Chien-Ning Hsu
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Left Ventricular ◽  
Differentially Expressed ◽  
Surrogate Markers ◽  
Differentially Expressed Proteins ◽  
Apolipoprotein C ◽  
Lv Mass

Cardiovascular disease (CVD) is an evolving process that begins in the early stages of chronic kidney disease (CKD) in children. Several surrogate markers, such as ambulatory blood pressure monitoring (ABPM), left ventricular (LV) mass, and arterial stiffness assessment, allow for the early detection of subclinical CVD in pediatric CKD. Four groups of plasma samples (n = 3/group) from congenital anomalies of the kidney and urinary tract (CAKUT), as well as non-CAKUT patients with or without BP abnormalities, were studied to screen differentially expressed proteins using isobaric tags for relative and absolute protein quantification (iTRAQ)-based proteomics. As a result, 20 differentially expressed proteins associated with hypertension in children with CKD were discovered. Among them, apolipoprotein C-II (apoC-II) was found to have the highest abundance among the CKD patients with hypertension. As such, we hypothesized that apoC-II and apolipoprotein C-III (apoC-III) levels were related to BP abnormalities and CVD in children suffering from mild-to-moderate CKD. We examined their associations with surrogate markers of CV risk in 88 pediatric patients with CKD stages G1–G4. Children with CKD stages G2–G4 had a higher plasma apoC-II level than G1 patients (6.35 vs. 5.05 mg/dl, p < 0.05). We observed that ABPM abnormalities, LV mass, and arterial stiffness parameters were greater in CKD children who had stages G2–G4 than in those who had stage G1 (all p < 0.05). Plasma levels of apoC-II and apoC-III were positively correlated with total cholesterol, triglyceride, and low-density lipoprotein (LDL) (all p < 0.001). In multivariate linear regression analyses, apoC-II was correlated with a high LV mass index and an abnormal ABPM profile, and apoC-III was correlated with 24-h hypertension (r = 0.303, p = 0.003) and asleep hypertension (r = 0.379, p < 0.001). Early evaluations of apoC-II and apoC-III, ABPM, and surrogate markers of CV risk will aid in early preventative interventions to reduce the risk of CV in youths suffering from CKD.

scholarly journals The Association between Nitric Oxide Pathway, Blood Pressure Abnormalities, and Cardiovascular Risk Profile in Pediatric Chronic Kidney Disease

2019 ◽  
Vol 20 (21) ◽  
pp. 5301 ◽  
Author(s):  
Hsu ◽  
Lu ◽  
Lo ◽  
Lin ◽  
Tain
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Children And Adolescents ◽  
Young Patients ◽  
Left Ventricular ◽  
Stiffness Index ◽  
Lv Mass

Cardiovascular disease (CVD) is common in chronic kidney disease (CKD), while major CV events are rare in young CKD patients. In addition to nitric oxide (NO)-related biomarkers, several surrogate markers have been assessed to stratify CV risk in youth with CKD, including 24-h ambulatory blood pressure monitoring (ABPM), carotid artery intima-media thickness (cIMT), pulse wave velocity (PWV), ABPM-derived arterial stiffness index (AASI), flow-mediated dilatation (FMD), and left ventricular mass index (LVMI). The aim of this study was to identify subclinical CVD through the analysis of indices of CV risk in children and adolescents with CKD. Between 2016 and 2018, the prospective observational study enrolled 125 patients aged 3 to 18 years with G1–G4 CKD stages. Close to two-thirds of young patients with CKD exhibited blood pressure (BP) abnormalities on ABPM. CKD children with abnormal office BP showed lower plasma arginine levels and arginine-to-asymmetric dimethylarginine (ADMA) ratio, but higher ratios of ADMA-to-symmetric dimethylarginine (SDMA) and citrulline-to-arginine. High PWV and AASI, indices of arterial stiffness, both strongly correlated with high BP load. Additionally, LV mass and LVMI exhibited strong correlations with high BP load. Using an adjusted regression model, we observed the citrulline-to-arginine ratio was associated with 24-h systolic and diastolic BP, systolic blood pressure (SBP) load, and diastolic blood pressure (DBP) load. Early assessments of NO-related parameters, BP load abnormalities, arterial stiffness indices, and LV mass will aid in early preventative care toward decreasing CV risk later in life for children and adolescents with CKD.

scholarly journals Cardiovascular Risk in Chronic Kidney Disease: Role of the Sympathetic Nervous System

2012 ◽  
Vol 2012 ◽  
pp. 1-8 ◽  
Author(s):  
Jeanie Park
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Renal Failure ◽  
Nervous System ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Sympathetic Nervous System ◽  
Renal Disease ◽  
Left Ventricular ◽  
Sympathetic Nervous

Patients with chronic kidney disease are at significantly increased risk for cardiovascular disease and sudden cardiac death. One mechanism underlying increased cardiovascular risk in patients with renal failure includes overactivation of the sympathetic nervous system (SNS). Multiple human and animal studies have shown that central sympathetic outflow is chronically elevated in patients with both end-stage renal disease (ESRD) and chronic kidney disease (CKD). SNS overactivation, in turn, increases the risk of cardiovascular disease and sudden death by increasing arterial blood pressure, arrythmogenicity, left ventricular hypertrophy, and coronary vasoconstriction and contributes to the progression renal disease. This paper will examine the evidence for SNS overactivation in renal failure from both human and experimental studies and discuss mechanisms of SNS overactivity in CKD and therapeutic implications.

scholarly journals Can we IMPROVE cardiovascular outcomes through phosphate lowering in CKD? Rationale and protocol for the IMpact of Phosphate Reduction On Vascular End-points in Chronic Kidney Disease (IMPROVE-CKD) study

BMJ Open ◽  
2019 ◽  
Vol 9 (2) ◽  
pp. e024382 ◽  
Author(s):  
Nicole Lioufas ◽  
Nigel D Toussaint ◽  
Eugenia Pedagogos ◽  
Grahame Elder ◽  
Sunil V Badve ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Compliance ◽  
Left Ventricular ◽  
Serum Phosphate ◽  
Lanthanum Carbonate ◽  
Cardiovascular Morbidity And Mortality ◽  
Fgf 23 ◽  
The Impact

IntroductionPatients with chronic kidney disease (CKD) are at heightened cardiovascular risk, which has been associated with abnormalities of bone and mineral metabolism. A deeper understanding of these abnormalities should facilitate improved treatment strategies and patient-level outcomes, but at present there are few large, randomised controlled clinical trials to guide management. Positive associations between serum phosphate and fibroblast growth factor 23 (FGF-23) and cardiovascular morbidity and mortality in both the general and CKD populations have resulted in clinical guidelines suggesting that serum phosphate be targeted towards the normal range, although few randomised and placebo-controlled studies have addressed clinical outcomes using interventions to improve phosphate control. Early preventive measures to reduce the development and progression of vascular calcification, left ventricular hypertrophy and arterial stiffness are crucial in patients with CKD.Methods and analysisWe outline the rationale and protocol for an international, multicentre, randomised parallel-group trial assessing the impact of the non-calcium-based phosphate binder, lanthanum carbonate, compared with placebo on surrogate markers of cardiovascular disease in a predialysis CKD population—the IMpact of Phosphate Reduction On Vascular End-points (IMPROVE)-CKD study. The primary objective of the IMPROVE-CKD study is to determine if the use of lanthanum carbonate reduces the burden of cardiovascular disease in patients with CKD stages 3b and 4 when compared with placebo. The primary end-point of the study is change in arterial compliance measured by pulse wave velocity over a 96-week period. Secondary outcomes include change in aortic calcification and biochemical parameters of serum phosphate, parathyroid hormone and FGF-23 levels.Ethics and disseminationEthical approval for the IMPROVE-CKD trial was obtained by each local Institutional Ethics Committee for all 17 participating sites in Australia, New Zealand and Malaysia prior to study commencement. Results of this clinical trial will be published in peer-reviewed journals and presented at conferences.Trial registration numberACTRN12610000650099.

Renal bone disease: a dietitian's perspective

2020 ◽  
Vol 5 (1) ◽  
pp. 18-25
Author(s):  
Ruth Kander
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Dietary Restriction ◽  
Bone Disease ◽  
Morbidity And Mortality ◽  
Phosphate Binders ◽  
Renal Bone Disease ◽  
High Phosphate

Renal bone disease increases morbidity and mortality in patients with chronic kidney disease by increasing the risk for fractures, osteoporosis and other bone problems and its association with cardiovascular disease, including calcification and arterial stiffness. Treatment of renal bone disease is through a combination of three main methods to reduce phosphate levels: dietary restriction of high-phosphate foods; dialysis clearance; and the use of phosphate binders to prevent its absorption.

scholarly journals Chronic Kidney Disease and Disproportionally Increased Cardiovascular Damage: Does Oxidative Stress Explain the Burden?

2017 ◽  
Vol 2017 ◽  
pp. 1-15 ◽  
Author(s):  
Anila Duni ◽  
Vassilios Liakopoulos ◽  
Karolos-Pavlos Rapsomanikis ◽  
Evangelia Dounousi
Keyword(s):  
Oxidative Stress ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular ◽  
Antioxidant Defenses ◽  
Pon1 Activity ◽  
Pathophysiological Mechanism ◽  
Ros Production ◽  
Cardiovascular Damage

Chronic kidney disease (CKD) patients are among the groups at the highest risk for cardiovascular disease and significantly shortened remaining lifespan. CKD enhances oxidative stress in the organism with ensuing cardiovascular damage. Oxidative stress in uremia is the consequence of higher reactive oxygen species (ROS) production, whereas attenuated clearance of pro-oxidant substances and impaired antioxidant defenses play a complementary role. The pathophysiological mechanism underlying the increased ROS production in CKD is at least partly mediated by upregulation of the intrarenal angiotensin system. Enhanced oxidative stress in the setting of the uremic milieu promotes enzymatic modification of circulating lipids and lipoproteins, protein carbamylation, endothelial dysfunction via disruption of nitric oxide (NO) pathways, and activation of inflammation, thus accelerating atherosclerosis. Left ventricular hypertrophy (LVH) and heart failure are hallmarks of CKD. NADPH oxidase activation, xanthine oxidase, mitochondrial dysfunction, and NO-ROS are the main oxidative pathways leading to LVH and the cardiorenal syndrome. Finally, a subset of antioxidant enzymes, the paraoxonases (PON), deserves special attention due to abundant clinical evidence accumulated regarding reduced serum PON1 activity in CKD as a contributor to the increased burden of cardiovascular disease. Future, meticulously designed studies are needed to assess the effects of antioxidant therapy on patients with CKD.

scholarly journals Cardiovascular Risk Factors and Chronic Kidney Disease—FGF23: A Key Molecule in the Cardiovascular Disease

2014 ◽  
Vol 2014 ◽  
pp. 1-9 ◽  
Author(s):  
Rika Jimbo ◽  
Tatsuo Shimosawa
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Fibroblast Growth Factor 23 ◽  
Left Ventricular ◽  
Cardiovascular Risks ◽  
Mineral And Bone Disorder ◽  
Promising Target ◽  
Increased Risk

Patients with chronic kidney disease (CKD) are at increased risk of mortality, mainly from cardiovascular disease. Moreover, abnormal mineral and bone metabolism, the so-called CKD-mineral and bone disorder (MBD), occurs from early stages of CKD. This CKD-MBD presents a strong cardiovascular risk for CKD patients. Discovery of fibroblast growth factor 23 (FGF23) has altered our understanding of CKD-MBD and has revealed more complex cross-talk and endocrine feedback loops between the kidney, parathyroid gland, intestines, and bone. During the past decade, reports of clinical studies have described the association between FGF23 and cardiovascular risks, left ventricular hypertrophy, and vascular calcification. Recent translational reports have described the existence of FGF23-Klotho axis in the vasculature and the causative effect of FGF23 on cardiovascular disease. These findings suggest FGF23 as a promising target for novel therapeutic approaches to improve clinical outcomes of CKD patients.

scholarly journals Nontraditional Biomarkers for Cardiovascular Disease in Patients With Chronic Kidney Disease

2020 ◽  
Vol 43 (2) ◽  
pp. 51-60
Author(s):  
Ittikorn Spanuchart ◽  
Arkom Nongnuch ◽  
Youg Liu
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Arterial Stiffness ◽  
Mineral Metabolism ◽  
Uremic Toxins ◽  
Calcium Balance ◽  
The Novel ◽  
Cvd Risk ◽  
Chd Risk

Cardiovascular disease (CVD) is the leading cause of death among patients who have chronic kidney disease (CKD). Nowadays, CKD per se is considered one of the coronary heart disease (CHD) risk equivalents. Apart from traditional CVD risk factors, there are several possible determinants for CVD in patients with CKD, for example, uremic toxins, increased inflammatory stage, abnormal bone mineral metabolism, and positive calcium balance. In this narrative review, we offer a summary of the extensively studied biomarkers for CVD in patients with CKD, including uremic toxins (p-cresol, indoxyl sulfate, and advanced glycated end products), and a novel indicator of arterial stiffness, cardio-ankle vascular index (CAVI), which is an independent prognostic predictor for CVD. For the uremic toxins, we reviewed their metabolisms, particularly, how the reduced renal function in CKD patients affect their clearance and their clearance with dialysis. Also, we pay attention to the recent evidence on how those uremic toxins contribute to CVD and their clinical associations. We do not include the possible treatment targeting at those uremic toxins. As for the novel indicator of arterial stiffness, we reviewed the clinical application of CAVI in comparison to the standard indicator for arterial stiffness, pulse wave velocity.  

scholarly journals Prevalence of anemia and cardiovascular diseases in chronic kidney disease patients: a single tertiary care centre study

2017 ◽  
Vol 4 (1) ◽  
pp. 247 ◽  
Author(s):  
Swaraj Sathyan ◽  
Sunil George ◽  
Poornima Vijayan
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Cardiovascular Diseases ◽  
Kidney Disease ◽  
Strong Association ◽  
Left Ventricular ◽  
Newly Diagnosed ◽  
National Kidney Foundation ◽  
Study Population ◽  
Prevalence Of Anemia

Background: Chronic kidney disease (CKD) is recognized as a global health issue having high mortality and morbidity rates putting a substantial burden on global resources. CKD has become a recognised independent risk factor for several adverse health outcomes including cardiovascular disease (CVD). Anaemia is an anticipated consequence as renal function declines, and can develop at any stage of CKD. There is a strong association between anemia and cardiovascular complications in CKD patients and many studies have proven that anemia plays a key role in worsening CVD in CKD patients. The objective of this study was to study the prevalence of anemia and cardiovascular diseases in CKD patients and establish an association between them.Methods: This study was conducted between January 2008 and June 2008 for a period of six months at a Government tertiary referral institution in south India. During this period, all newly diagnosed cases of chronic kidney disease based on the National Kidney foundation definition were included in this study. All the patients were evaluated based on detailed history taking, clinical examination and laboratory investigations after an informed consent was obtained from them. Staging of CKD was done based on the national kidney foundation (NKF/KDIGO) staging system. GFR was estimated using the abbreviated MDRD (Modification of Diet in Renal Disease) formula.Results: Of the 333 newly diagnosed CKD patients, a large majority (264, 79.28%) of the patients in the study presented in stage 5 CKD. The mean Hb in the study was 8.42±2.20 g/dl. Anemia was present in 90.39% while 25.53% had an Hb of <7g/dl. The prevalence of anemia increased from stage 3 (66.6%) to stage 5 (94.7%) and this correlation was statistically significant (p<0.0005). 167 (50.15% ) were found to have some form of cardiovascular disease, of which 120 (71.86%) were males and 47 (28.14%) were females. 83.93% had left ventricular hypertrophy, 16.17% had ischemic heart disease and 7.78% had congestive heart failure. 56.3% of patients in the age group 41-60 years had cardiovascular disease. The correlation between cardiovascular disease and age was statistically significant (p = 0.04139). And it was found that cardiovascular disease was more common when the cause of CKD was Diabetic nephropathy (65.8%) and hypertensive nephrosclerosis (84.6%). The correlation between the cardiovascular disease and etiological diagnosis of CKD was statistically significant. (p<0.0005).Cardiovascular disease was present in 61.2 % of the study population with diabetes mellitus and in 56.4% of the study population with hypertension. The correlations between CVD and diabetes and hypertension were statistically significant. Cardiovascular disease was present in 61.2% of the study population with Hemoglobin <7 gm/dl, 41.7% with Hb between 7-11 gm/dl and the correlation between cardiovascular disease and the level of Hb was highly significant in CKD patients.Conclusions: Thus there is a strong association between the clinical trial of anemia, CKD and CVD and prompt identification and management of common risk factors and adequate correction of anemia is necessary to slow progression of CKD and prevent cardiovascular events.

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