scholarly journals The Effect of Hemodialysis on Kinetic Segment of Left Ventricular in Stage V Chronic Kidney Diseases Patients

2018 ◽  
Vol 3 (1) ◽  
pp. 10
Author(s):  
Systriana Esi Kamasita ◽  
Suryono Suryono ◽  
Yudha Nurdian ◽  
Yuli Hermansyah ◽  
Edy Junaidi ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricle ◽  
Left Ventricular ◽  
Wilcoxon Test ◽  
Disease Stage ◽  
Electrolyte Balance ◽  
Uremic Toxin ◽  
Ckd Stage

Chronic kidney disease (CKD) stage V attacks other organs such as heart that can cause cardiovascular disease (CVD). One of them is CVD caused by CKD stage V that is the kinetic segment of left ventricle. Cardiovascular disease occurs due to excess fluid and buildup of uremic toxin. Chronic kidney disease stage V can not be cured so it requires therapy that is hemodialysis (HD). Hemodialysis can reduce excess fluid, uremic toxin, and maintain electrolyte balance in stage V stage. Improved fluid and decreased uremic toxin can reduce the burden of the heart and strain so that blood supply to certain myocardial areas increases and the left ventricular kinetic segment increases. The purpose of this study is to determine the effect of HD on left ventricular kinetic changes in CKD stage V patients in dr. Soebandi hospital in Jember. The research design used was quasi-experimental one group pretest-postest design. The sample was 30 patients. Respondents were determined by nonprobability sampling technique with purposive sampling method. The data used are primary data and secondary data. Data analysis using Wilcoxon test. Based on the results of the study, the distribution of the sample based on the age of the most in the range of 45-54 years, based on the sex obtained more women, based on the duration of hemodialysis obtained the period of most hemodialysis> 24 months and based on blood pressure before and after hemodialysis obtained patients with hypertension. Hypothesis test using Wilcoxon test got p-value (0.000). From the results of the analysis can be concluded that there is influence of hemodialysis on kinetic segment of left ventricle in patient of CKD stage V in dr. Soebandi hospital in Jember.   

scholarly journals Hemodialysis Effect on Systolic Left Ventricular Function in Stage V Chronic Kidney Disease Patients

2018 ◽  
Vol 4 (3) ◽  
pp. 128
Author(s):  
Hazbina Fauqi Ramadhan ◽  
Yuli Hermansyah ◽  
Desie Dwi Wisudanti ◽  
Suryono Suryono
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Left Ventricular Function ◽  
Ventricular Function ◽  
Cardiovascular Function ◽  
Left Ventricular ◽  
Wilcoxon Test ◽  
World Health ◽  
Uremic Toxin ◽  
Systolic Left Ventricular Function

Chronic kidney diasease (CKD) is one of world health problem with increased incidence. Kidney function impairment contribute to cardiovascular complication that has been the main cause of CKD patient death. The impairment of cardiovascular function mainly caused by decreased of systolic left ventricular function. Stage V CKD patients need renal replacement therapy such as hemodialysis. Hemodialysis known to has positive effect on cadiovascular function by decreasing volume overload and uremic toxin. Echocardiography is a non-invasive method to assess cardiovascular function i.e. systolic left ventricular function. The aim of this study is to describe the improvement of  systolic left ventricular function in stage V CKD patients after going through hemodialysis. The subject of this study are 30 patients, ≥18 years old diagnosed with Stage V CKD and undergo routine hemodialysis in RSD dr. Soebandi Jember. The data analyzed with Wilcoxon test and shown significance (p=0,000). This study concludes there is a significant improvement on systolic left ventricular function in CKD patients before and after hemodialysis in RSD dr. Soebandi Jember. Keywords: Systolic Left Ventricular Function, Hemodialysis, Chronic Kidney Disease, Echocardiography

MO145CAROTID PLAQUE THICKNESS COMPARED WITH SEVERITY OF CAROTID AND CORONARY ARTERY CALCIFICATION IN PATIENTS WITH CHRONIC KIDNEY DISEASE STAGE 3

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Sasha Saurbrey Bjergfelt ◽  
Ida Maria Hjelm Soerensen ◽  
Henrik Oeder Hjortkjaer ◽  
Nino Emanuel Landler ◽  
Ellen Linnea Freese Ballegaard ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Coronary Arteries ◽  
Chronic Kidney Disease Stage ◽  
Disease Stage ◽  
Arterial Calcification ◽  
Carotid Plaques ◽  
Ckd Stage ◽  
Computed Tomography Scanning

Abstract Background and Aims Chronic kidney disease (CKD) accelerates both atherosclerosis and arterial calcification. The aim of the present study was to explore whether maximal carotid plaque thickness (cPT max) was increased in patients with CKD stage 3 compared to controls and associated with cardiovascular disease and severity of calcification in the carotid and coronary arteries. Method The study group consisted of 200 patients with CKD stage 3 from the Copenhagen CKD Cohort and 121 age- and sex-matched controls. cPT max was assessed by ultrasound and arterial calcification by computed tomography scanning. Results Carotid plaques were present in 58% of patients (n=115) compared with 40% of controls (n=48), P=0.002. Among participants with plaques, cPT max (median, interquartile range) was significantly higher in patients compared with controls (1.9 (1.4-2.3) versus 1.5 (1.2-1.8) mm, P=0.001. Cardiovascular disease was present in 9.4% of patients without plaques (n=85), 23.2% of patients with cPT max 1.0-1.9 mm (n=69) and 34.8% of patients with cPT max >1.9 mm (n=46), P=0.001. Carotid and coronary calcium scores >400 were present in 0.0% and 4.0%, respectively, of patients with no carotid plaques, in 19.1% and 24.2% of patients with cPT max 1.0-1.9 mm, and in 47.5% and 52.6% of patients with cPT max >1.9 mm, P<0.001. Conclusion This is the first study showing that cPT max is increased in patients with CKD stage 3 compared to controls and closely associated with prevalent cardiovascular disease and severity of calcification in both the carotid and coronary arteries.

scholarly journals Uremic toxin indoxyl sulfate promotes proinflammatory macrophage activation by regulation of β-catenin and YAP pathways

2021 ◽  
Author(s):  
Ying Li ◽  
Jing Yan ◽  
Minjia Wang ◽  
Jing Lv ◽  
Fei Yan ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Inflammatory Response ◽  
Macrophage Polarization ◽  
Indoxyl Sulfate ◽  
Uremic Toxin ◽  
Lps Challenge ◽  
Hla Dr ◽  
M1 Macrophage

AbstractEvidence has been shown that indoxyl sulfate (IS) could impair kidney and cardiac functions. Moreover, macrophage polarization played important roles in chronic kidney disease and cardiovascular disease. IS acts as a nephron-vascular toxin, whereas its effect on macrophage polarization during inflammation is still not fully elucidated. In this study, we aimed to investigate the effect of IS on macrophage polarization during lipopolysaccharide (LPS) challenge. THP-1 monocytes were incubated with phorbol 12-myristate-13-acetate (PMA) to differentiate into macrophages, and then incubated with LPS and IS for 24 h. ELISA was used to detect the levels of TNFα, IL-6, IL-1β in THP-1-derived macrophages. Western blot assay was used to detect the levels of arginase1 and iNOS in THP-1-derived macrophages. Percentages of HLA-DR-positive cells (M1 macrophages) and CD206-positive cells (M2 macrophages) were detected by flow cytometry. IS markedly increased the production of the pro-inflammatory factors TNFα, IL-6, IL-1β in LPS-stimulated THP-1-derived macrophages. In addition, IS induced M1 macrophage polarization in response to LPS, as evidenced by the increased expression of iNOS and the increased proportion of HLA-DR+ macrophages. Moreover, IS downregulated the level of β-catenin, and upregulated the level of YAP in LPS-stimulated macrophages. Activating β-catenin signaling or inhibiting YAP signaling suppressed the IS-induced inflammatory response in LPS-stimulated macrophages by inhibiting M1 polarization. IS induced M1 macrophage polarization in LPS-stimulated macrophages via inhibiting β-catenin and activating YAP signaling. In addition, this study provided evidences that activation of β-catenin or inhibition of YAP could alleviate IS-induced inflammatory response in LPS-stimulated macrophages. This finding may contribute to the understanding of immune dysfunction observed in chronic kidney disease and cardiovascular disease.

scholarly journals Atorvastatin treatment does not abolish inflammatory mediated cardiovascular risk in subjects with chronic kidney disease

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Renate M. Hoogeveen ◽  
Simone L. Verweij ◽  
Yannick Kaiser ◽  
Jeffrey Kroon ◽  
Hein J. Verberne ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Cardiovascular Risk ◽  
Kidney Disease ◽  
Arterial Wall ◽  
Ldl Cholesterol ◽  
Statin Treatment ◽  
Receptor Expression ◽  
Disease Stage ◽  
Cellular Inflammation

AbstractIndividuals with chronic kidney disease are at an increased risk for cardiovascular disease. This risk may partially be explained by a chronic inflammatory state in these patients, reflected by increased arterial wall and cellular inflammation. Statin treatment decreases cardiovascular risk and arterial inflammation in non-CKD subjects. In patients with declining kidney function, cardiovascular benefit resulting from statin therapy is attenuated, possibly due to persisting inflammation. In the current study, we assessed the effect of statin treatment on arterial wall and cellular inflammation. Fourteen patients with chronic kidney disease stage 3 or 4, defined by an estimated Glomerular Filtration Rate between 15 and 60 mL/min/1.73 m2, without cardiovascular disease were included in a single center, open label study to assess the effect of atorvastatin 40 mg once daily for 12 weeks (NTR6896). At baseline and at 12 weeks of treatment, we assessed arterial wall inflammation by 18F-fluoro-deoxyglucose positron-emission tomography computed tomography (18F-FDG PET/CT) and the phenotype of circulating monocytes were assessed. Treatment with atorvastatin resulted in a 46% reduction in LDL-cholesterol, but this was not accompanied by an attenuation in arterial wall inflammation in the aorta or carotid arteries, nor with changes in chemokine receptor expression of circulating monocytes. Statin treatment does not abolish arterial wall or cellular inflammation in subjects with mild to moderate chronic kidney disease. These results imply that CKD-associated inflammatory activity is mediated by factors beyond LDL-cholesterol and specific anti-inflammatory interventions might be necessary to further dampen the inflammatory driven CV risk in these subjects.

scholarly journals The Copenhagen chronic kidney disease echo study (COInCYDE)

2020 ◽  
Vol 41 (Supplement_2) ◽  
Author(s):  
N Landler ◽  
S Bro ◽  
B Feldt-Rasmussen ◽  
D Hansen ◽  
A.L Kamper ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Chronic Kidney Disease ◽  
Cohort Study ◽  
Kidney Disease ◽  
Cardiac Function ◽  
Left Ventricular ◽  
Funding Source ◽  
Ckd Stage ◽  
Significant Difference ◽  
Stage 1

Abstract Background The cardiovascular mortality of patients with chronic kidney disease (CKD) is 2–10 times higher than in the average population. Purpose To estimate the prevalence of abnormal cardiac function or structure across the stages CKD 1 to 5nonD. Method Prospective cohort study. Patients with CKD stage 1 to 5 not on dialysis, aged 30 to 75 (n=875) and age-/sex-matched controls (n=173) were enrolled consecutively. All participants underwent a health questionnaire, ECG, morphometric and blood pressure measurements. Blood and urine were analyzed. Echocardiography was performed. Left ventricle (LV) hypertrophy, dilatation, diastolic and systolic dysfunction were defined according to current ESC guidelines. Results 63% of participants were men. Mean age was 58 years (SD 12.6 years). Mean eGFR was 46.7 mL/min/1,73 m (SD 25.8) for patients and 82.3 mL/min/1,73 m (SD 13.4) for controls. The prevalence of elevated blood pressure at physical exam was 89% in patients vs. 53% in controls. Patients were more often smokers and obese. Left ventricular mass index (LVMI) was slightly, albeit insignificantly elevated at CKD stages 1 & 2 vs. in kontrols: 3.1 g/m2, CI: −0.4 to 6.75, p-value 0.08. There was no significant difference in LV-dilatation between patients and controls. Decreasing diastolic and systolic function was observed at CKD stage 3a and later: LVEF decreased 0.95% (CI: −1.5 to −0.2), GLS increased 0.5 (CI: 0.3 to 0.8), and OR for diastolic dysfunction increased 3.2 (CI 1.4 to 7.3) pr. increment CKD stage group. Conclusion In accordance to previous studies, we observe in the CPHCKD cohort study signs of early increase of LVMI in patients with CKD stage 1 & 2. Significant decline in systolic and diastolic cardiac function is apparent already at stage 3 CKD. Figure 1. Estimated GFR vs. GLS & histogram of GLS Funding Acknowledgement Type of funding source: Public hospital(s). Main funding source(s): The Capital Region of Denmark

scholarly journals Analysof Reticulocyte Hemoglobin Equivalent Levels in Patients with Chronic Kidney Disease Stage IV and V

2021 ◽  
Vol 15 (1) ◽  
Author(s):  
Agri Febria Sari ◽  
Rikarni Rikarni ◽  
Deswita Sari
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Iron Status ◽  
Chronic Kidney Disease Stage ◽  
Stage Iv ◽  
Disease Stage ◽  
Cross Sectional ◽  
Iron Storage ◽  
Laboratory Installation ◽  
Ckd Stage

Reticulocyte hemoglobin equivalent (RET-He) represents hemoglobin content in reticulocyte. Reticulocyte hemoglobin equivalent test can be used to asses iron status of chronic kidney disease (CKD). Iron deficiency happens in 40% CKD and could lead to anemia manifestation. Level of RET-He gives real-time assesment of iron availability for hemoglobin production and the level will getting lower when iron storage for erythropoiesis decreasing. Reticulocyte hemoglobin equivalent is more stabil than feritin and transferin saturation in assessing iron status. Aim of this study is to determine RET-He level in patients with CKD stage IV and V. This study is  a cross sectional descripstive study. Subjects were 96 CKD stage IV and V patients that met inclusion and exclusion criterias. Subjects conducted blood tests at Central Laboratory Installation Dr. M. Djamil Hospital Padang from July to September 2020. Examination of RET-He level was analyzed by Sysmex XN-1000 flowcytometry fluorescense method. Data was presented in frequency distribution table. The RET-He level below cutoff (<29,2 pg) indicates the need for iron suplementation therapy for CKD stage IV and V patients. Samples with RET-He level below cutoff were 48 (50%) and 48 (50%) were above cutoff.

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.

MO448MICRORNAS IMPLICATED IN CHRONIC KIDNEY DISEASE

2021 ◽  
Vol 36 (Supplement_1) ◽  
Author(s):  
Laurent Metzinger
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Clinical Outcomes ◽  
Molecular Mechanisms ◽  
Neointimal Hyperplasia ◽  
Uremic Toxins ◽  
University Hospital ◽  
Transcriptional Level ◽  
Uremic Toxin ◽  
Ckd Stage

Abstract Background and Aims The gene program is controlled at the post-transcriptional level by the action of small non-coding RNAs known as microRNAs (miRNAs), short, single-stranded molecules that control mRNA stability or translational repression via base pairing with regions in the 3' untranslated region of their target mRNAs. Recently, considerable progress has been made to elucidate the roles of miRNAs in vascular pathogenesis and develop the use of miRNAs as biomarkers, and innovative drugs. We demonstrated during the last decade that miRNAs miR-126 and miR-223 are implicated in the course of chronic kidney disease (CKD) and cardiovascular damage. miR-223 expression is enhanced in vascular smooth muscle cells (VSMCs) subjected to an uremic toxin and also in aortas of a murine model of CKD. As restenosis is a common complication of angioplasty, in which neointimal hyperplasia results from migration of VSMCs into the vessel lumen we measured the effect of miR-223 modulation on restenosis in a rat model of carotid artery after balloon injury. We over-expressed and inhibited miR-223 expression using adenoviral vectors, coding a pre-miR-223 sequence or a sponge sequence, used to trap endogenous microRNA, respectively. We demonstrated that inhibiting miR-223 function significantly reduced neointimal hyperplasia by almost half in carotids. Thus down-regulating miR-223 could be a potential therapeutic approach to prevent restenosis after angioplasty. We also correlated miR-126 and miR-223 expression with clinical outcomes in a large cohort of CKD patients, in collaboration with the University Hospital of Ghent (Belgium) and Ambroise Paré Hospital, France. We evaluated both miRNA’s link with all-cause mortality and cardiovascular and renal events over a 6-year follow-up period. The serum levels of miR-126 and miR-223 were decreased as CKD stage advanced, and patients with higher levels of miR-126 and miR-223 had a higher survival rate. Similar results were observed for cardiovascular and renal events. In conclusion, CKD is associated with a decrease in circulating miR-126 and miR-223 levels in CKD patients. We will also present links between several uremic toxin concentrations and miRNA concentration in the patients of this cohort. Finally, anemia is a common feature of CKD that is associated with cardiovascular disease and poor clinical outcomes. A mixture of uremic toxins accumulates in the blood of CKD patients during the course of the disease, and there is good evidence that they modulate erythropoiesis, explaining at least partly anemia. The exact molecular mechanisms implicated are however poorly understood, although recent progresses have been made to identify key components in the CKD process. We will present results on the effect of uremic toxins on erythropoiesis, having an impact on cell metabolism during this process. Taken together, our findings could be of interest to both researchers and clinicians working in the field since they might shed new light on the molecular mechanisms involved in the CKD process. MicroRNAs implicated in Chronic Kidney Disease Pr. Laurent Metzinger, UR-UPJV 4666 HEMATIM, CURS, Université de Picardie Jules Verne, CHU Amiens Sud, Avenue René Laënnec, Salouel, F-80054, Amiens, France. Tel: (+33) 22 82 53 56, Email: [email protected]

CHRONIC KIDNEY DISEASE AND THE STATE OF THE CARDIOVASCULAR SYSTEM IN LOCOMOTIVE CREW WORKERS

2021 ◽  
Author(s):  
V.A. Zhmurov ◽  
◽  
D.V. Zhmurov ◽  
V.G. Yarkova
Keyword(s):  
Chronic Kidney Disease ◽  
Kidney Disease ◽  
Cardiovascular System ◽  
Cardiovascular Events ◽  
Ventricular Remodeling ◽  
Myocardial Hypertrophy ◽  
Left Ventricular Remodeling ◽  
Left Ventricular ◽  
Professional Activities ◽  
Ckd Stage

Abstract: 967 employees of locomotive crews (drivers and their assistants of the Sverdlovsk railway of JSC «Russian Railways») were examined. It was revealed that CKD occurs in 12, 09% of employees of locomotive crews. As the CKD stage increases, the progression of changes in the cardiovascular system was found in locomotive crew workers. A high percentage of the prognostically unfavorable variant of left ventricular remodeling - eccentric myocardial hypertrophy (25% - 39.1%, depending on the stage of CKD) was found. These changes may be a factor of adverse cardiovascular events in employees of locomotive crews, which must be taken into account when admitting to professional activities.

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