scholarly journals There Is No Impact of Diabetes on the Endothelial Function of Chronic Kidney Disease Patients

2018 ◽  
Vol 2018 ◽  
pp. 1-8 ◽  
Author(s):  
Mariana Nogueira Coutinho ◽  
Aluizio Barbosa Carvalho ◽  
Maria Aparecida Dalboni ◽  
Margaret Gori Mouro ◽  
Elisa Mieko Suemitsu Higa ◽  
...  

Background. Patients with chronic kidney disease (CKD) and type 2 diabetes mellitus (DM) have increased risk of endothelial dysfunction, cardiovascular disease, and mortality. Several studies have separately analyzed endothelial function in these populations. However, data of patients with both CKD and DM are scarce. The aim of this study was to evaluate whether the presence of DM has any additional effect on the endothelial dysfunction of CKD patients.Methods. We measured endothelial progenitor cells (EPCs), stromal-derived factor 1 alpha (SDF-1α), serum and urinary nitric oxide (NO), flow-mediated dilation (FMD), and pulse wave velocity (PWV) in 37 CKD patients with DM (CKD-DM group) and in 37 without DM (CKD group).Results. CKD-DM group had a higher prevalence of obesity (P<0.01), previous myocardial infarction (P=0.02), myocardial revascularization (P=0.04), and a trend for more peripheral artery disease (P=0.07). Additionally, CKD-DM group had higher EPC (P=0.001) and PWV (P<0.001) values. On the other hand, no difference in SDF-1αand serum or urinary NO and FMD was observed between the groups.Conclusions. Endothelial dysfunction is frequent in CKD patients, and an additive effect of diabetes cannot be implicated, suggesting the predominant role of uremia in this condition.

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Yooju Nam ◽  
Seonyeong Lee ◽  
Hyung Woo Kim ◽  
Jae Hyun Chang ◽  
Tae-Hyun Yoo

Abstract Background and Aims Osteoprotegerin (OPG), which is an osteoclastic inhibitory factor, is associated with type 2 diabetes mellitus, severity of vascular calcification, coronary artery disease, and chronic kidney disease. Obesity is a risk factor for diabetes, and cardiovascular disease, however there are few studies about the relationship between OPG and obesity, especially in patients with CKD. This study aimed to investigate association between OPG level and obesity in a large-scale prospective cohort. Method Among 2,238 patients with non-dialysis CKD enrolled in the KoreaN cohort study for Outcome in patients With Chronic Kidney Disease (KNOW-CKD), 1,970 patients who measured body mass index (BMI), waist circumference (WC) and OPG level were included in the analysis. Obesity were defined as having a BMI &gt;25 kg/m2 and WC &gt; 90 cm in male, &gt; 85 cm in female. Results The mean age was 53.6 ± 12.2 years and 1,196 (60.7%) patients were males. At baseline, obesity by BMI, WC, and composite of BMI and WC were found in 814 (41.3%), 208 (26.9%) and 1,137 (57.7%) patients. A multivariate logistic regression model showed that log transformed OPG level was independently associated with the prevalence of obesity by BMI, WC, composite of BMI and WC (odds ratio [OR], 0.33; 95% confidence interval [CI], 0.16-0.65, P&lt;0.001 and OR, 0.37; 95% CI, 0.18-0.75, P=0.006, and OR, 0.33, 95% CI, 0.16-0.69, P=0.003, respectively). Among patients without baseline obesity, 207 (19.3%) patients developed obesity by BMI, 202 (21.7%) by WC, and 194 (23.3%) by composite of BMI and WC. In the fully adjusted multivariable Cox models, risks of developing obesity by BMI, WC and composite of BMI and WC were significantly higher with increased level of OPG (hazard ratio [HR], 0.59; 95% CI, 0.38-0.92; P=0.019, HR, 0.63; 95% CI, 0.41-0.98; P=0.001). Conclusion We showed that serum OPG levels are associated with obesity in patients with non-dialysis CKD.


2017 ◽  
Vol 89 (10) ◽  
pp. 87-94
Author(s):  
I T Murkamilov ◽  
I S Sabirov ◽  
V V Fomin ◽  
F A Yusupov

In recent years, one of the promising areas in clinical medicine is the study of impaired ments in endothelial function and arterial wall stiffness, which can be referred to as one of the important predictors of cardiovascular events in patients with chronic kidney disease, including that of diabetic etiology. There is strong evidence that endothelial function and great artery stiffness may be used as reliable clinical and instrumental indicators to evaluate the efficiency of therapeutic measures and the rate of progression of cardiovascular disorders in type 2 diabetes mellitus. The article presents data on the role of endothelial dysfunction and arterial wall stiffness in the progression of chronic kidney disease in type 2 diabetes mellitus and discusses the possibility of their correction with pharmacological agents.


2021 ◽  
Author(s):  
Resham L Gurung ◽  
Rajkumar Dorajoo ◽  
Yiamunaa M ◽  
Ling Wang ◽  
Sylvia Liu ◽  
...  

Abstract Background Chronic kidney disease (CKD) is common among type 2 diabetes (T2D) and increases the risk of kidney failure and cardiovascular diseases. Shorter leukocyte telomere length is associated with CKD in patients with T2D. We previously reported single nucleotide polymorphisms (SNPs) associated with leukocyte telomere length in Asian population. In this study, we elucidated the association of these SNPs with CKD in patients with T2D using Mendelian randomization (MR) approach. Methods The cross-sectional association of 16 leukocyte telomere length SNPs with CKD, defined as an estimated glomerular filtration rate of less than 60 ml/min/1.73m2 was assessed among 4,768 (1,628 cases, 3,140 controls) participants in the Singapore Study of Macro-angiopathy and Micro-vascular Reactivity in Type 2 Diabetes and Diabetic Nephropathy cohorts. MR analysis was performed using the random-effect inverse-variance weighted (IVW) method, the weighted median, MR-Egger and Radial MR adjusted for age and sex-stratified by cohorts and ethnicity (Chinese and Malays), then meta-analysed. Results Genetically determined shorter leukocyte telomere length was associated with increased risk of CKD in patients with T2D (meta-IVW adjusted odds ratio = 1.51 [95% confidence interval, 1.12 - 2.12; P = 0.007; Phet= 0.547]). Similar results were obtained following sensitivity analysis. MR-Egger analysis (intercept) suggested no evidence of horizontal pleiotropy (β  =  0.010, P = 0.751). Conclusions Our findings suggest that genetically determined leukocyte telomere length is associated with CKD in patients with T2D. Further studies are warranted to elucidate the causal role of telomere length in CKD progression.


2021 ◽  
Vol 22 (19) ◽  
pp. 10549
Author(s):  
Ophélie Fourdinier ◽  
Griet Glorieux ◽  
Benjamin Brigant ◽  
Momar Diouf ◽  
Anneleen Pletinck ◽  
...  

Chronic kidney disease (CKD) is a major cause of death worldwide and is associated with a high risk for cardiovascular and all-cause mortality. In CKD, endothelial dysfunction occurs and uremic toxins accumulate in the blood. miR-126 is a regulator of endothelial dysfunction and its blood level is decreased in CKD patients. In order to obtain a better understanding of the physiopathology of the disease, we correlated the levels of miR-126 with several markers of endothelial dysfunction, as well as the representative uremic toxins, in a large cohort of CKD patients at all stages of the disease. Using a univariate analysis, we found a correlation between eGFR and most markers of endothelial dysfunction markers evaluated in this study. An association of miR-126 with all the evaluated uremic toxins was also found, while uremic toxins were not associated with the internal control, specifically cel-miR-39. The correlation between the expression of endothelial dysfunction biomarker Syndecan-1, free indoxyl sulfate, and total p-cresyl glucuronide on one side, and miR-126 on the other side was confirmed using multivariate analysis. As CKD is associated with reduced endothelial glycocalyx (eGC), our results justify further evaluation of the role of correlated parameters in the pathophysiology of CKD.


Pharmacophore ◽  
2021 ◽  
Vol 12 (3) ◽  
pp. 91-94
Author(s):  
Mishal Yousef Alqurashi ◽  
Khalid Faisal Alharthi ◽  
Abdulaziz Abdulrahman Alshehri ◽  
Yazeed Khalid Alharbi ◽  
Mohammad Abdulmunem Sanousi ◽  
...  

2016 ◽  
Vol 31 (suppl_1) ◽  
pp. i302-i302
Author(s):  
Aleix Cases ◽  
Manel Vera ◽  
Marta Palomo ◽  
Susana Martin-Rodriguez ◽  
Josep Maria Cruzado ◽  
...  

2019 ◽  
Vol 20 (15) ◽  
pp. 3775 ◽  
Author(s):  
Cesar A. Meza ◽  
Justin D. La Favor ◽  
Do-Houn Kim ◽  
Robert C. Hickner

NADPH oxidases (NOX) are enzyme complexes that have received much attention as key molecules in the development of vascular dysfunction. NOX have the primary function of generating reactive oxygen species (ROS), and are considered the main source of ROS production in endothelial cells. The endothelium is a thin monolayer that lines the inner surface of blood vessels, acting as a secretory organ to maintain homeostasis of blood flow. The enzymatic production of nitric oxide (NO) by endothelial NO synthase (eNOS) is critical in mediating endothelial function, and oxidative stress can cause dysregulation of eNOS and endothelial dysfunction. Insulin is a stimulus for increases in blood flow and endothelium-dependent vasodilation. However, cardiovascular disease and type 2 diabetes are characterized by poor control of the endothelial cell redox environment, with a shift toward overproduction of ROS by NOX. Studies in models of type 2 diabetes demonstrate that aberrant NOX activation contributes to uncoupling of eNOS and endothelial dysfunction. It is well-established that endothelial dysfunction precedes the onset of cardiovascular disease, therefore NOX are important molecular links between type 2 diabetes and vascular complications. The aim of the current review is to describe the normal, healthy physiological mechanisms involved in endothelial function, and highlight the central role of NOX in mediating endothelial dysfunction when glucose homeostasis is impaired.


Sign in / Sign up

Export Citation Format

Share Document