Search

Cardiovascular disease (CVD) incidence is high in patients with chronic kidney disease (CKD) and is the most frequent cause of mortality in this population. Advanced age, hypertension, uremic toxins, endothelial dysfunction, atherosclerosis, hyperhomocysteinemia, oxidative stress, and inflammation are among the leading causes of increased CVD in advanced stages of CKD. Although defined as a decrease in muscle strength associated with aging, sarcopenia is also prevalent in CKD patients. Sarcopenia causes physical disability, low quality of life, and mortality. Regular exercise and nutritional supplementation may slow the progression of sarcopenia. Recent studies have shown that sarcopenia increases the risk of CVD and mortality in people with or without kidney disease. This review discusses the relationship between sarcopenia and CVD in light of the current literature., (© 2022. The Author(s), under exclusive licence to Springer Nature B.V.)

Endothelins including its most abundant isoform, endothelin-1 (ET-1), are peptides acting as vasoconstrictors when binding to ET A and ET B receptors, and, in addition to their distinct roles in normal physiology, endothelins have a central role in the pathophysiology of many diseases including cardiovascular and renal diseases. Endothelin-1 (ET-1), the most potent vasoconstrictor in the cardiovascular system, regulates basal vascular tone and glomerular hemodynamics. ET-1 is involved also in vascular and cardiac hypertrophy, inflammation, and in the development and progression of cardiovascular diseases - e.g. essential hypertension, atherosclerosis, coronary artery disease, congestive heart failure, pulmonary arterial hypertension and cerebrovascular disease and renal diseases - e.g. acute renal failure, polycystic kidney disease and chronic kidney disease. Not surprisingly, the ET system has become a target for therapeutic interventions that now include a few already established and some new promising agents. In this narrative review, we summarize physiologic properties of the ET system, focusing especially on ET-1, and its role in the pathophysiology of ET system activated diseases, and discuss the potentials of therapeutic interventions targeting the ET system in cardiovascular and renal diseases. While ET receptor antagonists have already revolutionized the management of idiopathic pulmonary arterial hypertension, so far, this class of drugs have failed as medication for congestive heart failure. Clinical trials continue to explore new applications of endothelin receptor antagonists in treatment-resistant hypertension and chronic kidney disease and have shown some benefits in the latter group by reducing proteinuria; however, they have not been approved yet. We conclude that larger clinical trials are needed to validate the use of ET receptor antagonists in ET system activated diseases., Competing Interests: Declaration of Competing Interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper., (Copyright © 2020 Elsevier B.V. All rights reserved.)

Cardiovascular events make up the primary cause of death in hemodialysis patients, and the risk for cardiovascular mortality is significantly increased by vascular calcification, a condition observed frequently in this patient population. The mechanisms underlying the pathogenesis of vascular calcification are complex, and many factors facilitate or hinder the development of calcification. In this review, we first summarize the main factors contributing to the pathogenesis of vascular calcification in patients with end-stage renal disease. We then explore the role of calcification inhibitors in the calcification process, as well as their effect on vascular dysfunction and mortality in hemodialysis patients., (© 2017 Wiley Periodicals, Inc.)

Background: Profilin-1 is a ubiquitous, actin-binding protein that plays an important role in the regulation of actin polymerization and cytoskeleton remodelling and contributes to vascular dysfunction. We conducted this study to investigate the association of serum profilin-1 levels with fatal and nonfatal CVE in a cohort of patients with stage 1-5 CKD., Materials and Methods: Serum concentrations of profilin-1 levels were determined by enzyme-linked immunosorbent assay. Endothelium-dependent vasodilatation (flow-mediated dilatation [FMD]) and endothelium-independent vasodilatation (nitroglycerine-mediated dilatation [NMD]) of the brachial artery were assessed noninvasively, using high-resolution ultrasound., Results: Both fatal and nonfatal CVE were significantly higher in patients with high profilin-1 levels. Kaplan-Meier survival curves showed that patients with profilin-1 below the median value (114 pg/mL) had higher cumulative survival compared with patients who had profilin-1 levels above the median value (log-rank test, P < .001)., Conclusions: This is the first study that demonstrates the serum profilin-1 is independently associated with endothelial dysfunction, cardiovascular events and survival in patients with CKD., (© 2017 Stichting European Society for Clinical Investigation Journal Foundation.)

Objective: Increased inflammation, associated with the increase in chronic kidney disease (CKD) stage, has a very important influence in vascular injury and cardiovascular diseases. In this study, we aimed to investigate the levels of IL-33 and ST2 in the different stages of CKD and to determine their effect on vascular damage and cardiovascular events (CVE)., Methods: This was an observational cohort study in which serum IL-33 and ST2 were obtained from 238 CKD (stages 1-5) patients. We examined the changes in IL-33/ST2 levels in CKD patients, as well as the association with a surrogate of endothelial dysfunction. Fatal and non-fatal CVE were recorded for a mean of 24 months. We also performed a COX regression analysis to determine the association of IL-33/ST2 levels with CVE and survival., Results: IL-33 and ST2 levels were significantly increased and estimated glomerular filtration rates (eGFR) were decreased. Flow-mediated dilatation (FMD) was significantly decreased from stage 1 to stage 5 CKD. IL-33 and ST2 levels were associated with FMD, and ST2 was a predictor. Multivariate Cox analysis showed that the presence of diabetes mellitus, smoking, and proteinuria and haemoglobin, Hs-CRP, IL-33, and ST2 were associated with the risk of CVE. Kaplan-Meier survival curves showed that patients with IL-33 and ST2 levels below the median value (IL-33 = 132.6 ng/L, ST2 = 382.9 pg/mL) had a higher cumulative survival compared with patients who had IL-33 and ST2 levels above the median value (log-rank test, p = 0.000)., Conclusion: This is the first study that demonstrates that serum IL-33 and ST2 are associated with vascular injury, cardiovascular events, and survival in CKD patients.

Aims: Cardiovascular disease is a major cause of mortality in renal transplant recipients. Paraoxonase-1 (PON-1) has been shown to protect against atherosclerosis by modifying lipoproteins. Epicardial fat tissue (EFT) has been proposed as a new cardiovascular risk factor. The aim of this study was to investigate the relationship between PON-1 activity and EFT in renal transplant recipients., Methods: Eighty renal transplant recipients were enrolled in this cross-sectional study. PON-1 activity was assessed from the rate of enzymatic hydrolysis of paraoxon to p-nitrophenol. EFT was measured by echocardiography., Results: The mean age of the patients was 40.4 ± 12.3 years and mean post transplant follow-up duration was 57.2 ± 46 months. Mean PON-1 activity was 68.5 ± 30 U/L. PON-1 activity was positively correlated with age and body mass index and negatively correlated with parathyroid hormone, dialysis duration and EFT. The mean EFT thickness was 0.64 ± 0.17 cm. Multiple linear regression analysis was used to define independent determinants of EFT in renal transplant recipients. According to linear regression analysis, PON-1 levels and age were found to be independent predictors of EFT., Conclusion: Reduced PON-1 activity was negatively associated with EFT and PON-1 activity independently predicts EFT in renal transplant recipients.

Introduction: Arterial stiffness is a risk marker for cardiovascular events in peritoneal dialysis (PD) patients. Strict volume control strategy has been shown to result in better cardiac functions and control of hypertension in these patients. The aim of the study was to identify the determinants of arterial stiffness and evaluate the changes in cardiac biomarkers in PD patients under strict volume control strategy., Methods: 58 PD patients were enrolled into this prospective observational study. Arterial stiffness determined by aortic pulse wave velocity (PWV), echocardiography, ambulatory blood pressure and NT-pro-BNP levels were measured at baseline and at first year., Results: The mean age of the patients was 46.4 ± 14 years. 30 patients were on automated PD (APD) and 28 on continuous ambulatory PD (CAPD) group. In both groups, there were significant differences in PWV values at baseline and at the end of the study. A similar decrease was observed with NT-proBNP and PWV levels. In addition, a significant improvement was found in echocardiographic parameters in all patients. Comparison of APD and CAPD groups with respect to change in one year, showed no difference in echocardiographic findings, while the reduction in PWV, NTproBNP and blood pressure values was higher in the CAPD group., Conclusions: In PD patients, strict volume control leads to a reduction in NT-pro-BNP levels, better control of blood pressure and significant improvements in cardiac functions and arterial stiffness.