Cardiovascular Risk in Peritoneal Dialysis

Author(s):  
S. Prichard
2007 ◽  
Vol 27 (2_suppl) ◽  
pp. 205-209 ◽  
Author(s):  
Elvia García–López ◽  
Juan J. Carrero ◽  
Mohamed E. Suliman ◽  
Bengt Lindholm ◽  
Peter Stenvinkel

Patients on peritoneal dialysis (PD) are at high cardiovascular risk. Although some risk factors are unmodifiable (for example, age, sex, genetics), others are exacerbated in the unfriendly uremic milieu (inflammation, oxidative stress, mineral disturbances) or contribute per se to kidney disease and cardiovascular progression (diabetes mellitus, hypertension). Moreover, several factors associated with PD therapy may both increase (by altered lipid profile, hyperinsulinemia, and formation of advanced glycation end-products) and decrease (by better blood pressure control and anemia management) cardiovascular risk. The present review discusses recent findings and therapy trends in cardiovascular research on the PD population, with emphasis on the roles of inflammation, insulin resistance, homocysteinemia, dyslipidemia, vascular calcification, and genetics/epigenetics.


2005 ◽  
Vol 65 (8) ◽  
pp. 739-745 ◽  
Author(s):  
F. M. Yilmaz ◽  
G. Yilmaz ◽  
M. Duranay ◽  
H. Parpucu ◽  
M. Şeneş ◽  
...  

2017 ◽  
Vol 37 (4) ◽  
pp. 375-383 ◽  
Author(s):  
Charlotte E. Grantham ◽  
Katherine L. Hull ◽  
Matthew P.M. Graham-Brown ◽  
Daniel S. March ◽  
James O. Burton

Cardiovascular mortality in the end-stage renal disease (ESRD) population remains the leading cause of death. Targeting traditional cardiovascular risk factors has proven unsuccessful in this patient population, and therefore attention has turned to risk factors related to chronic kidney disease (CKD). The toxicity of high-glucose peritoneal dialysis (PD) solutions has been well documented. The breakdown of glucose into glucose degradation products (GDP) and advanced glycation end-products (AGE) has the ability to alter cell viability and cause premature apoptosis and is strongly correlated with interstitial fibrosis and microvascular sclerosis. Biocompatible solutions have been introduced to combat the hostile milieu to which PD patients are exposed.Given the considerable cardiovascular burden for PD patients, little is known about the cardiovascular impact the new biocompatible solutions may have. This review analyzes the existing literature regarding the mechanisms through which low-GDP solutions may modulate cardiovascular risk. Interventions using low-GDP solutions have provided encouraging changes in structural cardiovascular measures such as left ventricular mass (LVM), although metabolic changes from reduced GDP and AGE exposure yield inconclusive results on vascular remodelling. It is thought that the local effects of reduced glucose exposure may improve membrane integrity and therefore fluid status. Further research in the form of a robust randomized controlled trial should be carried out to assess the true extent of the cardiovascular benefits these biocompatible solutions may hold.


2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii550-iii551
Author(s):  
Mooyong Park ◽  
Soo Jeong Choi ◽  
Seung Duk Hwang ◽  
Jin Kuk Kim ◽  
Hye Min Jo

2010 ◽  
Vol 90 ◽  
pp. 685
Author(s):  
M. J. Pérez-Sáez ◽  
K. Toledo ◽  
L. González-Burdiel ◽  
M. L. Agüera ◽  
D. Del Castillo ◽  
...  

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Juan Manuel Sacnun ◽  
Rebecca Herzog ◽  
Maria Bartosova ◽  
Claus Schmitt ◽  
Klaus Kratochwill

Abstract Background and Aims The composition of all currently available peritoneal dialysis (PD) fluids triggers morphological and functional changes in the peritoneal membrane. Periodic exposure leads to vasculopathy, hypervascularization, and diabetes-like damage of vessels, eventually leading to failure of the technique. Patients undergoing dialysis generally, have a high risk of cardiovascular events. It is currently unclear if there is a mechanistic link between peritoneal membrane failure and cardiovascular risk. In vitro and in vivo studies have shown that cytoprotective additives (e.g. dipeptide alanyl-glutamine (AlaGln) or kinase inhibitor lithium chloride (LiCl)) to PDF reduce peritoneal damage. Here, we developed an experimental model for investigating effects of these cytoprotective additives in PDF in the cardiovascular context. Method For modelling the peritoneal membrane in vitro, mesothelial and endothelial cells were co-cultured in transwell plates. Mesothelial cells were grown in the upper compartment and primary human umbilical vein endothelial cells (HUVEc) or primary microvascular cells were grown in the lower compartment. PDF with or without cytoprotective compounds, was added to the upper compartment to only expose mesothelial cells directly to different dilutions of the fluid. Effects on cell damage was assessed by quantification of lactate-dehydrogenase (LDH) release and live-dead staining of cells. Proteome profiles were analysed for both cell-types separately and in combination using two-dimensional difference gel electrophoresis (2D-DiGE) and liquid chromatography coupled to mass spectrometry (LC-MS). In vitro findings were related to PD-induced arteriolar changes based on abundance profiles of micro-dissected omental arterioles of children treated with conventional PD-fluids and age-matched controls with normal renal function. Results Marked cellular injury of HUVEc after PD-fluid exposure was associated with a molecular landscape of the enriched biological process clusters ‘glucose catabolic process’, ‘cell redox homeostasis’, ‘RNA metabolic process’, ‘protein folding’, ‘regulation of cell death’, and ‘actin cytoskeleton reorganization’ that characterize PD-fluid cytotoxicity and counteracting cellular repair process respectively. PDF-induced cell damage was reduced by AlaGln and LiCl both in mesothelial and endothelial cells. Proteome analysis revealed perturbation of major cellular processes including regulation of cell death and cytoskeleton reorganization. Selected markers of angiogenesis, oxidative stress, cell junctions and transdifferentiation were counter-regulated by the additives. Co-cultured cells yielded differently regulated pathways following PDF exposure compared to separate culture. Comparison to human arterioles confirmed overlapping protein regulation between endothelial cells in vitro and in vivo, proving harmful effects of PD-fluids on endothelial cells leading to drastic changes of the cellular process landscape. Conclusion In summary, this study shows harmful effects of PD-fluids also effecting endothelial cells and elucidates potential mechanisms by which cytoprotective additives may counteract the signalling axis between local peritoneal damage and systemic vasculopathy. An in vitro co-culture system may be an attractive approach to simulate the peritoneal membrane for testing direct and indirect effects of cytoprotective additives in PDF. When cultured and stressed in close proximity cells may respond differently. Characterisation of PD-induced perturbations will allow identifying molecular mechanisms linking the peritoneal and cardiovascular context, offering therapeutic targets to reduce current limitations of PD and ultimately decreasing cardiovascular risk of dialysis patients.


2015 ◽  
Vol 30 (suppl_3) ◽  
pp. iii542-iii542
Author(s):  
Nikolina Basic-Jukic ◽  
Josipa Radic ◽  
Bozidar Vujicic ◽  
Zeljka Grdan ◽  
Marko Jakic ◽  
...  

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