Next Article in Journal
Efficacy of Modified Treat-and-Extend Aflibercept Regimen for Macular Edema Due to Branch Retinal Vein Occlusion: 1-Year Prospective Study
Next Article in Special Issue
Impact of Short-Term Hypoxia on Sirtuins as Regulatory Elements in HUVECs
Previous Article in Journal
Mitochondrial DNA: Hotspot for Potential Gene Modifiers Regulating Hypertrophic Cardiomyopathy
Previous Article in Special Issue
Endothelial Dysfunction: A Contributor to Adverse Cardiovascular Remodeling and Heart Failure Development in Type 2 Diabetes beyond Accelerated Atherogenesis
Open AccessReview

Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update

1
Division of Nephrology and Hypertension, 1st Department of Internal Medicine, School of Medicine, AHEPA Hospital, Aristotle University of Thessaloniki, 54636 Thessaloniki, Greece
2
CNR-IFC (National Research Council of Italy, Centre of Clinical Physiology, Clinical Epidemiology of Renal Diseases and Hypertension Unit, Reggio Cal., c/o Ospedali Riuniti, 89124 Reggio Cal, Italy
*
Author to whom correspondence should be addressed.
J. Clin. Med. 2020, 9(8), 2359; https://doi.org/10.3390/jcm9082359
Received: 8 July 2020 / Revised: 20 July 2020 / Accepted: 21 July 2020 / Published: 23 July 2020
(This article belongs to the Special Issue Atherosclerosis: Endothelial Dysfunction and Beyond)
The vascular endothelium is a dynamic, functionally complex organ, modulating multiple biological processes, including vascular tone and permeability, inflammatory responses, thrombosis, and angiogenesis. Endothelial dysfunction is a threat to the integrity of the vascular system, and it is pivotal in the pathogenesis of atherosclerosis and cardiovascular disease. Reduced nitric oxide (NO) bioavailability is a hallmark of chronic kidney disease (CKD), with this disturbance being almost universal in patients who reach the most advanced phase of CKD, end-stage kidney disease (ESKD). Low NO bioavailability in CKD depends on several mechanisms affecting the expression and the activity of endothelial NO synthase (eNOS). Accumulation of endogenous inhibitors of eNOS, inflammation and oxidative stress, advanced glycosylation products (AGEs), bone mineral balance disorders encompassing hyperphosphatemia, high levels of the phosphaturic hormone fibroblast growth factor 23 (FGF23), and low levels of the active form of vitamin D (1,25 vitamin D) and the anti-ageing vasculoprotective factor Klotho all impinge upon NO bioavailability and are critical to endothelial dysfunction in CKD. Wide-ranging multivariate interventions are needed to counter endothelial dysfunction in CKD, an alteration triggering arterial disease and cardiovascular complications in this high-risk population. View Full-Text
Keywords: endothelial dysfunction; nitric oxide; ADMA; SDMA; cardiovascular risk; chronic kidney disease (CKD), end-stage kidney disease (ESKD) endothelial dysfunction; nitric oxide; ADMA; SDMA; cardiovascular risk; chronic kidney disease (CKD), end-stage kidney disease (ESKD)
Show Figures

Figure 1

MDPI and ACS Style

Roumeliotis, S.; Mallamaci, F.; Zoccali, C. Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update. J. Clin. Med. 2020, 9, 2359. https://doi.org/10.3390/jcm9082359

AMA Style

Roumeliotis S, Mallamaci F, Zoccali C. Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update. Journal of Clinical Medicine. 2020; 9(8):2359. https://doi.org/10.3390/jcm9082359

Chicago/Turabian Style

Roumeliotis, Stefanos; Mallamaci, Francesca; Zoccali, Carmine. 2020. "Endothelial Dysfunction in Chronic Kidney Disease, from Biology to Clinical Outcomes: A 2020 Update" J. Clin. Med. 9, no. 8: 2359. https://doi.org/10.3390/jcm9082359

Find Other Styles
Note that from the first issue of 2016, MDPI journals use article numbers instead of page numbers. See further details here.

Article Access Map by Country/Region

1
Search more from Scilit
 
Search
Back to TopTop