Vascular inflammation and media calcification are already present in early stages of chronic kidney disease

Benz, Kerstin; Varga, Ildikó; Neureiter, Daniel; Câmpean, Valentina; Daniel, Christoph; Heim, Christian; Reimann, Albrecht; Weyand, Michael; Hilgers, Karl F.; Amann, Kerstin

doi:10.1016/j.carpath.2017.01.004

Cited by 51 publications

(38 citation statements)

References 45 publications

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“…CKD is a representative condition wherein inflammation and VC share pathogenesis. Indeed, a recent report claims that vascular media calcification and related inflammation exist even in the early stages of CKD [296]. It has also been reported that mRNA levels of components of the Nalp3 inflammasome complex, including Nalp3, ASC, and caspase-1 were upregulated in calcifying VSMCs.…”

Section: Inflammation and Immune Dysregulation In The Pathogenesis Ofmentioning

confidence: 98%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

254

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Vascular calcification (VC), which is categorized by intimal and medial calcification, depending on the site(s) involved within the vessel, is closely related to cardiovascular disease. Specifically, medial calcification is prevalent in certain medical situations, including chronic kidney disease and diabetes. The past few decades have seen extensive research into VC, revealing that the mechanism of VC is not merely a consequence of a high-phosphorous and -calcium milieu, but also occurs via delicate and well-organized biologic processes, including an imbalance between osteochondrogenic signaling and anticalcific events. In addition to traditionally established osteogenic signaling, dysfunctional calcium homeostasis is prerequisite in the development of VC. Moreover, loss of defensive mechanisms, by microorganelle dysfunction, including hyper-fragmented mitochondria, mitochondrial oxidative stress, defective autophagy or mitophagy, and endoplasmic reticulum (ER) stress, may all contribute to VC. To facilitate the understanding of vascular calcification, across any number of bioscientific disciplines, we provide this review of a detailed updated molecular mechanism of VC. This encompasses a vascular smooth muscle phenotypic of osteogenic differentiation, and multiple signaling pathways of VC induction, including the roles of inflammation and cellular microorganelle genesis.

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Section: Inflammation and Immune Dysregulation In The Pathogenesis Ofmentioning

confidence: 98%

Vascular Calcification—New Insights into Its Mechanism

Lee

Jeon

2020

IJMS

254

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“…Vascular inflammation and mVC are a coexisting phenomenon currently shown for patients with early-stage of chronic kidney disease. 33 Thereby, inflammation either can occur initially or further promote mineralization as well. 34 Chronic inflammation is associated with arterial stiffness and inhibition of tumor-necrosis-factor-α (TNFα) resulting in decreased PWV.…”

Section: Inflammationmentioning

confidence: 99%

In times of tobacco‐free nicotine consumption: The influence of nicotine on vascular calcification

Babic

Schuchardt

Tölle

et al. 2019

Eur J Clin Investigation

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Background Smoking remains the most important avoidable cause of global mortality. Even though the number of cigarette smokers declines in first world countries, the uses of alternative nicotine delivery products increase and may even surpass the sells of cigarettes. In this light, the explicit role of nicotine in the development of cardiovascular diseases should be elucidated. Objectives This narrative review attempts to connect current literature about possible effects of nicotine on the environment of the vasculature to the pathogenesis of vascular calcification, focusing on the tunica media of the vessel wall. Methods For this review, papers found on Pubmed and Medline until December 2018 by searching for the keywords nicotine, vascular calcification, oxidative stress, osteoblastic transdifferentiation and matrix degradation were considered. Results Nicotine creates an environment that probably facilitates and maybe even induces osteogenic transdifferentiation of VSMC by inflammation, endothelial dysfunction and reactive oxygen species. This process is believed to be a key event in calcification of the tunica media of the vessel wall. Furthermore, nicotine could lead to the formation of nucleation sites for hydroxyapatite by facilitating matrix vesicles and extracellular matrix degradation. Conclusions There is a growing body of evidence implicating that nicotine alone could impair vascular function and lead to vascular calcification. Further research is necessary to elucidate the explicit influence of nicotine on arteriosclerosis.

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“…But beyond the obvious infective, hemodynamic and anatomic injury potential, their linkage to vascular immunoreactivity found in CKD is of growing concern. This latter may be reflected in the noted proinflammatory state reported in CKD wherein immunoinflammatory activation could trigger or amplify formation of the biomass [17,18]. This altered environment in CKD is thought to be important in the development of adverse cardiovascular (CV) outcomes, and we ask whether such vascular immunoreactivity ultimately contributes to characteristic vascular pathology in the form of accelerated coronary atherosclerotic disease found in hemodialysis patients [19][20][21][22][23].…”

Section: Introductionmentioning

confidence: 99%

Hemodialysis Catheter-related Masses Case Report the Pro Inflammatory State in Chronic Kidney Disease

2019

JCRC

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Indwelling venous catheters provide essential functional vascular access for patients requiring emergent or urgent hemodialysis, though their long-term use is practically limited by known complications including increased rates of infection as compared with surgically created arteriovenous (AV) fistulas. Converging lines of evidence also support that chronic kidney disease (CKD) represents a pro-inflammatory state, an environment with active cellular and inflammatory pathobiology. Accordingly, implantation of catheters for even short-term use is associated with a fibrinthrombin-cellular matrix often forming around the catheter. This "biomass" long considered innocuous, can cause occlusion of the catheter, contributing to reduced flow rates during dialysis. It may also result in embolic injury of downstream structures. This case report identifies a complex catheter-related biomass remaining after removal of the hemodialysis catheter and focuses on two concerns. First, intravenous masses associated with the catheter, or remaining after removal may provoke embolic and direct hemodynamic-related injury. But perhaps less obvious is their potential linkage to vascular immunoreactivity found in CKD. This latter potential may need to be part of the larger discussion surrounding the outcomes of such pathologic immunoresponsiveness in CKD patients on hemodialysis. www.opastonline.com J Clin Rev Case Rep, 2019 Volume 4 | Issue 1 | 2 of 4 www.opastonline.com J Clin Rev Case Rep, 2019 Volume 4 | Issue 1 | 4 of 4 Copyright: ©2019 Dr. John D Rozich, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Vascular inflammation and media calcification are already present in early stages of chronic kidney disease

Cited by 51 publications

References 45 publications

Vascular Calcification—New Insights into Its Mechanism

Vascular Calcification—New Insights into Its Mechanism

In times of tobacco‐free nicotine consumption: The influence of nicotine on vascular calcification

Hemodialysis Catheter-related Masses Case Report the Pro Inflammatory State in Chronic Kidney Disease

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