American Journal of Kidney Diseases

2019

DOI: 10.1053/j.ajkd.2018.09.012

|View full text |Cite

|

Sign up to set email alerts

|

Use of Measures of Inflammation and Kidney Function for Prediction of Atherosclerotic Vascular Disease Events and Death in Patients With CKD: Findings From the CRIC Study

Richard L. Amdur

¹

,

Harold I. Feldman

²

,

Elizabeth A. Dominic

³

et al.

Help me understand this report

Search citation statements

Order By: Relevance

Paper Sections

Select...

Discussion1

Effects Of Uts On Endothelial and Endothelial Progenitor1

Novel Risk Factors and Biomarkers1

Introduction1

Citation Types

Supporting

2

Mentioning

74

Contrasting

1

Year Published

2019

2019

2023

2023

Publication Types

Select...

Article6

Book2

Preprint1

Other1

Relationship

Self Cite0

Independent10

Authors

Journals

Cited by 111 publications

(77 citation statements)

References 40 publications

Supporting

2

Mentioning

74

Contrasting

1

Order By: Relevance

“…MCP-1 together with IL-6, also upregulated by DOCA treatment and reduced by EV administration, are multifunctional microinflammatory cytokines involved in immunoreaction and inflammation in hypertensive kidney disease 44 . Moreover, IL-6 is commonly found at high levels in the plasma of CKD patients 45 and has been associated with CKD progression through a mechanism involving promotion of renal injury and induction of chronic vascular disease 46 . Interestingly, recent reports highlighted the hypertensive state in DOCA-salt mice as an inflammation progress, where the inflammasome deficiency induces a fall in high BP, along with reduction of macrophages and pro-inflammatory cytokines in the kidneys compared to controls 47 .…”

Section: Discussionmentioning

confidence: 99%

Adipose Mesenchymal Cells-Derived EVs Alleviate DOCA-Salt-Induced Hypertension by Promoting Cardio-Renal Protection

¹

,

²

,

³

et al. 2020

Molecular Therapy - Methods & Clinical Development

View full text Add to dashboard Cite

Hypertension is a long-term condition that can increase organ susceptibility to insults and lead to severe complications such as chronic kidney disease (CKD). Extracellular vesicles (EVs) are cell-derived membrane structures that participate in cell-cell communication by exporting encapsulated molecules to target cells, regulating physiological and pathological processes. We here demonstrate that multiple administration of EVs from adipose-derived mesenchymal stromal cells (ASC-EVs) in deoxycorticosterone acetate (DOCA)-salt hypertensive model can protect renal tissue by maintaining its filtration capacity. Indeed, ASC-EVs downregulated the pro-inflammatory molecules monocyte chemoattracting protein-1 (MCP-1) and plasminogen activating inhibitor-1 (PAI1) and reduced recruitment of macrophages in the kidney. Moreover, ASC-EVs prevented cardiac tissue fibrosis and maintained blood pressure within normal levels, thus demonstrating their multiple favorable effects in different organs. By applying microRNA (miRNA) microarray profile of the kidney of DOCA-salt rats, we identified a selective miRNA signature associated with epithelial-mesenchymal transition (EMT). One of the key pathways found was the axis miR-200-TGF-β, that was significantly altered by EV administration, thereby affecting the EMT signaling and preventing renal inflammatory response and fibrosis development. Our results indicate that EVs can be a potent therapeutic tool for the treatment of hypertension-induced CKD in cardio-renal syndrome.

“…MCP-1 together with IL-6, also upregulated by DOCA treatment and reduced by EV administration, are multifunctional microinflammatory cytokines involved in immunoreaction and inflammation in hypertensive kidney disease 44 . Moreover, IL-6 is commonly found at high levels in the plasma of CKD patients 45 and has been associated with CKD progression through a mechanism involving promotion of renal injury and induction of chronic vascular disease 46 . Interestingly, recent reports highlighted the hypertensive state in DOCA-salt mice as an inflammation progress, where the inflammasome deficiency induces a fall in high BP, along with reduction of macrophages and pro-inflammatory cytokines in the kidneys compared to controls 47 .…”

Section: Discussionmentioning

confidence: 99%

Adipose Mesenchymal Cells-Derived EVs Alleviate DOCA-Salt-Induced Hypertension by Promoting Cardio-Renal Protection

¹

,

²

,

³

et al. 2020

Molecular Therapy - Methods & Clinical Development

View full text Add to dashboard Cite

Hypertension is a long-term condition that can increase organ susceptibility to insults and lead to severe complications such as chronic kidney disease (CKD). Extracellular vesicles (EVs) are cell-derived membrane structures that participate in cell-cell communication by exporting encapsulated molecules to target cells, regulating physiological and pathological processes. We here demonstrate that multiple administration of EVs from adipose-derived mesenchymal stromal cells (ASC-EVs) in deoxycorticosterone acetate (DOCA)-salt hypertensive model can protect renal tissue by maintaining its filtration capacity. Indeed, ASC-EVs downregulated the pro-inflammatory molecules monocyte chemoattracting protein-1 (MCP-1) and plasminogen activating inhibitor-1 (PAI1) and reduced recruitment of macrophages in the kidney. Moreover, ASC-EVs prevented cardiac tissue fibrosis and maintained blood pressure within normal levels, thus demonstrating their multiple favorable effects in different organs. By applying microRNA (miRNA) microarray profile of the kidney of DOCA-salt rats, we identified a selective miRNA signature associated with epithelial-mesenchymal transition (EMT). One of the key pathways found was the axis miR-200-TGF-β, that was significantly altered by EV administration, thereby affecting the EMT signaling and preventing renal inflammatory response and fibrosis development. Our results indicate that EVs can be a potent therapeutic tool for the treatment of hypertension-induced CKD in cardio-renal syndrome.

“…A correlation between IAA levels and CRP in CKD patients was also confirmed in another report [ 13 ]. In a cohort of 2399 CKD patients followed for 7.3 years as well as in a cohort of HD patients, increased inflammation and IS levels were independently associated with atherosclerotic vascular disease [ 53 , 54 ].…”

Section: Effects Of Uts On Endothelial and Endothelial Progenitormentioning

confidence: 99%

Molecular Mechanisms Underlying the Cardiovascular Toxicity of Specific Uremic Solutes

¹

,

²

2020

View full text Add to dashboard Cite

Mounting evidence strongly suggests a causal link between chronic kidney disease (CKD) and cardiovascular disease (CVD). Compared with non-CKD patients, patients with CKD suffer disproportionately from CVD and derive suboptimal benefits from interventions targeting conventional CVD risk factors. Uremic toxins (UTs), whose plasma levels rapidly rise as CKD progresses, represent a unique risk factor in CKD, which has protean manifestations on CVD. Among the known UTs, tryptophan metabolites and trimethylamine N-oxide are well-established cardiovascular toxins. Their molecular mechanisms of effect warrant special consideration to draw translational value. This review surveys current knowledge on the effects of specific UTs on different pathways and cell functions that influence the integrity of cardiovascular health, with implication for CVD progression. The effect of UTs on cardiovascular health is an example of a paradigm in which a cascade of molecular and metabolic events induced by pathology in one organ in turn induces dysfunction in another organ. Deciphering the molecular mechanisms underlying such cross-organ pathologies will help uncover therapeutic targets to improve the management of CVD in patients with CKD.

“…35 Plasma levels of fibrinogen, IL-6, and TNF-α have been shown to have positive independent associations with a composite of incident MI, PAD, stroke, and death. 36 Moderate kidney disease has also been shown to inhibit the regression of atherosclerosis in a mouse model as a result of impaired chemokine receptor 7 signaling. This resulted in macrophage accumulation in the atherosclerotic lesions that may increase foam cell formation.…”

Section: Novel Risk Factors and Biomarkersmentioning

confidence: 99%

<p>Mild to moderate chronic kidney disease and cardiovascular events in patients with type 2 diabetes mellitus</p>

Stavropoulos²,

Papademetriou³

2019

View full text Add to dashboard Cite

Chronic kidney disease (CKD) has become a major public health problem in the USA and worldwide. A large majority of patients with CKD have mild to moderate disease and microalbuminuria. It has increasingly been noted that patients with CKD have a significantly higher risk of cardiovascular outcomes compared to patients with normal kidney function. Many studies have shown increased risk beginning at stage 3 CKD but risk has been elevated in patients with milder degrees of kidney dysfunction in some studies. This risk may be better predicted by the degree of albuminuria in the earlier stages of CKD. Data addressing interventions to improve outcomes in patients with mild to moderate CKD are scarce. In this paper, we examined data and post hoc analyses from the ORIGIN and ACCORD trials. Data indicate that intensive treatment of diabetes in patients with CKD actually may result in adverse outcomes. The mechanism by which CKD results in increased cardiovascular risk is not clear. Patients with CKD frequently have the traditional risk factors that cause cardiovascular disease and there are mechanisms that are unique to CKD that promote the development of cardiovascular disease. In this article, we describe in some detail traditional, newer and novel risk factors that play a role in the development of CKD and heart disease.

scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.

Contact Info

customersupport@researchsolutions.com

10624 S. Eastern Ave., Ste. A-614

Henderson, NV 89052, USA

Product

Browser Extension Assistant by scite Citation Statement Search Reference Check Visualizations Dashboards Explore Journals Explore Organizations Explore Funders Embedding Badge Embedding Citation Search Pricing

Resources

Blog Help & FAQ Accessibility Statement API Terms For Universities & Governments For Researchers For Publishers For Corporate, Pharma & Enterprise Author Marketing Become an Affiliate Get an organization trial or quote scite Data & Services

About

News & Press Careers Read our Paper Coverage

This site is protected by reCAPTCHA and the Google Privacy Policy and Terms of Service apply.

Blog Terms and Conditions API Terms Privacy Policy Contact Cookie Preferences Do Not Sell or Share My Personal Information

Copyright © 2025 scite LLC. All rights reserved.

Made with 💙 for researchers

Part of the Research Solutions Family.