Circulating Progenitor Cells Affect Thrombosis of Dialysis Arteriovenous Fistulas

Chen, Tsung Yan; Lin, Ting Tse; Hsieh, Mu-Yang; Lin, Lin; Yang, Chung-Wei; Chuang, Shao Yuan; Huang, Po Hsun; Wu, Chih‐Cheng

doi:10.1159/000452428

Cited by 6 publications

(6 citation statements)

References 33 publications

(38 reference statements)

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“…Delayed reendothelialization secondary to decreased endothelial cell proliferation and migration is related to increased risk for delayed thrombosis observed after endovascular therapy in CKD patients [37,38]. This is especially relevant to CKD patients, as adequate vascular access sites for hemodialysis (HD) often serve as their lifeline, and these sites are especially susceptible to thrombosis in the setting of repeated endothelial injury [39][40][41].…”

Section: Alteration Of the Procoagulant Function Of Endothelial Cellsmentioning

confidence: 99%

Molecular Mechanisms Underlying the Cardiovascular Toxicity of Specific Uremic Solutes

Ravid

Chitalia

2020

Cells

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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.

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Section: Alteration Of the Procoagulant Function Of Endothelial Cellsmentioning

confidence: 99%

Molecular Mechanisms Underlying the Cardiovascular Toxicity of Specific Uremic Solutes

Ravid

Chitalia

2020

Cells

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“…In CKD patients, endothelium dysfunction begins in the early stages of CKD [ 42 ] and takes a substantial part in thrombotic events [ 43 ]. In hemodialysis patients, endothelial injury is associated with an increased risk of AVF thrombosis [ 44 , 45 , 46 ]. The modifications of hemodynamic stress in vascular access and the accumulation of uremic toxins play a major role in endothelium dysfunction [ 45 ].…”

Section: Thrombotic Mechanisms Induced By Tryptophan-derived Uremimentioning

confidence: 99%

Tryptophan-Derived Uremic Toxins and Thrombosis in Chronic Kidney Disease

Addi

Dou

Burtey

2018

Toxins

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Patients with chronic kidney disease (CKD) display an elevated risk of thrombosis. Thrombosis occurs in cardiovascular events, such as venous thromboembolism, stroke, and acute coronary syndrome, and is a cause of hemodialysis vascular access dysfunction. CKD leads to the accumulation of uremic toxins, which exerts toxic effects on blood and the vessel wall. Some uremic toxins result from tryptophan metabolization in the gut through the indolic and the kynurenine pathways. An increasing number of studies are highlighting the link between such uremic toxins and thrombosis in CKD. In this review, we describe the thrombotic mechanisms induced by tryptophan-derived uremic toxins (TDUT). These mechanisms include an increase in plasma levels of procoagulant factors, induction of platelet hyperactivity, induction of endothelial dysfunction/ impairment of endothelial healing, decrease in nitric oxide (NO) bioavailability, and production of procoagulant microparticles. We focus on one important prothrombotic mechanism: The induction of tissue factor (TF), the initiator of the extrinsic pathway of the blood coagulation. This induction occurs via a new pathway, dependent on the transcription factor Aryl hydrocarbon receptor (AhR), the receptor of TDUT in cells. A better understanding of the prothrombotic mechanisms of uremic toxins could help to find novel therapeutic targets to prevent thrombosis in CKD.

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“…Endothelial progenitor cells have been shown to mobilize and incorporate into the denuded vessel wall, a process associated with accelerated re-endothelialization [ 61 ]. Clinical studies have shown progenitor cell deficiency to be associated with restenosis and thrombosis after endovascular intervention [ 62 , 63 , 64 ]. Indoxyl sulfate has a deleterious effect on progenitor cell function, which may precipitate thrombosis through delayed re-endothelialization [ 36 ].…”

Section: Indoxyl Sulfate and Thrombosis Of Dialysis Vascular Accesmentioning

confidence: 99%

Impact of Indoxyl Sulfate on Progenitor Cell-Related Neovascularization of Peripheral Arterial Disease and Post-Angioplasty Thrombosis of Dialysis Vascular Access

Hung

Kuo

et al. 2017

Toxins

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Patients with chronic kidney disease (CKD) have an increased risk of vascular disease, which is associated with considerable health care costs. Vascular disease in CKD differs clinically and pathobiologically from that in patients with normal renal function. Besides the traditional risk factors, retention of uremic toxins contributes to the pathogenesis of vascular disease in patients with CKD. Indoxyl sulfate is a protein-bound uremic toxin and is inefficiently removed by conventional dialysis. Accumulating evidence suggests that indoxyl sulfate is a vascular toxin involved in atherosclerosis, arteriosclerosis, vascular calcification and vascular repair. Clinically, indoxyl sulfate is associated with total and cardiovascular mortality in patients with CKD. Recent studies have indicated that in addition to coronary and cerebral arteries, indoxyl sulfate plays a role in peripheral artery disease (PAD) and dialysis graft thrombosis. Emerging evidence suggests that indoxyl sulfate is implicated via novel mechanisms, including progenitor cell-related neovascularization and tissue factor-related hypercoagulability. These findings raise the possibility that strategies targeting serum indoxyl sulfate may have the potential to improve the outcomes of PAD and dialysis vascular access in patients with CKD.

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Circulating Progenitor Cells Affect Thrombosis of Dialysis Arteriovenous Fistulas

Cited by 6 publications

References 33 publications

Molecular Mechanisms Underlying the Cardiovascular Toxicity of Specific Uremic Solutes

Molecular Mechanisms Underlying the Cardiovascular Toxicity of Specific Uremic Solutes

Tryptophan-Derived Uremic Toxins and Thrombosis in Chronic Kidney Disease

Impact of Indoxyl Sulfate on Progenitor Cell-Related Neovascularization of Peripheral Arterial Disease and Post-Angioplasty Thrombosis of Dialysis Vascular Access

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