Candidate Gene Analysis of Arteriovenous Fistula Failure in Hemodialysis Patients

Verschuren, Jeffrey J. W.; Ocak, Gürbey; Dekker, Friedo W.; Rabelink, Ton J.; Jukema, J. Wouter; Rotmans, Joris I.

doi:10.2215/cjn.11091012

Cited by 15 publications

(17 citation statements)

References 44 publications

(48 reference statements)

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“…Thrombophilia (genetic abnormalities associated with a hypercoagulable state, such as factor V Leiden, prothrombin mutation, or decreased activity of protein S or C) was present in 9% of 219 patients undergoing AVF creation and was associated with a 2.2-fold higher risk for AVF failure (63). Another prospective study of 479 patients with new AVFs investigated the association of AVF failure with 43 single-nucleotide polymorphisms (SNPs) in 26 candidate genes related to proliferation, inflammation, endothelial function, vascular remodeling, coagulation, and calcium/phosphate metabolism (64). Only two of the candidate SNPs studied (one for factor V and one for LDL receptor-related protein 1), accounting for 17% of the study cohort, were associated with AVF failure.…”

Section: Answermentioning

confidence: 99%

A Patient with Recurrent Arteriovenous Graft Thrombosis

Allon¹

2015

Clinical Journal of the American Society of Nephrology

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Arteriovenous grafts (AVGs) are prone to frequent thrombosis that is superimposed on underlying hemodynamically significant stenosis, most commonly at the graft-vein anastomosis. There has been great interest in detecting AVG stenosis in a timely fashion and performing preemptive angioplasty, in the belief that this will prevent AVG thrombosis. Three surveillance methods (static dialysis venous pressure, flow monitoring, and duplex ultrasound) can detect AVG stenosis. Whereas observational studies have reported that surveillance with preemptive angioplasty substantially reduces AVG thrombosis, randomized clinical trials have failed to confirm such a benefit. There is a high frequency of early AVG restenosis after angioplasty caused by aggressive neointimal hyperplasia resulting from vascular injury. Stent grafts prevent AVG restenosis better than balloon angioplasty, but they do not prevent AVG thrombosis. Several pharmacologic interventions to prevent AVG failure have been evaluated in randomized clinical trials. Anticoagulation or aspirin plus clopidogrel do not prevent AVG thrombosis, but increase hemorrhagic events. Treatment of hyperhomocysteinemia does not prevent AVG thrombosis. Dipyridamole plus aspirin modestly decreases AVG stenosis or thrombosis. Fish oil substantially decreases the frequency of AVG stenosis and thrombosis. In patients who have exhausted all options for vascular access in the upper extremities, thigh AVGs are a superior option to tunneled internal jugular vein central vein catheters (CVCs). An immediate-use AVG is a reasonable option in patients with recurrent CVC dysfunction or infection. Tunneled femoral CVCs have much worse survival than internal jugular CVCs.Clin J Am Soc Nephrol 10: 2255-2262, 2015. doi: 10.2215/CJN.00190115 Patient PresentationThe following vignette illustrates the numerous challenges in optimizing arteriovenous graft (AVG) patency in hemodialysis patients. A 28-year-old woman initiated peritoneal dialysis when she developed ESRD because of focal glomerular sclerosis. She was hospitalized with an intracerebral bleed caused by a ruptured aneurysm 1.5 years later. A ventricular-peritoneal shunt was placed to treat hydrocephalus, and she was anticoagulated with warfarin to keep the shunt patent. Because of residual left-sided weakness and inadequate family support, she was no longer able to perform peritoneal dialysis. A tunneled central vein catheter (CVC) was placed in the right internal jugular vein, and she was switched to maintenance hemodialysis. A left forearm arteriovenous fistula (AVF) clotted 2 weeks after its creation. A subsequent looped left upper-arm AVG was successfully cannulated 5 weeks after its creation. It clotted four times during the ensuing 6 months and was treated each time by an interventional radiologist or nephrologist, who performed percutaneous thrombectomy, in conjunction with angioplasty of a venous anastomotic stenosis. The patient resumed hemodialysis with an internal jugular CVC when the AVG failed. A right radiocephalic AV...

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Section: Answermentioning

confidence: 99%

A Patient with Recurrent Arteriovenous Graft Thrombosis

Allon¹

2015

Clinical Journal of the American Society of Nephrology

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“…While recent genomic studies of these populations exist, they are centered on kidney disease risk or progression, associated dialysis complications like arteriovenous fistula failure, or patient survival (2–4) rather than phenotypes related to drug response. But, a few potentially important pharmacogenomics associations have been explored.…”

Section: Pharmacogenomics Of Dialysis and Chronic Kidney Diseasementioning

confidence: 99%

Role of pharmacogenomics in dialysis and transplantation

Birdwell

2014

Current Opinion in Nephrology and Hypertension

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Purpose of Review Pharmacogenomics is the study of differences in drug response based on individual genetic background. With rapidly advancing genomic technologies and decreased costs of genotyping, the field of pharmacogenomics continues to develop. Application to patients with kidney disease provides growing opportunities for improving drug therapy. Recent Findings Pharmacogenomics studies are lacking in patients with chronic kidney disease and dialysis but are abundant in the kidney transplant field. A clinically actionable genetic variant exists in the CYP3A5 gene, with the initial tacrolimus dose selection optimized based on CYP3A5 genotype. Though many pharmacogenomics studies have focused on transplant immunosuppression pharmacokinetics, an expanding literature on pharmacodynamic outcomes like calcineurin inhibitor toxicity and new onset diabetes is providing new information on patients at risk. Summary Appropriately powered pharmacogenomics studies with well-defined phenotypes are needed to validate existing studies and unearth new findings in patients with kidney disease, especially the chronic kidney disease and dialysis population.

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“…Verschuren JJ et al, [32] studied 479 incident hemodialysis patients between January 1997 and April 2004. Follow-up lasted 2 years or until AVF failure, in total, 207 (43.2%) patients developed AVF failure.…”

Section: Discussionmentioning

confidence: 99%

Tumor Necrosis Factor Alpha 308 Genepolymorphism and Serum Osteoprotogerin Inarteriovenous Fistula Dysfunction Inhemodialysis Patients

2015

IJSR

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Introduction: The preservation of patent, well-functioning dialysis fistulas is one of the most difficult clinical problems in the long-term treatment of patients undergoing dialysis. Arteriovenous fistula (AVF) dysfunction remains a major contributor to the morbidity and mortality of hemodialysis patients. The goal is to identify a dysfunctional AVF early enough to intervene in a timely manner to either assist with the maturation process or to prevent thrombosis. Over the past years, numerous clinical studies have consistently reported higher serum levels of OPG in association with cardiovascular outcome including coronary artery disease (CAD), vascular calcification, advanced atherosclerosis.Genes encoding for TNF-alpha are potential genetic risk factors for atherosclerosis and have functional variants that regulate their expressions. Polymorphisms at the position -308 in the promoter region of the TNF-alpha gene have been implicated as risk factors for atherosclerosis.Factor V Leiden mutation (G1691A) has been recognized to be the most prevalent genetic risk factor for venous thrombosis. Aim of the work: The aim of the present work is to investigate TNF-alpha 308 gene polymorphism,factor V Leiden mutation (G1691A), and serum osteoprotogerin level in patients on maintenance hemodialysis suffering from vascular access dysfunction. Subjects & methods: The study included 60 end stage renal disease patients from Alexandria University Hospitals on maintenance hemodialysis who were divided into 2 groups; 40 patients with AVF dysfunction, 20 patients with normal functioning AVF , 20 age and sex matched healthy subjects of matched age & sex were used as a control group. Investigations include serum level of Osteoprotogerin by ELISA technique, Serum TNF-alpha-308G>A-polymorphism by real time PCR and factor VLeiden gene mutation was assessed using 5' Nuclease assay as well as Doppler ultrasound for vascular access. Results: As regard TNF alpha 308 genepolymorphism there was statistically significant difference in the group with dysfunctioning AVF compared to the other two groups while factor V laden gene mutation showed statistical significant difference in group with AVF dysfunction &control group while no significant difference between them and those with functioning AVF. OPG was higher in group with AVF dysfunction compared to those with functioning AVF &control group while there was no significant difference betweenfunctioning AVF &control group. Conclusion: both OPG and the genotype distribution of TNF-α -308 G > A can be used as potential markers on HD patients to detect AVF dysfunction while, the role Factor V Leiden gene mutations may need further research and investigations.

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Candidate Gene Analysis of Arteriovenous Fistula Failure in Hemodialysis Patients

Cited by 15 publications

References 44 publications

A Patient with Recurrent Arteriovenous Graft Thrombosis

A Patient with Recurrent Arteriovenous Graft Thrombosis

Role of pharmacogenomics in dialysis and transplantation

Tumor Necrosis Factor Alpha 308 Genepolymorphism and Serum Osteoprotogerin Inarteriovenous Fistula Dysfunction Inhemodialysis Patients

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