Platelet Glycoprotein IIb HPA-3 a/b Polymorphism Is Associated with Native Arteriovenous Fistula Thrombosis in Chronic Hemodialysis Patients

Wan, Jin; Zhang, Ding-Wu; Cheng, Xiaolan; Shi, Hui; Fan, Yanbo

doi:10.3109/0886022x.2012.706865

Cited by 5 publications

(4 citation statements)

References 17 publications

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“…Certain alleles of these genes have been correlated with higher rates of access thrombosis. 83 Studies examining genetic predispositions to AVF failure lend credence and support to the current understanding of the molecular changes leading to AVF failure. Future work aiming at gene-specific therapy may help alleviate IH.…”

Section: Geneticsmentioning

confidence: 89%

The Biology of Hemodialysis Vascular Access Failure

Brahmbhatt

Misra

2016

Semin intervent Radiol

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Arteriovenous fistulas (AVFs) are essential for patients and clinicians faced with end-stage renal disease (ESRD). While this method of vascular access for hemodialysis is preferred to others due to its reduced rate of infection and complications, they are plagued by intimal hyperplasia. The pathogenesis of intimal hyperplasia and subsequent thrombosis is brought on by uremia, hypoxia, and shear stress. These forces upregulate inflammatory and proliferative cytokines acting on leukocytes, fibroblasts, smooth muscle cells, and platelets. This activation begins initially with the progression of uremia, which induces platelet dysfunction and primes the body for an inflammatory response. The vasculature subsequently undergoes changes in oxygenation and shear stress during AVF creation. This propagates a strong inflammatory response in the vessel leading to cellular proliferation. This combined response is then further subjected to the stressors of cannulation and dialysis, eventually leading to stenosis and thrombosis. This review aims to help interventional radiologists understand the biological changes and pathogenesis of access failure.

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Section: Geneticsmentioning

confidence: 89%

The Biology of Hemodialysis Vascular Access Failure

Brahmbhatt

Misra

2016

Semin intervent Radiol

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“… 167 In a study examining Chinese Han patients, a glycoprotein IIb human platelet antigen 3 a/b polymorphism, specifically the b allele was linked to native AVF thrombosis. 168 These studies show that changes in the vessel wall lead to increased thrombogenicity, which is further compounded by systemic uremia.…”

Section: Thrombosismentioning

confidence: 99%

The molecular mechanisms of hemodialysis vascular access failure

Brahmbhatt

Remuzzi

Franzoni

et al. 2016

Kidney International

196

211

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The arteriovenous fistula has been used for more than 50 years to provide vascular access for patients undergoing hemodialysis. More than 1.5 million patients worldwide have end stage renal disease and this population will continue to grow. The arteriovenous fistula is the preferred vascular access for patients, but its patency rate at 1 year is only 60%. The majority of arteriovenous fistulas fail because of intimal hyperplasia. In recent years, there have been many studies investigating the molecular mechanisms responsible for intimal hyperplasia and subsequent thrombosis. These studies have identified common pathways including inflammation, uremia, hypoxia, sheer stress, and increased thrombogenicity. These cellular mechanisms lead to increased proliferation, migration, and eventually stenosis. These pathways work synergistically through shared molecular messengers. In this review, we will examine the literature concerning the molecular basis of hemodialysis vascular access malfunction.

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“…The HPA-3 (rs5910) polymorphism results from a thymine to guanine base change that leads to the replacement of isoleucine (HPA-3a) by serine (HPA-3b) at codon 843 of GPIIb ( ITGA2B ). This polymorphism may potentially influence the activity of the GPIIb/IIIa complex and associate with thrombosis [10]. …”

Section: Introductionmentioning

confidence: 99%

Identification ofITGA2BandITGB3Single-Nucleotide Polymorphisms and Their Influences on the Platelet Function

Xiang

Zhang

et al. 2016

BioMed Research International

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The aim of the study was to investigate ITGA2B and ITGB3 genetic polymorphisms and to evaluate the variability in the platelet function in healthy Chinese subjects. The genetic sequence of the entire coding region of the ITGA2B and ITGB3 genes was investigated. Adenosine diphosphate-induced platelet aggregation, glycoprotein IIb/IIIa content, bleeding time, and coagulation indexes were detected. Thirteen variants in the ITGA2B locus and 29 variants in the ITGB3 locus were identified in the Chinese population. The rs1009312 and rs2015049 were associated with the mean platelet volume. The rs70940817 was significantly correlated with the prothrombin time. The rs70940817 and rs112188890 were related with the activated partial thromboplastin time, and ITGB3 rs4642 was correlated with the thrombin time and fibrinogen. The minor alleles of rs56197296 and rs5919 were associated with decreased ADP-induced platelet aggregation, and rs55827077 was related with decreased GPIIb/IIIa per platelet. The rs1009312, rs2015049, rs3760364, rs567581451, rs7208170, and rs117052258 were related with bleeding time. Further studies are needed to explore the clinical importance of ITGA2B and ITGB3 SNPs in the platelet function.

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Platelet Glycoprotein IIb HPA-3 a/b Polymorphism Is Associated with Native Arteriovenous Fistula Thrombosis in Chronic Hemodialysis Patients

Cited by 5 publications

References 17 publications

The Biology of Hemodialysis Vascular Access Failure

The Biology of Hemodialysis Vascular Access Failure

The molecular mechanisms of hemodialysis vascular access failure

Identification ofITGA2BandITGB3Single-Nucleotide Polymorphisms and Their Influences on the Platelet Function

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