title: Coagulation, thrombophilia and patency of arteriovenous fistula in children undergoing haemodialysis compared with healthy volunteers: a prospective analysis.
abstract: This study aimed to assess whether markers of coagulation, fibrinolysis or thrombophilia are increased in children on haemodialysis compared with controls and whether measurement of any of these factors could help to identify patients at an increased risk of arteriovenous fistula (AVF) occlusion. Blood samples were taken from 55 children immediately before a session of haemodialysis and from 20 healthy volunteers. Thrombin-antithrombin (TAT), D-dimer, plasmin-antiplasmin (PAP) and anticardiolipin immunoglobulin G (ACA-Ig G) were measured by ELISA. Factor V Leiden mutation (G1691A) was determined by gene polymorphism [restriction fragment length polymorphism (RFLP)]. Determination of the patency of the AVF was prospectively followed up for a minimum of 4 years or until the AVF was nonfunctioning. Fifty-five patients were studied with a median follow-up of 659 days (range 30-1670 days). A significant increase was found in the levels of D-dimer, PAP and ACA-Ig G in haemodialysis patients with thrombosed and nonthrombosed native AVFs vs.
  
  
  METHODS
  There was a significant difference between both chronic haemodialysis patients with thrombosed and nonthrombosed native AVF with regard to ACA-IgG levels. At 1 year follow-up, primary patency was 61.4% (27 patients). In multivariate analysis, D-dimer was inversely associated with secondary patency.Thrombophilia may predispose children with end stage renal disease to access failure. The promising finding is that in children on haemodialysis, D-dimer levels were increased and inversely correlated with secondary patency. Further evaluation is required into the possible role of D-dimer as a biomarker of AVF occlusion.
authors.affiliation: aPediatrics Department, Faculty of Medicine, Cairo UniversitybPediatrics DepartmentcClinical & Chemical Pathology Department, National Research Centre, Cairo, Egypt.
authors.forename: Fatina I
authors.initials: FI
authors.lastname: Fadel
authors.forename: Manal F
authors.initials: MF
authors.lastname: Elshamaa
authors.forename: Safaa M
authors.initials: SM
authors.lastname: Abdel-Rahman
authors.forename: Eman H
authors.initials: EH
authors.lastname: Thabet
authors.forename: Solaf
authors.initials: S
authors.lastname: Kamel
authors.forename: Dina
authors.initials: D
authors.lastname: Kandil
authors.forename: Mona H
authors.initials: MH
authors.lastname: Ibrahim
authors.forename: Mostafa
authors.initials: M
authors.lastname: El-Ahmady
mesh_terms: D000293:Adolescent; D017153:Antibodies, Anticardiolipin / Q000097:blood; D000990:Antithrombin III / Q000378:metabolism; D001164:Arteriovenous Fistula / Q000097:blood* / Q000150:complications / Q000175:diagnosis / Q000628:therapy; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D005165:Factor V / Q000235:genetics / Q000378:metabolism; D005260:Female; D005338:Fibrin Fibrinogen Degradation Products / Q000378:metabolism; D005341:Fibrinolysin / Q000378:metabolism; D006801:Humans; D007074:Immunoglobulin G / Q000097:blood; D007676:Kidney Failure, Chronic / Q000097:blood* / Q000150:complications / Q000175:diagnosis / Q000628:therapy; D008297:Male; D009154:Mutation; D010447:Peptide Hydrolases / Q000378:metabolism; D011446:Prospective Studies; D006435:Renal Dialysis; D019851:Thrombophilia / Q000097:blood* / Q000150:complications / Q000175:diagnosis / Q000628:therapy; D000979:alpha-2-Antiplasmin / Q000378:metabolism
chemical_list: D017153:Antibodies, Anticardiolipin; D015415:Biomarkers; D005338:Fibrin Fibrinogen Degradation Products; D007074:Immunoglobulin G; D000979:alpha-2-Antiplasmin; C046193:antithrombin III-protease complex; C095381:factor V Leiden; C036309:fibrin fragment D; C037742:plasmin-plasmin inhibitor complex; D000990:Antithrombin III; D005165:Factor V; D010447:Peptide Hydrolases; D005341:Fibrinolysin