title: Prevalence of heparin-induced antibody in African-American hemodialysis patients--comparison to non-dialysis patients.
abstract: OBJECTIVE
  Heparin-induced antibody formation and thrombocytopenia are well-established complications of heparin use and may be associated with thromboembolic events. Our study aimed to establish the prevalence of heparin-induced antibodies (HIA), otherwise known as platelet factor 4 (PF4) antibodies, and their relationship to thrombocytopenia and thrombotic events in a group of predominantly African-American hemodialysis patients over 12 months. For comparison, the prevalence of HIA in thrombocytopenic patients with serum creatinine of less than 2.0 mg/dl tested for the antibody in the same period was evaluated.
  
  
  METHODS
  36 hemodialysis patients on thrice-weekly, in-center treatments receiving heparin on dialysis were selected to have blood drawn predialysis for PF4 heparin antibodies (HIA). Complete blood counts (CBC) were also checked that day and monthly for the next 3 months. Outpatient records were reviewed for thromboembolic events, including thrombosis of dialysis access lines, grafts and fistulas. The HIA results for the dialysis patients were compared with HIA performed at the same lab for non-dialysis thrombocytopenic patients during the same period.
  
  
  RESULTS
  17 out of 36 (47%) hemodialysis patients had detectable HIA. There were no differences in gender, ethnicity, disease states, or duration of hemodialysis. None of the patients had thrombocytopenia, and the incidence of thromboembolic events was statistically not different from patients without HIA. The non-CKD thrombocytopenic group had a lower incidence, 16/88 (18%) of positive HIA.
  
  
  CONCLUSIONS
  Heparin-induced antibodies are relatively common in patients receiving hemodialysis. However, their presence does not appear to be associated with clinical consequences. Therefore, testing for HIA should be done only if a clinical indication is present.
authors.affiliation: Department of Nephrology, Temple University School of Medicine, Philadelphia, PA, USA. benjam@temple.edu
authors.forename: J
authors.initials: J
authors.lastname: Benjamin
authors.forename: S
authors.initials: S
authors.lastname: Moldavsky
authors.forename: J
authors.initials: J
authors.lastname: Lee
authors.forename: R
authors.initials: R
authors.lastname: Rubin
mesh_terms: D000328:Adult; D001741:Black or African American; D000368:Aged; D000369:Aged, 80 and over; D000906:Antibodies / Q000032:analysis*; D003404:Creatinine / Q000097:blood; D005260:Female; D006493:Heparin / Q000276:immunology*; D006801:Humans; D007070:Immunoglobulin A / Q000097:blood; D007074:Immunoglobulin G / Q000097:blood; D007075:Immunoglobulin M / Q000097:blood; D007676:Kidney Failure, Chronic / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D015995:Prevalence; D006435:Renal Dialysis / Q000009:adverse effects*; D013921:Thrombocytopenia / Q000097:blood / Q000209:etiology; D013927:Thrombosis / Q000097:blood / Q000209:etiology
chemical_list: D000906:Antibodies; D007070:Immunoglobulin A; D007074:Immunoglobulin G; D007075:Immunoglobulin M; D006493:Heparin; D003404:Creatinine