title: Frequency, potential risk and therapeutic intervention in end-stage renal disease patients with antiphospholipid antibody syndrome: a multicenter study.
abstract: BACKGROUND
  Antiphospholipid antibody syndrome (APAS) is characterized by the presence of anticardiolipin antibodies (ACA) in association with thrombotic disorders of arterial and/or venus systems, spontaneous abortion(s) or thrombocytopenia.
  
  
  METHODS
  In this multicenter study, 502 end-stage renal disease (ESRD) patients awaiting renal transplants were screened to determine the frequency of APAS, the potential risk associated with APAS, and strategies for therapeutic intervention. Ninety-three patients (19%) had high titers of ACA. Twenty-three patients had documented evidence of one or more of the thrombotic disorders such as lupus, frequent abortions, frequent thrombosis of arteriovenous shunts, biopsy-proven microrenal angiopathy, or thrombocytopenia and thus were diagnosed with APAS. Of these 23 patients, 11 received kidney transplants either with (4 patients) or without (7 patients), concomitant anticoagulation therapy.
  
  
  RESULTS
  All seven of the patients with APAS not treated with anticoagulation therapy lost their allografts within 1 week as a result of renal thrombosis. In contrast, three out of four transplant patients with APAS treated with anticoagulation therapy maintained their allografts for over 2 years. The fourth patient lost his graft within a week because of thrombosis. Of the remaining 70 patients with high titers of ACA but no evidence of thrombotic disorders, 37 received kidney transplants. None lost their allografts as a result of thrombosis. Our data suggest that, although 19% of our ESRD patients exhibit high titer of ACA, only 5% of the patients have APAS.
  
  
  CONCLUSIONS
  In conclusion, our data suggest that the patients with APAS are at high risk of posttransplant renal thrombosis. Anticoagulation therapy could prevent patients from posttransplant thrombosis in patients with APAS.
authors.affiliation: University of Texas Medical Branch, Galveston 77555-0178, USA. svaidya@utmb.edu
authors.forename: S
authors.initials: S
authors.lastname: Vaidya
authors.forename: R
authors.initials: R
authors.lastname: Sellers
authors.forename: P
authors.initials: P
authors.lastname: Kimball
authors.forename: T
authors.initials: T
authors.lastname: Shanahan
authors.forename: J
authors.initials: J
authors.lastname: Gitomer
authors.forename: K
authors.initials: K
authors.lastname: Gugliuzza
authors.forename: J C
authors.initials: JC
authors.lastname: Fish
mesh_terms: D017153:Antibodies, Anticardiolipin / Q000032:analysis; D000925:Anticoagulants / Q000627:therapeutic use; D016736:Antiphospholipid Syndrome / Q000150:complications* / Q000188:drug therapy* / Q000453:epidemiology; D005260:Female; D006084:Graft Rejection / Q000209:etiology; D006085:Graft Survival / Q000187:drug effects; D006801:Humans; D007674:Kidney Diseases / Q000150:complications / Q000517:prevention & control; D007676:Kidney Failure, Chronic / Q000150:complications* / Q000601:surgery*; D016030:Kidney Transplantation; D008297:Male; D015995:Prevalence; D012307:Risk Factors; D013927:Thrombosis / Q000150:complications / Q000517:prevention & control; D014859:Warfarin / Q000627:therapeutic use
chemical_list: D017153:Antibodies, Anticardiolipin; D000925:Anticoagulants; D014859:Warfarin