CASE REPORT Plasmapheresis in a patien o p

as Sofue et al. BMC Nephrology 2014, 15:167 http://www.biomedcentral.com/1471-2369/15/167states that an initiating “first hit ” injury disrupts theIkenobe, Miki-cho, Kita-gun, Kagawa 761-0793, Japan Full list of author information is available at the end of the articleBackground Early graft thrombosis and bleeding complications remain important causes of early graft loss following kidney trans-plantation in patients with antiphospholipid syndrome (APS) [1-4]. APS is a multisystem autoimmune disorder characterized clinically by recurrent arterial and/or venous thrombosis and/or pregnancy morbidity, and serologically by the presence of antiphospholipid antibodies (aPL), in-cluding lupus anticoagulant (LA), anticardiolipin (aCL) and anti-β2-glycoprotein I (anti-β2GPI) antibodies. APS can be classified as primary or secondary to systemic lupus erythematosus (SLE). aCL antibody has been regarded as a major antiphospholipid antibody and a marker for APS. In contrast, anti-β2GPI antibody is a relatively new disease-specific antibody for APS and considered a cause of throm-botic complications [5,6]. The “two hit ” model of thrombosis in APS patient