Abstract
298 Antiphospholipid antibody syndrome (APAS) is a condition with a set of distinct clinical features including recurrent arterial and venus thrombosis, repeated fetal loss, thrombocytopenia either with or without lupus. In this study we have evaluated impact of APAS on renal transplant outcome. A total of 174 patients awaiting renal transplant were evaluated to determine if they had APAS as evidenced by their coagulation profiles and previous history of clotting disorders. In addition, several serum samples from each of these patients were tested for the presence of antiphospholipid antibody (APA) of IgG or IgM subtype by ELISA method. Of these 174 patients, 78 received renal transplants. Six (6) of these 78 patients had APAS as evidenced by either recurrent microrenal angiopathy (2 patients), or thrombocytopenia (1 patient) or frequent A-V shunt thrombosis (3 patients) along with high titers of APA of either IgM or IgG or both subtypes at the time of their transplants. All of these 6 patients thrombosed their renal allografts within a week of their transplants which had to be nephrectomized. One (1) of these 78 transplanted patients had high titer of APA (IgM and G both) but no evidence of any clotting disorder. He is doing well one year post transplant. The other 71 transplanted patients with no history of clotting disorder or APA are all doing well one year post transplant. The association between APAS and post-transplant renal thrombosis among these patients is highly significant(p<0.0005). In contrast, there is no association between post-transplant thrombosis and prior sensitization to HLA molecules as none of these six patients had either donor specific or panel specific HLA antibodies. In addition none of these patients developed anti-HLA antibodies following their transplant nephrectomies. Furthermore, biopsics of their nephrectomized kidneys showed no evidence of immunological rejection as evidenced by absence of IgG, M, A or C3. There does not appear to be any relationship between cold ischemia time and post-renal thrombosis among these patients as some of the thrombosed patients received living related renal transplants. Furthermore, there was no association between other non-HLA antibodies and post-renal thrombosis as none of these patients had positive skin crossmatches. In conclusion, our data suggest that patients with antiphospholipid antibody syndrome are at high risk for development of post-transplant renal thrombosis. Additionally, patients with APAS have circulating levels of antiphospholipid antibodies, however, patients with antiphospholipid antibodies without any clotting disorder do not appear to be at risk of post-transplant renal thrombosis.
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