Antiphospholipid Antibodies in Renal Allograft Recipients

Abstract

Introduction: Antiphospholipid antibodies (APLA) are the most common cause of acquired thrombophilia. Among renal transplant recipients APLA are an additional risk factor for graft loss due to arterial or venous thrombosis or thrombotic microangiopathy (TMA). Graft thrombosis ranges from 0,5-8% and it usually leads to graft loss. Objective: The aim of the study was to determine the relation between APLA and thrombosis in renal allograft recipients. Patients and methods: The study included 37 Caucasian renal transplant recipients: 17 women and 20 men aged 22-69 years; 25 patients (67%) received first allografts; main cause of ESRD was glomerulonephritis (51%); mean time after transplantation was 27,8 months, mean observation time was 12 months. Each patients were given steroids+CNI+MMF/MPS. Patients were divided into 2 groups: 27 patients with no clinically significant thrombotic history T(-) and 10 patients T(+) with previous strong thrombotic events (thrombosis 1) defined as a vascular graft thrombosis or recurrent (at least three times) thrombosis of arterio-venous fistulas. A single case of deep vein thrombosis or single case of thrombosis of arterio-venous fistulas were not considered to be strong thrombotic factor. APLA consist of LA (lupus anticoagulant), ACL (anticardiolipin) IgM and IgG antibodies, anti-β2GPI (anti-β2Glicoprotein I) IgM and IgG antibodies, anti-PT (anti-prothrombin) IgM and IgG antibodies. APLA were detected in serum twice in 6 months interval. Eight patients were lost for follow-up. Results: APLA incidence in renal recipients is higher than in general population and ranges from 0-16,22%. There were no statistically significant difference in APLA between T(-) and T(+), as well as examination1 and 2. Graft function remained stable in T(-) and T(+) with no significant difference in serum creatinine concentration (2,0 mg/dl and 1,6 mg/dl, respectively). During follow-up we reported in one APLA(+) patient the thrombosis of arterio-venous fistula and TMA of the graft despite to LMWH administration and she returned to hemodialysis. Discussion: As potential reasons for the lack of differences in APLA titres in both groups we considered: immunosupresive therapy, long time between thrombosis 1 and examination 1 (mean: 49,9 months), spontaneous APLA elimination from the circulation or potentially, previous thrombotic events in T(+) were due to surgical complication after transplantation with no impact of APLA. All patient T(+) were given LMWH, what potentially prevented from thrombotic events during follow-up. However, a small group and short observation time may also affect the results. Conclusion: Due to the presence of additional factors affecting APLA (steroids, long time between thrombosis 1 and examination 1, short period of observation, LMWH administration), based on the tested group, we can not clearly determine APLA importance as a marker of thrombosis after transplantation. A study designed on larger group is required.