anuria. He had not stopped or omitted his immuno- suppressive therapy. One year and 2 months prior,. Case. aCL antibodies IgG isotype were detected, in low ...
Nephrol Dial Transplant (1999) 14: 472–474
Nephrology Dialysis Transplantation
Case Report
Late renal transplant arterial thrombosis in a patient with systemic lupus erythematosus and antiphospholipid syndrome Fotini B. Karassa1, Konstandina Avdikou2, Paris Pappas4, Lidia Nakopoulou5, Alkiviadis Kostakis3 and John N. Boletis2 Departments of 1Pathophysiology and 5Pathology, University of Athens, Laikon Hospital, Departments of 2Nephrology, 3Transplantation, and 4Radiology, Laikon Hospital, Athens, Greece
Key words: antiphospholipid syndrome; renal artery thrombosis; transplantation; systemic lupus erythematosus
Introduction Acute thrombosis of the renal transplant artery is a well-known vascular complication of renal allografts that usually occurs within the first month after transplantation [1,2]. There is an apparent association between a history of venous thrombosis and/or arterial occlusions and the presence of antiphospholipid (aPL) antibodies namely lupus anticoagulant (LA) and anticardiolipin (aCL) antibodies [3,4]. To the best of our knowledge, late acute thrombosis of the renal transplant artery has not been reported in association with aPL antibodies. We describe the case of a 22-year-old man with systemic lupus erythematosus (SLE ) who developed renal transplant artery thrombosis, 2 years after transplantation, in association with aPL antibodies.
Case The patient, a 22-year-old man, presented at the age of 9 years in 1985 with Raynaud’s phenomenon. He had no other symptoms until 1987 when he developed arthritis, malar rash and livedo reticularis in both lower extremities. Laboratory tests revealed positive antinuclear antibodies (ANA), anti dsDNA, anti Sm and anti RNP antibodies, while C C were low. SLE 3, 4 was diagnosed based on American College of Rheumatology 1982 criteria [5]. A direct Coombs’ test was positive and therapy with methylprednisolone 32 mg daily was began in our department. In 1989, the patient developed renal involvement which manifested primarily with hypertension, massive Correspondence and offprint requests to: John Boletis MD, 25 Feidiou Str., 155 62 Athens, Greece.
proteinuria, and renal failure. The kidney biopsy revealed diffuse proliferative gromeluronephritis with activity and chronicity indices 19 and 0 respectively. Despite treatment with intravenous cyclophosphamide his serum creatinine rose to 3.5 mg/dl. A second kidney biopsy was done in February 1990 and revealed crescentic glomerulonephritis (mainly fibrous crescents) with severe tubulointersitial disease. He received an additional pulse of cyclophosphamide, but 6 months later started haemodialysis because of end-stage renal disease. In 1995, the patient underwent a two-antigen match, HLA B and HLA DR , cadaveric renal transplanta8 5 tion. The transplant renal artery was anastomized endto-side to the recipient’s external iliac artery. The posttransplant course was uneventful and thereafter he was stable on maintance immunosuppressive therapy consisting of methylprednisolone 4 mg daily, cyclosporin 4 mg/kg daily, and azathioprine 1 mg/kg daily. His serum creatinine was 1.9 mg/dl. Two years after transplantation the patient was admitted to the transplant unit complaining of acute pain at the site of the renal graft, high fever, and anuria. He had not stopped or omitted his immunosuppressive therapy. One year and 2 months prior, aCL antibodies IgG isotype were detected, in low and moderate titres respectively (aCL IgG: 116 and 254 binding units, normal values
