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Nephrol Dial Transplant (1999) 14: 2297-2303
© 1999 European Renal Association-European Dialysis and Transplant Association

Invited Comments

Renal allograft thrombosis: can thrombophilia explain the inexplicable?

Ashley Irish

Department of Nephrology, Royal Perth Hospital, Perth, Western Australia, Australia

Correspondence and offprint requests to: Ashley Irish FRACP, Department of Nephrology, Royal Perth Hospital, GPO Box X2213, Perth, Western Australia 6001.

Introduction

Renal allograft thrombosis is responsible for approximately 2–7% of early allograft loss [1–3]. Data from the Australian and New Zealand Dialysis and Transplant Registry demonstrate a constant rate of grafts lost due to thrombosis over the last 10 years [4]. Graft thrombosis is characterized by sudden anuria and almost inevitable irreversible loss of function. Venous thrombosis is more common, usually occurs within the first 2 weeks, and is accompanied by graft pain and swelling, frequently with allograft rupture. Arterial thrombosis may be painless and without swelling or rupture; however, thrombosis of both arterial and venous conduits can occur, and distinguishing the site of origin of thrombus may be impossible. Until recently, mechanisms for this catastrophic event were considered to reflect general and non-specific perturbations of coagulation associated with or exacerbated by the dialysis or surgical procedure, immunosuppressive drugs, technical errors, donor vessel abnormalities, vascular . . . [Full Text of this Article]

Blood coagulation, fibrinolysis and anticoagulant systems

Thrombophilia

Activated protein C resistance

Prothrombin gene G20210A polymorphism

Fibrinolysis

Homocysteine

Antiphospholipid antibodies and the lupus anticoagulant

Gene–gene and gene–environment interactions

Renal disease and transplantation

Cyclosporin and allograft thrombosis

Primary thrombophilia and allograft thrombosis

Screening

Prevention

Summary

References


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