Renal allograft thrombosis.

Renal allograft thrombosis may be responsible for 2–7% of early allograft losses in adults [1] and up to 35% in children [2]. The North American Pediatric Renal Transplant Cooperative Study (NAPRTCS) reported that graft thrombosis represented the main cause of graft failure in the first year. Most cases of renal allograft thrombosis occur early in the postoperative period with a peak incidence of 48 h. However, thrombus formation may be delayed until after the first week [3]. Thrombosis may initially involve the renal artery or more frequently the renal vein, but in some cases it is difficult to ascertain where the thrombosis originated. Several factors may be involved in the pathogenesis of graft thrombosis. Thrombosis may be caused by technical errors, by vascular clamp injury or perfusion cannulation injury. Although vascular abnormalities in the donor kidney may be responsible for graft thrombosis [4] (thrombosis is reported in up to 36% of allografts with multiple renal arteries), however, in a multivariate analysis, the presence of atheroma was the only independent factor associated with the risk of arterial renal thrombosis [5]. Paediatric transplant recipients of kidneys from cadaver donors <5 years of age had a significantly higher thrombosis rate than did recipients from older donors [6]. This increased risk is attributable to the discrepancy in the size between the vessels of the donor and the recipient. In the past, cases of arterial thrombosis have been reported with cadaveric paediatric ‘en bloc’ transplantation. Recent results with this technique are excellent with no vascular thrombosis [7,8]. An increased risk of graft thrombosis was reported in kidney transplants from elderly donors [9,10]. This is probably because donor hypotension together with ischaemiareperfusion injury may cause the activation of a proco-