Abstract
Recurrent or de novo diseases account for only 5% of graft failure in children, but have much to teach us about mechanisms. In children, almost the only metabolic disease with recurrence is type I hyperoxaluria, in which the poor long-term results of isolated renal transplantation make combined liver and renal transplantation, or even prophylactic liver transplantation before renal failure the preferable alternatives. While many forms of nephritis may show histological recurrence in allografts, it is notable that in many patients this is accompanied by no clinical manifestations or only mild disease: this is particularly so in mesangiocapillary glomerulonephritis (MCGN) type II, IgA-associated nephropathy and Henoch-Schönlein purpura. However focal segmental glomerulosclerosis and MCGN type I recur with sufficient frequency and severity to deter the use of living donors unless there is no alternative. The same is true of haemolytic-uraemic syndromes. As many as 10% of paediatric grafts may show de novo membranous nephropathy, but in the majority this is mild or not clinically evident. In contrast, the rare anti-glomerular basement membrane nephritis affecting some patients with Alport's syndrome usually results in graft failure, but occurs in only a minority of recipients with the syndrome. For all types of disease in allografts, risk factors for recurrence are poorly worked out, and attempts at treatment generally ineffective.