Glomerular diseases, including diabetes and various forms of GN, account for over 70% of patients undergoing renal transplantation. Among these patients, over 40% develop significant proteinuria and around 15% develop persistent nephrotic syndrome. The most common cause of post-TP proteinuria is chronic allograft nephropathy (60%), followed by recurrent (15%) and de novo (10%) GN. Persistent proteinuria is associated with a significantly reduced rate of graft survival but can often be controlled with non disease-specific therapy including angiotensin converting enzyme inhibitors and angiotensin receptor blockers with favorable effects on long-term prognosis.
Recurrent or de novo GN occurs in 6-20% of patients overall, and is more common in patients transplanted with GN. GN in the allograft is also associated with a reduction in long-term graft survival (40% vs 70% at 5 years). The most common diseases associated with allograft GN and their recurrence rates in transplants are idiopathic focal glomerular sclerosis (20-30%), IgA nephropathy (25%), membranoproliferative GN (Type I 25%, Type II 80%), membranous nephropathy (30%), and hemolytic-uremic syndrome (classical 10%, atypical 40%, familial 60%).
This presentation will review the current understanding of the immune mechanisms which underlie each of these diseases, the incidence of recurrence, the effects of recurrence on graft survival, risk factors for recurrence and management issues for nephrologists caring for patients with renal allografts. Proper donor selection, early diagnosis in high-risk patients and appropriate management can prolong graft survival and improve long-term outcomes.