A primer on recurrent and de novo glomerulonephritis in renal allografts

Accumulating evidence indicates that recurrent glomerulonephritis is the third most important cause of renal allograft loss at 10 years after transplantation. The proteinuria and elevated serum creatinine levels that result from recurrent glomerulonephritis are associated with cardiovascular morbidity and mortality. The exact prevalence of either recurrent or de novo post-transplantation glomerulonephritis is unknown because a considerable number of patients never undergo allograft biopsy, meaning that glomerulonephritis remains undiagnosed and a diagnosis of,chronic rejection/chronic allograft nephropathy' is sometimes presumed. The lack of consensus regarding evaluation of kidney transplant recipients who exhibit slow deterioration of graft function is a major reason for underdiagnosis. All forms of glomerular disease can recur after transplantation, but the likelihood of recurrence differs according to type. Focal segmental glomerulosclerosis, membranoproliferative glomerulonephritis, IgA nephropathy and idiopathic diarrhea-negative hemolytic uremic syndrome often recur. Membranous nephropathy, focal segmental glomerulosclerosis, anti-glomerular basement membrane nephritis associated with Alport syndrome, and drug-induced thrombotic microangiopathy are the most common forms of de novo glomerulonephritis. This Review discusses the prevalence, risk factors, pathogenesis, clinicopathological features, and effects on graft outcome of recurrent and de novo glomerulonephritis in renal allografts. Treatment options are briefly outlined.