Immunoglobulin A Nephropathy. Recurrence After Renal Transplantation

Abstract

IgA nephropathy (IgAN) is the most common primary glomerular disease worldwide. The disease generally runs an indolent course but may lead to ESRD in 20–30% of patients in 20 years or more after diagnosis. Patients with IgA nephropathy are ideal candidates for renal transplant because they are generally relatively young and with few comorbidities. Their graft survival is better or comparable to that of controls at 10 years, though few data are available after 10 years of follow-up. Recurrence of the original disease in the graft is a well-known complication of transplant in IgAN and is a significant cause of deterioration of graft function. Recurrent IgAN rarely manifests clinically before 3 years post transplantation. Recurrence rate is estimated to be around 30% with considerable differences among different series. Despite these factors there is no certain recurrence predictor, young age at renal transplant, rapid progression of the original disease and higher levels of circulating galactose-deficient IgA1 and IgA-IgG immune complexes are all associated with a higher rate of recurrence. Which pathogenetic mechanisms are responsible for the progression of the recurrence to graft function deterioration, and what therapy can prevent or slow down the progression of the disease in the graft, are open questions. The aim of this review is to describe the clinical outcome of renal transplantation in IgA patients with attention to the rate and the predictors of recurrence and to discuss the available therapeutic options for the management of recurrence.

Regulatory T cells for minimising immune suppression in kidney transplantation: phase I/IIa clinical trial

“…Because high immunosuppression by thymoglobuline and weaning of steroids correlates with decreased and enhanced risk of immunoglobulin A nephropathy recurrence, respectively, we decided to change treatment back to the triple drug regimen. 42 43 We have seen an improvement in proteinurea and stable graft function for more than three years in this patient. Therefore, in both patients treatment was successfully reversed to the triple drug regimen.…”

Recurrent Glomerulonephritis after Renal Transplantation: The Clinical Problem

“…The pathogenesis of IgAN is not completely understood [ 36 ]. There appears to be a genetic predisposition in patients that develop this kind of nephropathy, with specific HLA types associated with high serum IgA concentration [ 37 , 38 ].…”

“…However, many patients with recurrent IgA do not have clinical signs and the diagnosis can be histological only with mesangial IgA deposits with or without mesangial proliferation [ 36 , 60 ]. In a minority of cases cellular, fibro-cellular, or fibrous crescents are described at the graft biopsy and they are associated with a significantly worse graft survival [ 61 ].…”

The Role of IgA in the Pathogenesis of IgA Nephropathy

“…Moreover, latent IgA deposits in donor kidney are among frequently reported risk factors not only for IgAN recurrence, but also for delayed graft function and increased rejection rate of transplanted kidney [10]. However, it is noteworthy to mention that donor kidneys with IgA deposits when transplanted in non-IgAN recipients rapidly clear IgA deposits [5,11], which suggest that the basic cause of the disease is likely extra-renal.…”