33. The fate of mesangial IgA in the donor kidney: experience at the royal melbourne hospital

Abstract

Background Some authors claim that the presence of mesangial IgA (mlgA) in the donor kidney is associated with an increased risk of recurrent IgA glomerulonephritis in transplant recipients, particularly if the primary disease of the recipient was IgAGN (plgAGN). Aim To identify patients who had mlgA present in their donor kidney in the immediate post reperfusion biopsy (time zero biopsy) and to determine (a) its fate and (b) its impact on transplant and recipient survival. Methods Logbooks from 2000 to 2005 were retrospectively consulted to identify patients whose post reperfusion biopsies were positive for mlgA. Database searches were then conducted with particular emphasis on subsequent renal biopsies, serum eGFR and haematuria. Follow-up was until 2012. Results Twenty-one patients had mlgA in their post reperfusion biopsy. In subsequent biopsies 4 days to 3 years post transplant, 18 patients had no mlgA. Two patients who did not have follow-up biopsies have normal eGFR, no haematuria and appear to be disease-free. One patient had graft failure secondary to obstruction after four years of disease-free survival without evidence of recurrent IgA in the transplant nephrectomy. Seven of the patients with mlgA in their post reperfusion biopsy had plgA GN. Two of these did develop recurrent IgA glomerulonephritis, however this occurred some time after the mlgA initially present in the donor kidney had disappeared. Of the patients who did not have plgA GN as the cause of their ESRF, none developed IgA GN. Patients were disease-free and dialysis-free for a median of 7 years. Conclusions We conclude that the presence of mlgA in the donor kidney does not negatively impact on graft or recipient survival. We have shown that mlgA in the donor kidney disappears within a variable time frame. No adverse events can be directly attributable to the presence of mlgA in the donor kidney. Patients were disease-free and dialysis-free for a median of 7 years. The study supports the theory that factors inherent in the renal parenchyma are not involved in the pathogenesis of IgA GN. We confirm that the major risk factor for developing IgA glomerulonephritis in renal allografts is plgA GN.