BACKGROUND: Risk factors contributing to recurrence of IgA nephropathy (IgAN) after transplantation are unclear. Some (but not all) series have suggested greater degrees of human leukocyte antigen (HLA) matching play a role. METHODS: Using registry data including all kidney transplants performed in Australia and New Zealand between 1987 and 2004 we examined IgAN recurrence among living donors with zero HLA-mismatches. RESULTS: Of 1354 grafts performed in recipients with IgAN, live donors (LDs) accounted for 488 including 108 with zero HLA-mismatches. Biopsy-proven IgAN recurrence was reported for 110 (7%) of grafts overall, but 17% of those who received zero HLA-mismatched LD grafts (HR for recurrence free graft survival 2.7 [95% CI 1.5-5.1], P=0.001). There was no significant difference in recurrence rates between zero and >or=1 HLA-mismatched grafts from cadaveric donors (CDs). Recurrence of IgAN was associated with worse graft survival, more so among LD recipients (HR 8.5 [4.8-15.2], P<0.001) than CD recipients (HR 4.5 [2.6-7.5], P<0.001). However, there was no difference in graft survival between zero and >or=1 HLA mismatched LD recipients whose native disease was IgAN. In contrast, zero HLA mismatched recipients of kidneys with other primary renal disease enjoyed a graft survival advantage. No difference in recurrence rates was seen among those with HLA B12, B35 or DR4. CONCLUSIONS: The increased rates of IgAN-related graft loss among zero HLA-mismatched LD recipients counterbalance the advantage normally seen among zero HLA-mismatched recipients. However, since graft survivals are similar, there is no reason to avoid donor-recipient pairs with zero HLA-mismatches in this setting.
No takes yet. Share an insight, caveat, or question.
McDonald et al. (2006) studied this question.
Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context: