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Abstract: FR-PO769

Clinical and Native Histological Predictors of Recurrent IgA Nephropathy After Kidney Transplantation

Session Information

Category: Transplantation

  • 2002 Transplantation: Clinical

Authors

  • Chukwu, Chukwuma Austin, Salford Royal Hospital, Salford, Salford, United Kingdom
  • Holmberg, Christopher, Royal Liverpool University Hospital, Liverpool, Liverpool, United Kingdom
  • Middleton, Rachel, Salford Royal Hospital, Salford, Salford, United Kingdom
  • Kalra, Philip A., Salford Royal Hospital, Salford, Salford, United Kingdom
  • Shawki, Howida, Royal Liverpool University Hospital, Liverpool, Liverpool, United Kingdom
  • Rao, Anirudh, Royal Liverpool University Hospital, Liverpool, Liverpool, United Kingdom
Background

Although recurrent IgA Nephropathy (rIgAN) in kidney transplant recipients (KTR) has been regarded as benign, there is increasing evidence that rIGAN may lead to late allograft loss in a significant proportion of KTR. Data on the risk predictors and outcomes of rIgAN is limited. We investigated the incidence, clinical and histologic predictors,and outcomes of rIGAN in KTR.

Methods

KTR with biopsy-proven IgA nephropathy between 2005 and 2020 at 2 tirtiary nephrology centers in North-west England were evaluated. Demographic, clinical, and native kidney histological data were analysed. Risk factors and allograft outcomes were assessed using Cox proportional hazard method.

Results

rIgAN was diagnosed in 35 of 203KTR(17%). mean age was 45±13yr, and median follow-up was 7yr. Time to recurrence and from recurrence to graft loss was 4.8yr(IQR 2.7-6.7) and 2.9yr(IQR 1.3-4.3) respectively.
Factors associated with rIgAN include younger age(Hazard ratio[HR] 0.68, 95%CI 0.51-0.9; p=0.009); higher pre-transplant proteinuria(HR 1.21, 95% CI 1.09-1.35; p<0.001); living donor graft(HR 2.32, 95%CI 1.1 - 4.6;p=0.016), Cyclosporin use(HR 2.82, 95%CI 1.07-7.41;p=0.035); history of acute rejection(HR 2.33, 95%CI 1.14-4.77;p=0.020); higher proportion of native glomeruli with segmental sclerosis (HR 1.05, 95%CI 1.01-1.09; p=0.014).
Death censored graft loss was 11 times higher in recipients with rIgAN (HR 11.0, 95%CI 4.35-27.7; p<0.001).

Conclusion

KTR with rIgAN were 11 times more likely to lose their graft than those without recurrence. Younger age, higher pre-transplant proteinuria, living donor allograft, history of acute rejection, cyclosporin use and a higher degree of segmental sclerosis in the original disease are associated with rIgAN.