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Abstract: FR-PO770

Clinical and Histologic Predictors of Recurrent Focal Segmental Glomerulosclerosis 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
  • Rao, Anirudh, Royal Liverpool University Hospital, Liverpool, Liverpool, United Kingdom
  • Shawki, Howida, Royal Liverpool University Hospital, Liverpool, Liverpool, United Kingdom
Background

Recurrent FSGS (rFSGS) after transplantation is a major cause of allograft loss. Data on the clinical and native kidney histological predictors of rFSGS is limited. We investigated the clinical and histological predictors of rFSGS and its impact on allograft outcome

Methods

71 KTR with biopsy-proven FSGS transplanted between 2005 and 2020 at two tertiary nephrology centres in North-west England were evaluated. Demographic, clinical, and native kidney histological data were analysed. Risk factors of rFSGS and their impact on allograft outcomes were evaluated using Cox proportional hazard methods

Results

FSGS recurrence was diagnosed in 14 of 71 KTR(20%). Mean age at transplantation was 43.8±17yr, and median follow-up was 7yr. The median duration to rFSGS was 0.6yr(IQR 0.2-2.9) and the time from rFSGS to graft loss was 4.9yr(IQR 3-10). rFSGS was associated with higher pre-transplant proteinuria (HR 1.115,p=0.002); alemtuzumab induction(HR 3.38, p=0.035); younger donor age(HR 0.95, p=0.020); proteinuria at 12months post-transplant(HR 1.16, p<0.001); history of acute rejection(HR 3.17, p<0.039), lower baseline eGFR(HR 0.30, p<0.037), mesangial proliferation(HR 5.38,p=0.043); glomerular IgG(HR 20.5, p<0.033) and IgA(HR 12.1, p<0.001) deposits in the native disease. Death-censored graft loss adjusted for donor type, history of acute rejection and baseline eGFR was 6 times higher in KTR with rFSGS(HR 6.1, 95% CI 1.5-24.7;p=0.012)

Conclusion

rFSGS occurred early post-transplantation and was associated with a 6 fold increase in graft loss. Higher pre-and post-transplant proteinuria, alemtuzumab induction, acute rejection, low baseline eGFR, as well as mesangial proliferation, IgG and IgA deposits in native disease are factors associated with rFSGS