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Abstract: PO2563

Pediatric Donor Glomerulopathy in Pediatric En-Bloc Kidney Transplants

Session Information

Category: Transplantation

  • 1902 Transplantation: Clinical

Authors

  • Kendrick, Elizabeth A., University of California Los Angeles, Los Angeles, California, United States
  • Zuckerman, Jonathan E., University of California Los Angeles, Los Angeles, California, United States
  • Yabu, Julie M., University of California Los Angeles, Los Angeles, California, United States
  • Abdalla, Basmah A., University of California Los Angeles, Los Angeles, California, United States
  • Sisk, Anthony E., University of California Los Angeles, Los Angeles, California, United States
Background

Use of pediatric en-bloc kidneys (EBK) have equivalent outcomes to standard deceased donor kidneys and has helped expand the pool of donor kidneys. The size mismatch related hyperfiltration injury in pediatric EBK and pediatric single kidney allografts is associated with pediatric donor glomerulopathy whose effect on allograft outcomes is not well documented.

Methods

We retrospectively reviewed for cause biopsies of pediatric EBK from 1/2015 to 1/2020. Our center performed 37 transplants using pediatric EBK. Recipient weight criteria was < 75 kg to minimize donor-recipient size mismatch. One recipient died with a functioning graft at 4 months; one graft failed due to fungal infection of the vascular anastomosis requiring nephrectomy at 1 month.

Results

Fourteen biopsies were performed in 10 patients between 1 to 24 months after transplantation. Indications for biopsy were: graft dysfunction (10; 3 with proteinuria), proteinuria alone (2), BK viremia with proteinuria (1), and de novo donor specific antibody (DSA) (1).
Biopsies from 5 EBK recipients demonstrated pediatric donor glomerulopathy represented by the presence of glomerular abnormalities including subepithelial multi-layering/remolding of the basement membrane, segmental glomerulosclerosis, mesangial hypercellularity, mesangial sclerosis, podocyte hypertrophy, and/or segmental mild podocyte foot processes effacement. Ten biopsies also showed thin basement membranes (BM) on EM consistent with the age of the donor kidney.
Other diagnostic findings among the entire biopsy cohort were acute cellular rejection (ACR), antibody mediated rejection (AMR), or mixed ACR and AMR (5), acute tubular necrosis (ATN) (3), and pyelonephritis (1).
Biopsies with pediatric donor glomerulopathy were performed early after transplantation and were associated with proteinuria. Semiquantitative proteinuria in the 5 recipients at the time of biopsy was 1-3+; 1.2-9.5 g/day in 4. Follow up 4-39 months post-transplant (mean 17 months) in patients with pediatric donor glomerulopathy showed serum creatinine 0.55-2.07 mg/dl (mean 1.1) and urine protein 0.4 to 1.2 g/day (mean 0.73).

Conclusion

Overall, pediatric donor glomerulopathy seen early post transplant period did not appear to negatively affect long-term graft function; this outcome may be related to growth of these kidneys occurring early post transplant.