Abstract: SA-PO535

Clinical Findings, Pathology, Treatment, and Outcomes of PGNMID after Kidney Transplantation

Session Information

Category: Glomerular

  • 1005 Clinical Glomerular Disorders

Authors

  • Salameh, Hassan A., Mayo Clinic, Rochester, Minnesota, United States
  • Amer, Hatem, Mayo Clinic, Rochester, Minnesota, United States
  • Zand, Ladan, Mayo Clinic, Rochester, Minnesota, United States
  • Fervenza, Fernando C., Mayo Clinic, Rochester, Minnesota, United States
  • Leung, Nelson, Mayo Clinic, Rochester, Minnesota, United States
Background

Proliferative glomerulonephritis with monoclonal immunoglobulin deposits (PGNMID) is a rare form of glomerular disease caused by monoclonal immunoglobulin (Ig) deposition localized to the glomeruli. The outcome of recurrent PGNMID in renal allografts is not well known and to our knowledge has been reported in only 12 patients. We describe a single centers’ experience with PGNMID after kidney transplantation (KTx).

Methods

Between 2000 and 2016 we identified 20 patients with PGNMID who underwent KTx. We describe their clinical findings, labratory data, recurrence rates, biopsy findings, treatment and outcomes during the study period.

Results

The median age at the time of native kidney biopsy-proven PGNMID was 54 (range 23-74) years. Median time between the initial kidney biopsy to ESRD (KTx or dialysis) was 36 (range 2-146) months. Post-transplant, PGNMID recurred in 18 out of 20 patients (90%). The median time to recurrence in the kidney biopsy was 4 (range 1-48) months (Figure 1).
Four patients did not receive targeted treatment for the PGNMID recurrence and no graft loss was noted with median follow-up of 48.5 months. Three patients were treated with additional immunosuppressive agents including steroids and cyclophosphamide and 33% (n=1) had graft loss in this group. Seven patients received B-cell targeted therapy with Rituximab with graft loss rate of 28% (n=2). Four patients received plasmapheresis in addition to immunosuppressive therapy; graft lost in 75% (n=3); however; only 25% (n=1) was attributed to PGNMID with the other two loses due to rejection.

Conclusion

In our experience, PGNMID was associated with a very high rate of recurrence in allografts reaching 90%. Graft loss occurred in 33% of recurrent cases. The median time to graft loss was 67 (range 31-132) months. Graft loss incidence due to PGNMID was similar between the immunosuppression, Rituximab and plasmapheresis groups; however, the plasmapheresis group had more aggressive disease that lacked response to other treatment options.

Figure 1. Kaplan-Meier plots of (A) Cumulative incidence of PGNMID recurrence in grafts and (B) Graft loss in recurrent PGNMID.