Kidney Week

Abstract: TH-PO578

Allograft Membranous Nephropathy of Donor Origin – Response to the Immunological Environment of the Recipient

Session Information

• Trainee Case Reports - II
  October 25, 2018 | Location: Exhibit Hall, San Diego Convention Center
  Abstract Time: 10:00 AM - 12:00 PM

Category: Trainee Case Reports

• 1802 Transplantation: Clinical

Authors

• Zhong, Yan, LAC USC Medical Center, Los Angeles, California, United States

Yan Zhong,

• Carpenter, Philip M., University of Southern California, Los Angeles, California, United States

Philip M. Carpenter,

• Khine, Annika, LAC USC Medical Center, Los Angeles, California, United States

Annika Khine,

• Sharma, Neeraj, University of Southern California, Los Angeles, California, United States

Neeraj Sharma,

• Qazi, Yasir A., University of Southern California, Los Angeles, California, United States

Yasir A. Qazi,

• Maw, Thin Thin, University of Southern California, Los Angeles, California, United States

Thin Thin Maw,

• Smogorzewski, Miroslaw, University of Southern California, Los Angeles, California, United States

Miroslaw Smogorzewski,

Introduction

Primary membranous nephropathy (MN) is the common cause of nephrotic syndromes in adults. The exact mechanism of kidney injury remained elusive until discovery of the podocyte antigen PLA₂R and its IgG antibodies. We report a unique case of MN in the transplanted kidney.

Case Description

59-year-old Caucasian female with history of HTN, DM and ESRD on hemodialysis for 6 years underwent the deceased donor renal transplant (DDRT) (HLA A24:68/B35:57/DR18:11 to A2:2/B35:39/DR4:14) with DGF. She required hemodialysis four times post DDRT. The kidney frozen section obtained before transplantation show 135 glomeruli, 4% glomerulosclerosis, mild fibrosis and acute tubular necrosis. Eighteen days post DDRT, urine protein/creatinine ratio 34.2gm/gm was noted and SCr was 1.73 mg/dL on standard therapy (tacrolimus, mycophenolate mofetil, prednisone). Allograft biopsy done 40 days post-transplant show thickened glomerular basement membranes with strong positivity for IgG, C3 and PLA₂R1. Electron microscopy show subepithelial deposits along the basement membranes with spikes in between them. The original allograft biopsy performed at the time of transplant was stained with Jones silver and positive for PLA₂R1, confirming that MN was of donor origin. The recipient’s serum PLA₂R antibody was negative for 4 times over 8 months. Her serum albumin plummeted from 4.6g/dL to 2.4g/dL within 2 months after DDRT, but gradually improved to 4g/dL in 6 months. Proteinuria decreased to 1gm/24 hour and SCr remained 1.5-2.0mg/dL. Immunosuppression stays the same. We plan to repeat the allograft biopsy one year after DDRT to follow the expected histological recovery of the donor derived MN.

Discussion

This unique case of donor derived MN and subsequent clinical disease resolution after transplantation further supports the notion that PLA₂R antibody is critical for the pathogenesis of MN. It is possible that immune mediated GN may eventually clear from the transplanted kidney with no adverse effect on allograft function after kidney is removed from the donor auto-antigenicity environment. Thus, the future allograft biopsy should show disappearance of PLA₂R immune complex in the transplanted kidney.