Abstract: FR-PO1167
De Novo Minimal Change Disease After Acute Rejection in a Kidney Transplant Recipient with an APOL1 Risk Allele
Session Information
- Transplantation: Clinical - Transplant Access, Recipient Evaluation, Living Donors, Pregnancy, and More
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Earthineni, Geethika, Medical University of South Carolina, Charleston, South Carolina, United States
- Posadas, Maria Aurora C., Medical University of South Carolina, Charleston, South Carolina, United States
- Abdelkader, Ahmed I. Kamal, Medical University of South Carolina, Charleston, South Carolina, United States
- Barakat, Munsef, Medical University of South Carolina, Charleston, South Carolina, United States
- Edding, Sherida, Medical University of South Carolina, Charleston, South Carolina, United States
- Pasham, Vishwajeeth, Medical University of South Carolina, Charleston, South Carolina, United States
- McMahon, Blaithin A., Medical University of South Carolina, Charleston, South Carolina, United States
- Vaishnav, Sakshi, Medical University of South Carolina, Charleston, South Carolina, United States
Introduction
De novo minimal change disease (MCD) post-transplant is rare. Recipient APOL1 high-risk genotypes are associated with increased risk of T-cell mediated rejection (TCMR ) via T-cell/NK-cell immunomodulation, independent of donor genotype and recipient ancestry. To our knowledge, acute rejection with concurrent de novo MCD in an APOL1 G1/G1 recipient has not been previously reported.
Case Description
A 68 year old male with APOL-1-associated CKD (G1/G1), hypertension, prostate CA, s/p prostatectomy (2009), renal cell CA, s/p R nephrectomy (2015), previously treated HCV infection, underwent preemptive deceased donor kidney transplant (12/2025). He received basiliximab induction (cPRA 0%, HLA mismatch 1-2-1). Kidney transplant biopsy done 10 days post-transplant for rising serum creatinine and proteinuria (13 g/g) revealed Banff IIB TCMR with EM showing diffusely effaced foot processes. The patient received one dose of Methylprednisolone 250 mg IV and three doses of ATG 1.5 mg/kg, noted with improvement in serum creatinine and proteinuria (3.6 g/g). Repeat kidney biopsy done (3/2026) for increasing proteinuria (up to 23 g/g) showed de novo MCD. The patient received Methylprednisolone 500 mg IV x 3 doses, followed by a protracted course of Prednisone taper. Unfortunately, the patient’s clinical course was complicated by pulmonary and CNS aspergillosis, limiting treatment options. Allograft function stabilized with persistent nephrotic-range proteinuria (Fig 1).
Discussion
This case suggests probable mechanistic cascade: APOL1 G1/G1-driven immune dysregulation precipitating TCMR, with T-cell-mediated podocyte injury manifesting as MCD. Treatment of MCD, limited by active aspergillosis, presents further complexity. CNI optimization and cautious rituximab represent potential TCMR treatment options post-infection clearance. APOL1 genotyping may improve transplant risk stratification.
Fig 1: Pre and Post-transplant creatinine and proteinuria trends.