Abstract: SA-PO1185
APOL1: The Donor Connection? A Case of Collapsing Glomerulopathy Without an Identifiable Trigger in a Kidney Transplant Recipient
Session Information
- Transplantation: Clinical - Complications, Pediatrics, and Multi-Organ Considerations
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Farouji, Abdelhadi, Henry Ford Hospital, Detroit, Michigan, United States
- Pervez, Aqsa, Henry Ford Hospital, Detroit, Michigan, United States
- Ansari, Rehan, Henry Ford Hospital, Detroit, Michigan, United States
Introduction
High-risk Apolipoprotein L1 (APOL1) genotypes (G1/G2) are present in approximately 13% of the African American (AA) population. Donor kidneys carrying high-risk APOL1 alleles have been associated with adverse allograft outcomes, including rapid decline in renal function and collapsing glomerulopathy.
Case Description
A 71-year-old AA man with ESRD secondary to biopsy-proven hypertensive nephrosclerosis and six years of dialysis vintage underwent deceased donor kidney transplantation (KDPI 87%, cPRA 0%). Induction immunosuppression consisted of thymoglobulin, followed by tacrolimus, mycophenolate, and prednisone maintenance therapy. The donor was a 65-year-old AA woman without evidence of CKD (terminal creatinine 0.56 mg/dL, HbA1c 6%). Implant biopsy showed mild IFTA without arteriolar hyalinosis or nodular glomerulosclerosis.
Four months post-transplant, he developed progressive proteinuria (urine protein-to-creatinine ratio [UPCR] 2.52 g/g; albumin-to-creatinine ratio 1425 mg/g). Allograft biopsy demonstrated collapsing glomerulopathy with podocyte hyperplasia and foot process effacement, without immune complex deposition, rejection (C4d negative, no tubulitis), or viral nephropathy (negative SV40 and CMV immunohistochemical staining). Genetic testing from residual frozen biopsy tissue revealed a high-risk APOL1 genotype (G1/G2) with recipient G0/G0, supporting APOL1-associated nephropathy. Evaluation for secondary triggers, including CMV, EBV, BK virus, HIV, and COVID-19, was negative. Donor-specific antibodies were absent, tacrolimus levels remained therapeutic, and there was no evidence of sepsis or ischemia.
At 12 months post-transplant, serum creatinine increased to 5.1 mg/dL with worsening proteinuria (UPCR 9.65 g/g) despite supportive management. Notably, the mate kidney remained stable with a creatinine of 1.63 mg/dL during the same period.
Discussion
High-risk APOL1 variants are increasingly recognized as contributors to kidney disease and adverse allograft outcomes, particularly among donors of African ancestry. Although a “second hit” hypothesis has been proposed, no identifiable trigger was found in our case, suggesting APOL1-associated injury may occur independently or with unrecognized triggers. This case highlights donor-derived APOL1-associated collapsing glomerulopathy and supports donor APOL1 genotyping for risk stratification.