Abstract: SA-PO0141
Integrating Genetic Testing into Evaluation of Kidney Transplant Recipient Candidates: A Single-Center Experience
Session Information
- ADPKD and Cystic Kidney Disease - 3
October 24, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Genetic Diseases of the Kidneys
- 1201 Genetic Diseases of the Kidneys: Cystic (Monogenic)
Authors
- Bregman, Adam Philip, University of Wisconsin-Madison, Madison, Wisconsin, United States
- Benoy, Megan E., University of Wisconsin-Madison, Madison, Wisconsin, United States
- Mandelbrot, Didier A., University of Wisconsin-Madison, Madison, Wisconsin, United States
- Garg, Neetika, University of Wisconsin-Madison, Madison, Wisconsin, United States
Background
Genetic testing (GT) of kidney transplant recipient candidates (KTRCs) can identify cause of kidney disease in KTRCs, evaluate recurrence risk of native disease, identify a genetic cause of familial kidney disease and guide related donor testing. We sought to outline our single center experience of GT in KTRCs.
Methods
We identified all KTRCs evaluated at our center between June 1, 2018 and April 1, 2026 who underwent GT, analyzed indication for testing, results, impact on donor testing, and post-transplant management.
Results
75 KTRCs had GT, of which native disease was phenotypically identified as unknown in 23 (30.7%) despite biopsy performed in 11 (47.8%), thrombotic microangiopathy (TMA) in 14 (18.7%), focal segmental glomerulosclerosis (FSGS) in 11 (14.7%), polycystic kidney disease (PKD) in 8 (10.7%), and Alport syndrome in 5 (6.7%).
The most common reasons for GT were end stage kidney disease (ESKD) of unknown etiology in 41 (54.7%), evaluation of recurrence risk in 35 (46.7%), and to allow related donor cascade GT in 27 (36%). Comprehensive renal gene panels were utilized in 60 (45%), phenotype limited panels in 26 (34.7%), and single gene panels in 5 (6.7%).
37 (49.3%) of KTRCs GT had mutations in genes associated with ESKD phenotype. Of these, the most common was high risk APOL1 phenotype in 8 (21.6%). Of the remaining 29 patients, 26 had likely pathogenic (LP)/pathogenic (P) variants and 3 had variants of unknown significance (VUS) in genes correlating with the phenotype (Figure 1). GT in KTRCs led to sequential donor testing in 24 (32%), informed recipient prognosis in 24 (32%), and changed recipient treatment plan in 21 (28%).
Conclusion
In our single-center experience, GT provided an explanation for ESKD in half of cases, and informed decision making in over two-thirds.