Abstract: FR-PO0106
Validation of a Surface Plasmon Resonance Assay to Quantify Circulating APOL1 Protein After Living Donor Nephrectomy
Session Information
- Hereditary Glomerular and Tubulointerstitial Kidney Diseases
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Genetic Diseases of the Kidneys
- 1202 Genetic Diseases of the Kidneys: Non-Cystic (Complex and Non-Cystic Monogenic)
Authors
- Ferreira, Luisa Queiroga, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Tavares, Melissa Gaspar, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Ferreira, Guilherme De Sousa, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Godoi, Leonardo Moura, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Soares, Marina Oliveira Melo, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Oliveira Alves Lima, Roberta, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Finamor, Rhaon Pietro Santos, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Foresto, Renato Demarchi, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Medina-Pestana, Jose, Universidade Federal de Sao Paulo Hospital do Rim e Hipertensao, São Paulo, SP, Brazil
- Casarini, Dulce Elena, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
- Requiao-Moura, Lucio Roberto, Universidade Federal de Sao Paulo, São Paulo, SP, Brazil
Group or Team Name
- BRIDGES-APOL1
Background
APOL1 polymorphisms increase risk of nephropathy in individuals of African ancestry, yet not all carriers of risk alleles develop disease. Biomarkers are essential to predict who is at higher risk. Proteomics studies remain inconclusive regarding the correlation between APOL1 concentration and renal outcomes, and studies using Surface Plasmon Resonance (SPR) to determine APOL1 expression and its correlations are scarce.
Methods
This pilot study, conducted at Hospital do Rim(Brazil), aimed to validate an SPR-based method for quantifying APOL1 protein in blood from living kidney donors after nephrectomy, as part of the BRIDGES-APOL1 proteomics study designed to correlate APOL1 concentration with renal alterations. Living donors from 2008 to 2019 were stratified into 2 groups: high risk(≥1 allele G1 or G2) and low risk(G0G0).
Results
A total of 566 donors were included: 466(82.3%) G0G0 (low risk), 58(10.2%) G0G1, 32(5.7%) G0G2, 6(1.1%) G1G2, and 4(0.7%) G1G1; no G2G2 donors were identified. The APOL1 quantification protocol was standardized, confirming stable binding of the anti-APOL1 antibody and the reference protein. After establishing binding stability and the calibration curve, APOL1 was quantified in plasma from 20 donors: 10 low risk (G0G0) and 10 high risk. Preliminary results show APOL1 concentration was significantly higher in G1G1 donors compared with G0G0, with a trend toward significance for G1G2. Mean pre-donation eGFR was 102.9 mL/min/1.73 m2 in G0G0 versus 90.56 mL/min/1.73 m2 in high-risk donors. After a mean post-donation follow-up of 13.9 years (low risk) and 11.2 years (high risk), eGFR was 73.03 mL/min/1.73 m2 in G0G0 versus 70.54 mL/min/1.73 m2 in high risk. High-risk donors did not have a higher incidence of post-donation hypertension nor clinically significant albuminuria.
Conclusion
SPR is a sensitive method to quantify APOL1 in donors. In preliminary data, APOL1 concentration was significantly higher in G1G1 versus G0G0, with a trend toward significance for G1G2, suggesting biological relevance. Integrating SPR into APOL1 research may advance understanding of mechanisms underlying renal alterations in individuals of African ancestry with different genotypes. Additional analyses are needed to clarify remaining uncertainties regarding APOL1-associated kidney disease mechanisms.