Abstract: FR-PO1195
Association of Serum Uric Acid with Donor-Derived Cell-Free DNA and Inflammatory Plasma Proteins in Kidney Allograft Recipients
Session Information
- Transplantation: Clinical - Rejection, Biomarkers, and Pharmacology
October 23, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Transplantation
- 2002 Transplantation: Clinical
Authors
- Haririan, Abdolreza, University of Maryland Baltimore, Baltimore, Maryland, United States
- Woo, Jongmin, University of Maryland Baltimore, Baltimore, Maryland, United States
- Ugarte, Richard M., University of Maryland Baltimore, Baltimore, Maryland, United States
- Ibrahim, Mohamed M., University of Maryland Baltimore, Baltimore, Maryland, United States
- Gautam, Ujwal, University of Maryland Baltimore, Baltimore, Maryland, United States
- Ahmed, Hiba M., University of Maryland Baltimore, Baltimore, Maryland, United States
- Daniel, Emily, University of Maryland Baltimore, Baltimore, Maryland, United States
- Singh, Amit P., University of Maryland Baltimore, Baltimore, Maryland, United States
- Kalil, Roberto S., University of Maryland Baltimore, Baltimore, Maryland, United States
Background
Uric acid (UA), as a "danger signal" and product of DNA breakdown after cell injury stimulates macrophage/monocytes and inflammatory cytokines that can promote T-cell activation, and has been associated with worse kidney allograft survival. dd-cfDNA, resulting from cell injury in allograft is a biomarker of acute rejection, and can upregulate release of different cytokines and chemokines through activation of inflammasomes. AlloMap kidney (AM), a 5-gene expression score in peripheral blood mononuclear cells, is associated with allograft rejection. We sought to examine the association of serum UA with dd-cfDNA, AM, and targeted inflammatory pathway proteins in plasma.
Methods
This is a prospective cohort study in 30 kidney allograft recipients transplanted at our center between 2021-2023. Blood samples were collected at 1, 2, 3, 4, 6, 9, and 12 months post-transplant. dd-cfDNA and AM were analyzed at CareDx, UA was measured in local laboratory, and proteomic profiling was conducted at our center cytokine laboratories using nanoparticle enrichment.
Results
The characteristics of the 30 participants are summarized in the table. There was no significant correlation between UA, dd-cfDNA or AM in any of the time points. Moreover, none was predictive of graft loss during the 39.1±14.8 mo follow up. UA levels (6.8±1.6, n=21) correlated with ISG15, CD14, IFIT1, IFIT5, OAS2, OAS3, and MYD88 (ρ: 0.43-0.74, p=0.001-0.046), while AM scores (8.2±2.9, n=11) correlated with CRP, CD14, OAS2, OAS3 levels (ρ: 0.60-0.99, p=0.01-0.048). These proteins are upregulated by IFNγ and activation of innate immune system.
Conclusion
Although UA and dd-cfDNA both are released as a result of cell injury and death, we did not find any association between the two in kidney transplant recipients. dd-cfDNA was not associated with circulating inflammatory proteins, while UA and AM levels had significant correlation with INFγ-regulated and innate immune pathway targets. Further studies are needed to explore the role of these proteins in mediation of the impact of UA on allograft, and to investigate dd-cfDNA as a mediator vs byproduct of allograft injury/rejection.
Patient characteristics
| Recipient age | 51.7±12.5 | Donor age | 47.3±13.3 |
| Recipient male | 19 (63.3%) | Donor male | 16 (53.3%) |
| Recipient AA | 22 (73.3%) | HLA MM | 5.5±1.6 |
| Deceased donor | 24 (80%) | cPRA | 36.5±36.5 |
Funding
- Commercial Support – CareDx