Abstract: SA-PO0724
Shared and Distinct Urinary Proteomic Signatures of Lupus Nephritis and Other Glomerular Diseases
Session Information
- Glomerular Diseases: Profiling Through Multiomics
November 08, 2025 | Location: Exhibit Hall, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1401 Glomerular Diseases: Mechanisms, including Podocyte Biology
Authors
- Fava, Andrea, Johns Hopkins Medicine Division of Rheumatology, Baltimore, Maryland, United States
- Celia, Alessandra Ida, Universita degli Studi di Roma La Sapienza, Rome, Lazio, Italy
- Saksena, Daksh, Johns Hopkins Medicine Division of Rheumatology, Baltimore, Maryland, United States
- Lee, Chen-Yu, Johns Hopkins Medicine Division of Rheumatology, Baltimore, Maryland, United States
- Guthridge, Carla J, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, United States
- James, Judith A, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, United States
- Buyon, Jill P., New York University, New York, New York, United States
- Petri, Michelle, Johns Hopkins Medicine Division of Rheumatology, Baltimore, Maryland, United States
- Guthridge, Joel M, Oklahoma Medical Research Foundation, Oklahoma City, Oklahoma, United States
- Rovin, Brad, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
Group or Team Name
- The Accelerating Medicines Partnership: Autoimmune and Immune-Mediated Disease Program.
Background
Urinary biomarkers may detect histologically active lupus nephritis (LN). We tested candidate LN urinary proteins in other glomerular diseases to identify shared and specific biomarkers.
Methods
Urine samples from patients with LN (n=234), ANCA-associated glomerulonephritis (n=17), IgA nephropathy (IgAN, n=30), membranous nephropathy (MGN, n=30), and focal segmental glomerulosclerosis (FSGS, n=30) were collected near the time of biopsy and after screening for healthy controls (HC, n=31). Proteomic profiles were quantified using the Olink Explore HT platform (5,400-plex).
Results
IL-16 was elevated in Class III/IV LN and in a subset of ANCA patients. CD163 in proliferative LN, in a subset of ANCA, and unexpectedly in MGN. Galectin-1 was broadly elevated across glomerular diseases, but it was lower in class II LN, IgAN and FSGS. TNFSF13B (BAFF) was increased in all conditions, but higher in Class III, IV, and V LN, and in MGN, suggesting a stronger role in B cell–driven pathology in these conditions. Tenascin C was elevated in most, but highest in Class IV LN indicating prorepair and profibrotic pathways. C9 was elevated across all disease groups, indicating widespread complement activation.
Conclusion
Urinary biomarkers reveal both shared and disease-specific molecular pathways across glomerular diseases. distinct expression patterns suggest unique pathogenic processes. These findings offer mechanistic insight into glomerular inflammation and fibrosis and, importantly, raise the potential for repurposing targeted therapies across traditionally distinct kidney diseases. Analysis of the full urinary panel (~5,400) is ongoing.
Funding
- Other NIH Support