Abstract: TH-PO0466
Damage Accumulation over Time in an IgAN Cohort with Serial Kidney Biopsies
Session Information
- Glomerular Diseases: Clinical, Outcomes, and Therapeutics Research - IgAN
October 22, 2026 | Location: Exhibit Hall A, Convention Center
Abstract Time: 10:00 AM - 12:00 PM
Category: Glomerular Diseases
- 1402 Glomerular Diseases: Clinical, Outcomes, and Therapeutics
Authors
- Malvar, Ana, Hospital Fernandez, Buenos Aires, Argentina
- Flores, Andrea Jazmin, Hospital Fernandez, Buenos Aires, Argentina
- Gutierrez, Rocio Del Pilar, Hospital Fernandez, Buenos Aires, Argentina
- Navarro, Jordi Lionel, Hospital Fernandez, Buenos Aires, Argentina
- Olmos, Jhucelia, Hospital Fernandez, Buenos Aires, Argentina
- Rovin, Brad, The Ohio State University Wexner Medical Center, Columbus, Ohio, United States
Background
Recent epidemiologic studies demonstrate that IgA nephropathy (IgAN) often progresses to kidney failure. The evolution of histological damage in IgAN is unknown. To address this question, we characterized a longitudinal cohort of IgAN patients with repeat biopsies focusing on global and segmental glomerulosclerosis (GS, SS) and interstitial fibrosis and tubular atrophy (IFTA).
Methods
A cohort of 29 patients of Hispanic ethnicity followed for up to18 years had a diagnostic biopsy (Bx Dx) showing IgAN and at least one follow-up biopsy (Bx2). Proteinuria and eGFR (CKD-EPI) were measured. In addition to MEST-C scoring the percent GS,SS, and IFTA were determined on each biopsy. After diagnosis these patients were treated only with RASi or glucocorticoids.
Results
Patients were stratified into 4 groups by baseline proteinuria (none, <1g/d, 1-2g/d, and >2g/d) (Table). Six patients had no proteinuria and normal kidney function and were biopsied for glomerular hematuria. GS was present in 83% of patients at diagnosis. GS increased significantly with increasing baseline proteinuria (Table, p=0.003 for trend) and during the 3 years between Bx Dx and Bx2 (24±19% vs 32±16%, p=0.0006). Patients with no proteinuria at baseline had a low level of GS at diagnosis (6±9%) but this increased to 21±10% on Bx2, done 4 years later (p=0.03). Similarly, SS increased significantly between Bx Dx and Bx2 (8±10% vs 11.5±8.5%, p=0.02), but IFTA did not (16±11% vs 19±11%, p=0.25).
Conclusion
These data demonstrate GS is often already present at IgAN diagnosis, increases significantly over time and more rapidly than IFTA. Although GS is not reflected in the MEST-C score the high levels of glomerular obsolescence shown here are out of proportion to those expected with age and may represent an underrecognized marker of prognosis in IgAN.
Funding
- Clinical Revenue Support