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Peer-reviewedCC BY 4.0Frontiers in Immunology

Case Report: Renal amyloid A amyloidosis with crescent formation and elevated serum anti-glomerular basement membrane antibody titers in a patient with chronic systemic inflammation

5 affiliations
  1. 1Laboratory of Electron Microscopy, Pathological Center, Peking University First Hospital
  2. 2Renal Pathological Center, Institute of Nephrology, Peking University
  3. 3Renal Division, Department of Medicine, Peking University First Hospital
  4. 4Key Laboratory of Chronic Kidney Disease (CKD) Prevention and Treatment, Ministry of Education of China
  5. 5Key Laboratory of Renal Diseases, Ministry of Health of China

Abstract

We report a case of a 65-year-old Chinese man with chronic systemic inflammation, who presented with nephrotic syndrome and renal insufficiency, along with elevated serum anti-glomerular basement membrane (GBM) antibody titers, yet lacked the typical clinical features of rapidly progressive glomerulonephritis (GN). Renal biopsy demonstrated AA amyloid deposition in the glomerular mesangium, crescent formation in 33% of glomeruli, and patchy immunoglobulin G (IgG) staining. Persistent inflammation, mediated by pathways involving interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), is considered to be associated with the expression of serum amyloid A (SAA) and subsequent AA amyloidogenesis. Furthermore, we hypothesize that persistent inflammatory activity may be a contributory factor in the exposure of cryptic GBM antigens, thereby triggering the production of anti-GBM antibodies. In summary, we report a rare case of renal AA amyloidosis with crescent formation and elevated serum anti-GBM antibody titers in a patient with chronic systemic inflammation. However, the pathogenesis of crescent formation in this patient remains unclear and requires further investigation.

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BibTeX
@article{chen2026case,
  title = {{Case Report: Renal amyloid A amyloidosis with crescent formation and elevated serum anti-glomerular basement membrane antibody titers in a patient with chronic systemic inflammation}},
  author = {Kai Chen and Chen Tang and Yue-Yue Zhu and Lin Nie and Jin Xu and Xin Zhang and Li-Qiang Meng and Li-Jun Liu and Su-Xia Wang},
  journal = {Frontiers in Immunology},
  year = {2026},
  month = nov,
  doi = {10.3389/fimmu.2026.1970185},
  url = {https://www.frontiersin.org/articles/10.3389/fimmu.2026.1970185/full},
  note = {CC BY 4.0},
}
RIS
TY  - JOUR
TI  - Case Report: Renal amyloid A amyloidosis with crescent formation and elevated serum anti-glomerular basement membrane antibody titers in a patient with chronic systemic inflammation
AU  - Kai Chen
AU  - Chen Tang
AU  - Yue-Yue Zhu
AU  - Lin Nie
AU  - Jin Xu
AU  - Xin Zhang
AU  - Li-Qiang Meng
AU  - Li-Jun Liu
AU  - Su-Xia Wang
PY  - 2026
DA  - 2026/11/02
JO  - Frontiers in Immunology
DO  - 10.3389/fimmu.2026.1970185
UR  - https://www.frontiersin.org/articles/10.3389/fimmu.2026.1970185/full
AB  - We report a case of a 65-year-old Chinese man with chronic systemic inflammation, who presented with nephrotic syndrome and renal insufficiency, along with elevated serum anti-glomerular basement membrane (GBM) antibody titers, yet lacked the typical clinical features of rapidly progressive glomerulonephritis (GN). Renal biopsy demonstrated AA amyloid deposition in the glomerular mesangium, crescent formation in 33% of glomeruli, and patchy immunoglobulin G (IgG) staining. Persistent inflammation, mediated by pathways involving interleukin-1 (IL-1), interleukin-6 (IL-6), and tumor necrosis factor-α (TNF-α), is considered to be associated with the expression of serum amyloid A (SAA) and subsequent AA amyloidogenesis. Furthermore, we hypothesize that persistent inflammatory activity may be a contributory factor in the exposure of cryptic GBM antigens, thereby triggering the production of anti-GBM antibodies. In summary, we report a rare case of renal AA amyloidosis with crescent formation and elevated serum anti-GBM antibody titers in a patient with chronic systemic inflammation. However, the pathogenesis of crescent formation in this patient remains unclear and requires further investigation.
SN  - 1664-3224
ER  -