AKI
Anti-GBM glomerulonephritis
Antibody-mediated glomerular injury with crescent formation, proteinuria and rapidly declining kidney function.
Background and rationale
Administration of anti-glomerular basement membrane serum triggers complement activation, leukocyte recruitment and podocyte injury, producing a rapidly progressive glomerulonephritis. The model is well suited for anti-inflammatory and complement-targeted therapeutics, and for immune cell profiling of glomerular disease.
Typical study design
- Optional pre-immunisation to accelerate the autologous phase
- Dose-ranging of nephritogenic serum to reach the target level of proteinuria
- Metabolic cage or spot urine collection for albuminuria kinetics
- Terminal glomerular isolation available for transcriptomics
Readouts
- Urinary albumin-creatinine ratio and plasma creatinine, BUN, cystatin C
- Glomerular crescent, necrosis and sclerosis scoring on PAS with AI-assisted assessment
- Immunohistochemistry and multiplex immunofluorescence (IgG deposition, C3, macrophages, T cells)
- Electron microscopy and Magnephy super-resolved 3D imaging of the filtration barrier
- Luminex and Olink inflammatory profiling
Interested in this model?
We will walk you through severity levels, group sizes, dosing windows and endpoints, and propose a design matched to your compound.