AKI
Folic acid-induced AKI
Non-surgical crystal nephropathy model covering the full sequence from acute injury to established fibrosis.
Background and rationale
High-dose folic acid precipitates in the tubular lumen and injures proximal tubular epithelium, giving a reproducible acute injury that resolves incompletely and progresses to interstitial fibrosis. As no surgery is required, the model supports large group sizes and studies of the AKI-to-CKD transition.
Typical study design
- Single intraperitoneal injection with vehicle-matched controls
- Prevention and delayed-intervention dosing windows
- Body weight and food intake monitoring throughout
- Serial urine collection for injury and fibrosis biomarkers
Readouts
- Plasma creatinine, BUN and cystatin C
- Urinary NGAL, Kim-1 and albumin-creatinine ratio
- Sirius red and PAS histology with AI-assisted fibrosis scoring
- Immunohistochemistry for myofibroblasts and immune infiltration
- RNA sequencing and 10x spatial transcriptomics
- Transdermal GFR measurement
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.