CKD
Adenine-induced nephropathy
Diet-induced crystal nephropathy producing progressive CKD with mineral and bone disorder.
Background and rationale
Dietary adenine forms 2,8-dihydroxyadenine crystals in the tubules, causing tubulointerstitial inflammation and fibrosis with a graded loss of kidney function. The model reproduces the biochemical hallmarks of CKD, including hyperphosphataemia, secondary hyperparathyroidism and elevated FGF23, and is ideal for therapies targeting fibrosis or CKD-associated mineral bone disorder.
Typical study design
- Adenine dose and diet phosphate content selected for the target severity
- Stepwise or constant dosing schedules, with washout options
- Body weight, food intake and serial biochemistry monitoring
- Treatment start after CKD is established to test intervention rather than prevention
Readouts
- Plasma creatinine, BUN, cystatin C, phosphate, calcium, PTH and FGF23
- Urinary albumin-creatinine ratio and tubular injury markers
- Sirius red and PAS histology with AI-assisted fibrosis quantification
- Immunohistochemistry, multiplex immunofluorescence and RNAscope in situ hybridization
- Bulk and single nuclei RNA sequencing, spatial transcriptomics
- microCT for bone and vascular calcification
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.