AKI
Cisplatin-induced AKI
Nephrotoxic tubular injury model, available as single high-dose or repeated low-dose protocols.
Background and rationale
Cisplatin accumulates in proximal tubular cells and causes DNA damage, mitochondrial dysfunction and apoptosis. A single high dose gives severe acute injury within 72 hours, whereas repeated low-dose administration reproduces the inflammation and fibrosis of chemotherapy-associated chronic kidney disease.
Typical study design
- Single high-dose or weekly repeated low-dose protocol
- Body weight-adjusted dosing with hydration support
- Vehicle and nephroprotection arms with blinded histology
- Optional tumour-bearing designs to confirm preserved anti-tumour efficacy
Readouts
- Plasma creatinine, BUN and cystatin C
- Urinary NGAL, Kim-1 and albumin-creatinine ratio
- Histology (HE, PAS, Sirius red) with AI-assisted tubular injury and fibrosis quantification
- Apoptosis and DNA damage immunohistochemistry
- Bulk and single nuclei RNA sequencing
- Resazurin tubular function assay
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.