Nephritis is an immune complex-mediated autoimmune disease characterised by inflammation of the kidneys that develops through a mechanism that is not completely understood. Nephritis is clinically diagnosed through urine tests, blood tests, and kidney biopsies. Charles River has characterised a translational murine model of nephritis obtained by administration of nephrotoxic antiserum (NTS), preceded by administration of sheep immunoglobulin (IgG) in Complete Freund’s Adjuvant (CFA).
Readouts include in-life blood creatinine, proteinuria, pharmacokinetic and/or pharmacodynamic (PK/PD) blood collections and blood urea nitrogen (BUN) readings.
- PK/PD blood collections
- Blood creatinine analysis
- Clinical observations
- Histopathological evaluation
Figure 1: Flow cytometry of kidney immune infiltrates of mice with NTS nephritis is shown. NTS nephritis is characterised by an influx of CD4+ T cells in kidneys. Treatment with rapamycin reduces the levels of CD4+ T cells. Data is presented as a percentage of viable, single, and CD45+ cells.