Kidney Models

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).

How can we support your program?

Readouts include in-life blood creatinine, proteinuria, pharmacokinetic and/or pharmacodynamic (PK/PD) blood collections and blood urea nitrogen (BUN) readings.

Study Endpoints

  • PK/PD blood collections
  • BUN
  • Blood creatinine analysis
  • Proteinuria
  • Clinical observations
  • Histopathological evaluation

Validation Data

Flow cytometry of kidney immune infiltrates of mice with NTS nephritis

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.

IgG, IgG1, IgG2b and IgG2c levels in serum

Figure 6: Sera from mice with NTS nephritis were tested for mouse anti-sheep IgG in an end-point titre ELISA. Rapamycin administration causes a decrease in serum total IgG and serum IgG1, IgG2b, and IgG2c subclasses. Levels pre-disease induction were negligible.