Autoimmune Nephropathy

Autoimmune Nephropathy

Autoimmune Nephropathy refers to a group of kidney diseases caused by the body’s immune system mistakenly attacking the kidneys. These conditions can lead to inflammation and damage to the structures of the kidneys, impairing their function.                            

Model:
B6-hBAFF LN model

Features:

Lupus nephritis

B cell activation

Complement pathway

(clasiccall/alternative)

lgA/lgG/C3 deposition

Model:BSA+CCI4+LPS induced lgAN model

Features:

lgAN model

lgA / lgC deposition

Complement pathway

(lectin/alternative)

Model:
Humanized C3 Mouse

Features:

Accelerated C3

Glomerulopathy

Alternative complement

pathway

C3 deposition

Model:
CDH-KO mouse induced by NTS

Features:

C3 Glomerulopathy

Complement pathway

Model:
CBSA induced MN model

Features:

MN model

lgG deposition

Complement pathway

classical

BSA+CCl4+LPS induced IgA nephropathy mouse model 

This model closely mimics the key pathological features of human IgA nephropathy through a combination of BSA-induced immune complex formation, CCl₄-induced hepatic injury, and LPS-stimulated immune activation. It reliably induces mesangial IgA deposition, glomerular inflammation, elevated serum IgA levels, and proteinuria. This evidenced by increased mALB/CREA and UTP/CREA ratios which serve as hallmark indicators of renal damage. This model offers a robust and translational platform for investigating IgA nephropathy mechanisms and assessing potential immunomodulatory therapies.

Figure shows IgA deposition at Kidney after 4 weeks of LNP023 or Astrasentan treatment.