Diabetic nephropathy (DN) occurs in approximately 40% of the type 2 diabetes global population. It is also the single most common cause of end-stage renal failure worldwide. Early alterations in diabetic nephropathy include glomerular hyperfiltration, glomerular and tubular epithelial hypertrophy, and the development of microalbuminuria. In humans the typical early clinical presentation of diabetic nephropathy generally appears 5 to 15 years after the patient has been diagnosed with diabetes mellitus. It has always been a challenge to find reliable, robust and cost-effective animal disease models with which to explore the pathophysiological pathways and advance the knowledge on existing and discoverable pharmacological interventions for the prevention and alleviation of diabetic nephropathy.
Anti-glomerular basement membrane (GBM) glomerulonephritis accounts for 20% of all cases of rapidly progressive glomerulonephritis (GN) in the adult human population. End-stage renal disease develops in 40-70% of patients who have nephritis mediated by anti-GBM antibodies.? Recent investigations have proposed the concept that the immune system plays a role in the mechanisms of diabetic nephropathy.? Several components of the immune system including cytokines and resident chemokines, macrophage recruitment, T lymphocytes, and immune complex deposition that have been implicated in other glomerular diseases are now explored for their association with diabetic nephropathy.? Furthermore, anti-GBM nephritis shares several common downstream molecular mechanisms and targets with lupus nephritis making the anti-GBM nephritis animal model another relevant and effective model for lupus nephritis disease translation.