Diabetic kidney disease and immune modulation

- Inflammation is involved in the development and progression of DN.
- Macrophage depletion studies demonstrate a causal role in DN.
- Adoptive transfer of M2 macrophages or Tregs attenuates DN.
- Urinary MCP-1 correlates with albuminuria, tubular injury and progression of DN.
- Therapies targeting renal inflammation are undergoing clinical trials in DN.

Immune modulation is now known to contribute to the development of glomerulosclerosis, tubulointerstitial fibrosis and end-stage renal disease in a large number of kidney diseases. Similarly, diabetic nephropathy is increasingly considered an inflammatory disease, with immune modulation being involved in both the development and progression of the disease. Infiltration of immune cells including macrophages, T cells, B cells and mast cells into the kidney has been reported. A number of pro-inflammatory cytokines and chemokines also play a major role in pathogenesis of diabetic nephropathy. Consequently, a variety of therapeutic strategies involving modulation of the immune response are currently being investigated in diabetic kidney disease.