Prof A Richard Kitching
Department of Medicine - Monash Medical Centre
+61 3 9594 5520
We do not have a good understanding of how different forms of glomerulonephritis occur. Drugs that are current standard of care have significant toxic effects - without a better understanding of how disease occurs it will be difficult to rationally apply or develop new treatments. Prof Kitching's research aims to help understand the pathogenesis of immune renal disease. He has made important contributions to our understanding of how leukocytes mediate kidney disease in several areas.
- How T helper cells direct nephritogenic immune responses.
- Autoreactive CD4+ cells mediate injury in antineutrophil cytoplasmic antibody (ANCA)-associated vasculitis.
- T cell epitopes in autoimmune renal dsiease
- The unique biology of glomerular leukocyte recruitment and behaviour revealed by intravital and multiphoton microscopy (with Prof Michael Hickey)
- Leukocytes in acute kidney injury
Disease Models1) Our group uses a variety of models of murine glomerulonephritis, some of which are unique to our group.
These include autoimmune and non-autoimmune models, and models mediated by humoral
and cellular effectors.
We model all major types of rapidly progressive glomerulonephritis: anti-glomerular basement membrane disease, lupus nephritis and ANCA-associated vasculitis
2) We study acute kidney injury using murine models of cisplatin-induced acute kidney injury and unilateral and bilateral ischemia reperfusion injury
3) Although not currently a major research focus, renal fibrosis using murine unilateral ureteric obstruction as been used in the recent past.
Genetically Modified Organisms1) Mice geneticaly deficient in a number of different elements of the immune system
2) HLA transgenic mice
3) TCR transgenic mice specific for myeloperoxidase