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About Professor David Harris

David's passion for research is driven by the goal of defining novel therapies to slow and even reverse progressive chronic kidney disease.

Professor David Harris is a research leader in the field of progressive chronic kidney disease, internationally recognized especially for his contributions to understanding the role of tubulointerstitial injury in progressive disease.

David Harris is Associate Dean of the Western Clinical School, University of Sydney and Nephrologist in Sydney West Area Health Service.  For the past 2 decades his clinical research has focussed on dialysis in progressive kidney disease and his laboratory research on tubulointerstitial injury in models of chronic renal disease.  During that time he has made important contributions to knowledge in this area, including in regards to tubular hypermetabolism and oxidant damage, proteinuric tubular injury and more recently the pathogenic role of interstitial inflammatory cells and the therapeutic effect of regulatory cells and DNA vaccination.

He has published more than 160 articles, and about half of these have been specifically related to the role of the tubulointerstitium in progression of chronic kidney disease.  Almost half of his more than 80 invited national and international presentations have focussed specifically on his research into tubulointerstitial injury.  He has supervised a number of successful PhD and MSc candidates in this area and in conjunction with other senior members of his laboratory is currently supervising another 6 PhD students.

In 1998 he was awarded the TJ Neale prize of the Australian New Zealand Society of Nephrology for “Outstanding contributions to nephrological science” based on his contributions to the understanding of tubulointerstitial injury in chronic renal disease.  He was Chairman of the Scientific Programme Committee of the International Congress of Nephrology held in Sydney in 1997, and the World Congress of Nephrology held in Singapore in 2005.  He is Chair of the Medical and Scientific Advisory Committee of Kidney Health Australia and a Director of Kidney Health Australia.  He is Past-President of the Australian and New Zealand Society of Nephrology, Editor-in-Chief of the journal Nephrology and on the editorial board of Nephrology, Dialysis, Transplantation.  He is Chairman of the Advisory Committee of Australasian Clinical Trials Network and Executive Councillor of the International and Asian-Pacific Societies of Nephrology.  He has been invited to deliver the Ross Bailey lecture on chronic kidney disease at the 2008 Asian Pacific Congress of Nephrology.

Selected publications

  • Wang Y, Wang Y-P, Zheng G, Ouyang L, Lee VWE, Mahajan D, Chang DHH, Wang Y-M, Alexander SI, Harris DCH.  Amelioration of experimental chronic inflammatory renal disease using macrophages programmed ex vivo. Kidney Int 2007 (accepted 27 February 2007).(First description of the use of regulatory macrophages, with their phenotypes determined by cytokines in vitro, as a treatment for kidney disease).
  • Wang YM, Zhang GY, Wang Yiping, Hu M, Wu H, Watson D, Hori S, Alexander IE, Harris DCH, Alexander S. Foxp3 T regulatory cells protect against ADR.  J Am Soc Nephrol 2006 ; 17: 697-706.(First report of lymphocyte transduced with regulatory determinant as treatment for kidney disease).
  • Wu H, Wang Y-P, Tay YC, Zheng G, Zhang C, Alexander SI, Harris DCH.  DNA vaccination against MCP-1 RANTES is protective in chronic proteinuric renal disease. Kidney Int. 2005; 67: 2178-2186.(First description of use of DNA vaccination to treat chronic kidney disease).
  • Zheng G, Wang Y, Xiang S-H, Tay Y-C, Wu H, Watson, Coombes J, Rangan GK, Alexander SI and Harris DCH.  DNA Vaccination with CCL2 DNA Modified by the Addition of an Adjuvant Epitope Protects against “Nonimmune” Toxic Renal Injury.  J Am Soc Nephrol 2005; 17: 465-474.(Demonstrates the increased efficacy by modification of DNA vaccine against chemokine).
  • Kairaitis L, Wang Y-P, Tay Y-C, Wang Y, Harris DCH.  Blockade of CD40-CD40 ligand protects renal injury in chronic proteinuric renal disease. Kidney Int 2003; 64: 1265-1272.(First demonstration of potential importance of costimulatory blockade in interstitial inflammation of chronic kidney disease).
  • Wang Y-P, Wang Y, Feng X, Rangan GK, Harris DCH.  Depletion of  CD4+ T cells aggravates glomerular and interstitial injury in murine adriamycin nephropathy.  Kid Int 2001; 59: 975-984.(First demonstration of protective rather than damaging role of particular leucocyte subtypes in interstitium in non-immune chronic kidney disease).
  • Wang Y-P, Rangan GK, Goodwin B, Tay Y-C, Wang Y, Harris DCH. Lipopolysaccharide-induced MCP-1 gene expression in rat tubular epithelial cells is NFkB dependent.  Kid Int 2000; 57: 2011-2022.
  • Wang Y, Chen J, Chen L, Tay Y-C, Rangan GK, Harris DCH.  Induction of monocyte chemoattractant protein-1 in proximal tubule cells by urinary protein. J Am Soc Nephrol 1997; 8: 1537-1545.(First direct demonstration of chemokine production by tubular cells exposed to urinary protein).
  • Harris DCH, Chan L, Schrier RW. Remnant kidney hypermetabolism and progression of chronic renal failure.  Am J Physiol 1988; 254: F267-F276.(First proposal of tubular hypermetabolism as a mechanism of progression of chronic kidney disease). 
  • Harris DCH, Hammond WS, Burke TJ, Schrier RW. Verapamil protects against progression of chronic renal failure.  Kidney Int 1987; 31: 41-46.(Frequently cited paper (200 times) demonstrating first experimental evidence for a blood pressure independent effect of calcium channel blockers in chronic kidney disease).