Primary Research Area: Molecular & Cell Biology
Secondary Research Area: Genetics, Genomics & Proteomics
Translational Research Area: Complement-based kidney diseases and the translational aspects involved through clinical and basic research
Dr. Christoph Licht accepted a position as Assistant Professor at the University of Toronto in 2006 and joined the Division of Nephrology at The Hospital for Sick Children as a staff physician and the SickKids Research Institute as an Associate Scientist. In addition, he was appointed Associate Member of the Institute of Medical Science Graduate Faculty at the University of Toronto.
Dr Licht’s research focuses on complement-mediated renal diseases such as atypical haemolytic-uremic syndrome (aHUS) and membranoproliferative glomerulonephritis (MPGN). The nature of his research is translational and includes clinical and basic research. He established an international registry as well as clinical tests allowing for a comprehensive genetic and biochemical work-up of patients with complement-mediated renal diseases. In addition, Dr Licht established a research program focusing on the interface of complement and coagulation in platelets in HUS.
In collaboration with Dr. Walter Kahr, a SickKids haematologist, he works on the morphological and functional characterization of the components of the complement system, especially complement Factor H (CFH), in platelets. These results may ultimately change our understanding of the pathophysiology of aHUS and may allow for the development of new treatment strategies not only for aHUS but also other, clot related diseases.
Dr. Licht is member of the “European Pediatric Research Group for HUS” and associate member of the “European Working Party for the Genetics of Complement-Mediated Diseases”.
"My research has translational character and is mainly focused on complement-mediated renal diseases, i.e. atypical haemolytic-uremic syndrome (aHUS) and membranoproliferative glomerulonephritis (MPGN).
We identified a novel mutation in the regulatory domain of complement Factor H (CFH) resulting in the loss of CFH co-factor activity causes MPGN type II (dense deposit disease, DDD) [Licht al, Kidney Int 2006].
We demonstrated that a defect in CFH related proteins 1 and 3 (CFHR1/3) results in aHUS [Zipfel et al, PLoS Genetics 2007].
We defined a new aHUS sub-group termed DEAP HUS (deficiency of CFHR proteins and CFH autoantibody positive), which is characterized by the presence of CFH autoantibodies in patients with CFHR1/3 deficiency [Jozsi and Licht et al, Blood 2008].
Furthermore, I am interested in chronic proteinuric kidney diseases (e.g. Alport syndrome)."
Read about his work in the media: "Toronto hospital brings new dialysis treatment to children" (March 2016)