Dr. Farkash received his MD PhD degree from the University of Pennsylvania Medical School in 2007.  He completed residency in Anatomic and Clinical Pathology at the Massachusetts General Hospital in 2011, where he also served as Chief Resident of Clinical Pathology.  In 2013, he completed a joint research and clinical fellowship in Renal and Transplantation Pathology in the laboratory of Dr. Robert Colvin at MGH, also working closely with the Transplantation Biology Research Center.  During his fellowship training, Dr. Farkash studied the role of complement in the diagnosis of antibody mediated rejection in humans and the morphologic features of graft acceptance in mice.  He has experience in tissue diagnosis in large and small experimental animal models.  Dr. Farkash is certified in Anatomic and Clinical Pathology by the American Board of Pathology.

 Dr. Farkash’s laboratory studies factors that affect long term graft survival and patient outcomes after transplantation.  One complication of kidney transplants that can cause either acute or chonic graft loss is antibody mediated rejection, in which the immune system generates antibodies that recognize the donor kidney, cause direct or indirect endothelial injury, and recruit inflammation.  The gold standard test for antibody mediated rejection detects deposits of the complement fragment C4d in the capillaries of a renal biopsy.  While specific, this test lacks sensitivity.  Are there alternative biomarkers or diagnostic algorithms that can be performed on existing renal biopsy tissue that can supplement or replace the C4d assay? Another area of study is the relationship between BK polyomavirus and urinary tract cancers.  BK is a ubiquitous pathogen that causes few, if any, symptoms in immunocompetent people, but can reactivate in kidney and bone marrow transplant recipients and cause severe kidney and bladder infections.  BK is closely related to other polyomaviruses such as the known oncovirus Merkel Cell Polyomavirus, the major cause of Merkel Cell Carcinoma.  Although BK polyomavirus is not known to cause cancer in the general population, renal transplant recipients might susceptible to developing BK-driven cancers.  We have detected diffuse expression of BK antigens in a minority of kidney and bladder cancers that arise after kidney transplantation.  Is BK an oncovirus, and, if so, what are the molecular pathways and clinical factors that drive oncogenesis in these tumors?