David H. Ellison, M.D. is Professor of Medicine and Physiology & Pharmacology, Director of the Oregon Clinical and Translational Research Institute, and Associate Vice President for Clinical and Translational Research at Oregon Health & Science University. Prior to assuming these roles, he was Head of the Division of Nephrology and Hypertension for 13 years. He is also a Staff Physician at the Portland VA Medical Center. Dr. Ellison is board certified in Internal Medicine and Nephrology, past Chair of the Subspecialty Board in Nephrology for the American Board of Internal Medicine, and past Chair of the American Heart Association’s Council on the Kidney in Cardiovascular Disease. He was Program Chair for the American Society of Nephrology’s Kidney Week in 2010, and was recently elected by its members to its leadership Council. He is an elected member of the Association of American Physicians and is past chair of the Kidney Molecular Biology and Genitourinary Organ Development (KMBD) study section for NIH.
Dr. Ellison’s research centers on effects of diet on blood pressure, on mechanisms of salt transport by the kidney, on the genetic basis of human hypertension, and on diuretic treatment of edema. A long-term focus of his research is the thiazide-sensitive NaCl cotransporter (NCC). His early studies helped define the distal convoluted tubule of the kidney and how mutations of NCC can lead to Gitelman syndrome. Dr. Ellison showed that the antibiotic trimethoprim causes hyperkalemia in humans by disrupting transport along the distal convoluted tubule and showed that chronic treatment with high doses of loop diuretics causes hypertrophy of the distal nephron, work that is now being translated to help improve diuretic treatment of edema. Dr. Ellison has been a leader in defining how mutations in a novel kinase pathway cause Familial Hyperkalemic Hypertension by altering distal salt transport and has defined how a high potassium diet reduces kidney salt transport. Finally, his group has demonstrated that the immunosuppressive drug tacrolimus causes hyperkalemia and hypertension by activating the NCC; this work has been translated to an ongoing clinical trial. All of his work melds basic and clinical approaches and has been published in top journals including Nature Medicine, the Journal of Clinical Investigation, Cell Metabolism, and the Journal of the American Society of Nephrology.
