Photo of David H. Ellison, M.D.

David H. Ellison M.D.

  •      (503) 494-3442
    • Professor of Physiology and Pharmacology School of Medicine
    • Professor of Medicine, Division of Nephrology and Hypertension School of Medicine
    • Director Oregon Clinical and Translational Research Institute
    • Associate Vice President for Clinical and Translational Research OHSU Research & Innovation
    • Program in Molecular and Cellular Biosciences School of Medicine

David H. Ellison, M.D. is a professor of medicine and physiology and pharmacology, director of the Oregon Clinical and Translational Research Institute and associate vice president for Clinical and Translational Research at OHSU. 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. He is the 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 study section for NIH. He also was previously a standing member of the Renal Merit Review Study Section for the Department of Veterans Affairs.

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.

Dr. Ellison is also a practicing nephrologist and a dedicated teacher and mentor to medical students, residents, nephrology fellows and post-doctoral scientists.

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Areas of interest

  • Translational medicine
  • Nephrology

Education

  • B.S., Stanford University, Stanford California 1974
  • M.D., Rush Medical College, Chicago Illinois 1978
  • Residency:

    • Internal medicine - University of Oregon Health Sciences Center (Oregon Health & Science University), 1981
  • Fellowship:

    • Nephrology research - Oregon Health Sciences University (Oregon Health & Science University), 1982
  • Certifications:

    • American Board of Internal Medicine - internal medicine

Memberships and associations

  • Fellow of the American Heart Association

Publications

  • "Effects of calcium infusion on blood pressure in hypertensive and normotensive humans" Hypertension  1986
  • "Renal mineralocorticoid receptor and electrolyte homeostasis" American Journal of Physiology - Renal Fluid and Electrolyte Physiology  2015
  • "Diuretic Use in Edema and the Problem of Resistance"   2008
  • "WNK kinases and renal sodium transport in health and disease" Hypertension March 2008
  • "Evaluating hyponatremia" JAMA - Journal of the American Medical Association March 24 2015
  • "Rabbit distal convoluted tubule coexpresses NaCl cotransporter and 11β- hydroxysteroid dehydrogenase II mRNA" Kidney International  1998
  • "Chloride-dependent potassium secretion in early and late renal distal tubules" American Journal of Physiology - Renal Fluid and Electrolyte Physiology  1987
  • "Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter" Nature Medicine June 22 2015
  • "The physiologic basis of diuretic synergism" Annals of Internal Medicine May 15 1991
  • "Disorders of sodium and water." American Journal of Kidney Diseases  2005
  • "A quest - Halting the progression of autosomal dominant polycystic kidney disease" New England Journal of Medicine December 11 2014
  • "Stimulation of distal potassium secretion by low lumen chloride in the presence of barium." American Journal of Physiology - Renal Fluid and Electrolyte Physiology May 1985
  • "Hyperkalemia in elderly patients receiving standard doses of trimethoprim- sulfamethoxazole [1]" Annals of Internal Medicine  1994
  • "An Integrated View of Potassium Homeostasis" New England Journal of Medicine October 29 2015
  • "Distal convoluted tubule" Clinical Journal of the American Society of Nephrology  2014
  • "Bardoxolone methyl in type 2 diabetes and advanced chronic kidney disease" New England Journal of Medicine  2014
  • "SORLA/SORL1 functionally interacts with SPAK to control renal activation of Na+-K+-Cl- cotransporter 2" Molecular and Cellular Biology June 2010
  • "SPAK differentially mediates vasopressin effects on sodium cotransporters" Journal of the American Society of Nephrology : JASN February 28 2013
  • "Renal nerves, WNK4, glucocorticoids, and salt transport" Cell Metabolism June 8 2011
  • "Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride" Cell Metabolism January 6 2015
  • "Adrenal steroids stimulate thiazide-sensitive NaCl transport by rat renal distal tubules" American Journal of Physiology - Renal Fluid and Electrolyte Physiology  1996
  • "Gitelman's variant of Bartter's syndrome, inherited hypokalaemic alkalosis, is caused by mutations in the thiazide-sensitive Na-Cl cotransporter" Nature Genetics January 1996
  • "The effect of WNK4 on the Na+-Cl- cotransporter is modulated by intracellular chloride" Journal of the American Society of Nephrology : JASN August 1 2015
  • "Overexpression of the sodium chloride cotransporter is not sufficient to cause familial hyperkalemic hypertension" Hypertension November 2011
  • "Sympathetic stimulation of thiazide-sensitive sodium chloride cotransport in the generation of salt-sensitive hypertension" Hypertension  2014
  • "11β-hydroxysteroid dehydrogenase, mineralocorticoid receptor, and thiazide-sensitive Na-Cl cotransporter expression by distal tubules" Journal of the American Society of Nephrology : JASN August 1998
  • "Management of the Patient with Congestive Heart Failure"   2012
  • "Parathyroid hormone-induced hypotension" Journal of Investigative Medicine  1982
  • "Expression of the thiazide-sensitive Na-Cl cotransporter by rabbit distal convoluted tubule cells" Journal of Clinical Investigation  1995
  • "Training the next generation’s nephrology workforce" Clinical Journal of the American Society of Nephrology  2014

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