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.Read more
Areas of interest
- Translational medicine
- M.D., Rush Medical College, Chicago Illinois 1978
- B.S., Stanford University, Stanford California 1974
- Internal medicine - University of Oregon Health Sciences Center (Oregon Health & Science University), 1981
- Nephrology research - Oregon Health Sciences University (Oregon Health & Science University), 1982
- American Board of Internal Medicine - internal medicine
Memberships and associations
- Fellow of the American Heart Association
- "Compensatory distal reabsorption drives diuretic resistance in human heart failure." Journal of the American Society of Nephrology In: , Vol. 28, No. 11, 01.11.2017, p. 3414-3424.
- "Nephron remodeling underlies hyperkalemia in familial hyperkalemic hypertension." Journal of the American Society of Nephrology In: , Vol. 28, No. 9, 01.09.2017, p. 2555-2557.
- "Potassium sensing by renal distal tubules requires Kir4.1." Journal of the American Society of Nephrology In: , Vol. 28, No. 6, 01.06.2017, p. 1814-1825.
- "Calcineurin inhibitor cyclosporine A activates renal NA-K-CL cotransporters via local and systemic mechanisms." American Journal of Physiology - Renal Physiology In: , Vol. 312, No. 3, 01.03.2017, p. F489-F501.
- "WNK Kinase Signaling in Ion Homeostasis and Human Disease." Cell Metabolism In: , Vol. 25, No. 2, 07.02.2017, p. 285-299.
- "Gitelman syndrome : consensus and guidance from a Kidney Disease: Improving Global Outcomes (KDIGO) Controversies Conference." Kidney International In: , Vol. 91, No. 1, 01.01.2017, p. 24-33.
- "Renal tubular resistance is the primary driver for loop diuretic resistance in acute heart failure." European Journal of Heart Failure In: , 2017.
- "Anaesthesia recommendations for patients suffering from Liddle's syndrome." Anasthesiologie und Intensivmedizin In: , Vol. 57, No. 9, 01.09.2016, p. S500-S505.
- "Renal deletion of 12 kDa FK506-binding protein attenuates tacrolimus-induced hypertension." Journal of the American Society of Nephrology In: , Vol. 27, No. 5, 01.05.2016, p. 1456-1464.
- "Potassium and its discontents : New insight, new treatments." Journal of the American Society of Nephrology In: , Vol. 27, No. 4, 01.04.2016.
- "Diuretic Resistance." American Journal of Kidney Diseases In: , 23.02.2016.
- "Regulation of Renal Electrolyte Transport by WNK and SPAK-OSR1 Kinases." Annual Review of Physiology In: , Vol. 78, 10.02.2016, p. 367-389.
- "Degradation by Cullin 3 and effect on WNK kinases suggest a role of KLHL2 in the pathogenesis of Familial Hyperkalemic Hypertension." Biochemical and Biophysical Research Communications In: , Vol. 469, No. 1, 01.01.2016, p. 44-48.
- "Calcineurin and Sorting-Related Receptor with A-Type Repeats Interact to Regulate the Renal Na-K-2Cl Cotransporter." Journal of the American Society of Nephrology In: , Vol. 27, No. 1, 01.01.2016, p. 107-119.
- "Direct and indirect mineralocorticoid effects determine distal salt transport." Journal of the American Society of Nephrology In: , Vol. 27, No. 8, 2016, p. 2436-2445.
- "Outstanding translational science at American Society of Hypertension 2015." Journal of the American Society of Hypertension In: , Vol. 9, No. 11, 01.11.2015, p. 828-830.
- "An Integrated View of Potassium Homeostasis." The New England journal of medicine In: , Vol. 373, No. 18, 29.10.2015, p. 1786.
- "An integrated view of potassium homeostasis." New England Journal of Medicine In: , Vol. 373, No. 18, 29.10.2015, p. 1786.
- "Unique chloride-sensing properties of WNK4 permit the distal nephron to modulate potassium homeostasis." Kidney International In: , 30.09.2015.
- "The effect of WNK4 on the Na-Cl cotransporter is modulated by intracellular chloride." Journal of the American Society of Nephrology In: , Vol. 26, No. 8, 01.08.2015, p. 1781-1786.
- "Interleukin 18 function in atherosclerosis is mediated by the interleukin 18 receptor and the Na-Cl co-transporter." Nature Medicine In: , Vol. 21, No. 7, 22.06.2015, p. 820-826.
- "Evaluating hyponatremia." JAMA - Journal of the American Medical Association In: , Vol. 313, No. 12, 24.03.2015, p. 1260-1261.
- "Potassium modulates electrolyte balance and blood pressure through effects on distal cell voltage and chloride." Cell Metabolism In: , Vol. 21, No. 1, 06.01.2015, p. 39-50.
- "Distal convoluted tubule." Comprehensive Physiology In: , Vol. 5, No. 1, 01.01.2015, p. 45-98.
- "Renal mineralocorticoid receptor and electrolyte homeostasis." American Journal of Physiology - Regulatory Integrative and Comparative Physiology In: , Vol. 309, No. 9, 2015, p. R1068-R1070.
- "Why Your Mother Was Right : How Potassium Intake Reduces Blood Pressure." Transactions of the American Clinical and Climatological Association In: , Vol. 126, 2015, p. 46-55.
- "A quest - Halting the progression of autosomal dominant polycystic kidney disease." New England Journal of Medicine In: , Vol. 371, No. 24, 11.12.2014, p. 2329-2331.
- "Hyperkalemic hypertension-associated cullin 3 promotes WNK signaling by degrading KLHL3." Journal of Clinical Investigation In: , Vol. 124, No. 11, 03.11.2014, p. 4723-4736.
- "WNK-SPAK-NCC cascade revisited : WNK1 stimulates the activity of the Na-Cl cotransporter via SPAK, an effect antagonized by WNK4." Hypertension In: , Vol. 64, No. 5, 01.11.2014, p. 1047-1053.
- "Protein phosphatase 1 inhibitor-1 deficiency reduces phosphorylation of renal NaCl cotransporter and causes arterial hypotension." Journal of the American Society of Nephrology In: , Vol. 25, No. 3, 03.2014, p. 511-522.