Seminar: Dr. David Ellison

The distal convoluted tubule is the kidney's potassium homeostat

Date:
13 May 2014 00:00 hrs.
Location:
Figdor Lecture Theatre, 8th floor RIMLS Building, Geert Grooteplein 26-28, route 289
Title:
The distal convoluted tubule is the kidney's potassium homeostat
Speaker(s):

Dr. David Ellison, Oregon Health & Science University, Portland, USA

Host(s):

Prof. Peter Deen, Department of Physiology, Radboudumc

13-05-2014 00:00:00Europe/AmsterdamThe distal convoluted tubule is the kidney's potassium homeostat Figdor Lecture Theatre, 8th floor RIMLS Building, Geert Grooteplein 26-28, route 289Rimlsrimls@radboudumc.nl

Remarks / more information:

Ellison , DavidDavid H. Ellison, M.D. is Professor of Medicine and Physiology & Pharmacology and Associate Director of the Oregon Clinical and Translational Research Institute at Oregon Health & Science University. He was Head of the Division of Nephrology and Hypertension. He was Chair of the American Heart Association's Council on the Kidney in Cardiovascular Disease and Program Chair for the ASN's Kidney Week in 2010. Dr. Ellison's research is translational and centers on mechanisms of salt transport by the kidney, on the genetic basis of human blood pressure variation, and on diuretic treatment of edema. His work has been translational, since before the term was coined.  A long-term focus of his research is the protein target of thiazide diuretics, the thiazide-sensitive Na-Cl transporter (NCC). He has been a leader in defining a novel kinase pathway in the kidney that, when mutated, causes familial hyperkalemic hypertension and his group has demonstrated that the immunosuppressive drug tacrolimus causes hyperkalemia and hypertension by activating the NCC, knowledge which is now being used to design safer drugs to treat organ transplant recipients. 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 Hypertension.

Key Publications:

  • Ubiquitylation and the pathogenesis of hypertension. J Clin Invest 123: 546-548
  • The calcineurin inhibitor tacrolimus activates the renal sodium chloride cotransporter to cause hyper-tension. Nat Med 17: 1304-1309
  • A SPAK isoform switch modulates renal salt transport and blood pressure. Cell Metab 14: 352-364
  • Thiazide effects and adverse effects: insights from molecular genetics. Hypertension 54: 196-202



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