Paul A. WellingNorth American Coordinator
Joseph S. and Esther Handler Professor
Johns Hopkins Medical School
Department of Medicine and Physiology
720 Rutland Ave Ross 1167B
Baltimore, MD 21287, USA
F: +1 410 706 8341
Paul A. Welling, M.D. is the Joseph S. and Esther Handler Professor of Medicine, at Johns Hopkins University School of Medicine and the North American Coordinator of the Foundation Leducq Global Network of Excellence to understand the relationship between dietary potassium and blood pressure. He received his medical degree from the University of Kansas Medical School and completed his post-doctoral training at Yale University School of Medicine. Dr. Welling is an authority on the molecular bases of potassium and sodium balance, electrolyte disorders, and hypertension.
Dr. Welling’s laboratory is recognized for elucidating how ion transport molecules in the kidney control salt balance and discovering how these molecules go awry in disorders of electrolyte balance and hypertension. A major focus of Dr. Welling’s current research program seeks to understand how the kidney senses dietary potassium to regulate potassium, salt balance, and prevent high blood pressure. His research, which spans from gene discovery to animal studies to clinical-translational investigation, has been continuously funded by the National Institutes of Health (25 years) since his appointment on the faculty at Maryland.
Dr. Welling has served in many leadership and scientific advisory roles. Currently, he is a chair of the NIH study section, Kidney Molecular Biology, and Development. He is chair of the American Physiological Society Finance Committee. He is a Fellow of the American Heart Association (AHA) and is an elected Fellow of the American Association for the Advancement of Science. In his spare time, he enjoys cooking, gardening and traveling.
- Rapid Development of Vasopressin Resistance in Dietary Potassium Deficiency
Lama Al-Qusairi*, P. Richard Grimm*, Ava M. Zapf, and Paul A. Welling. journals.physiology.org/journal/ajprenal at Johns Hopkins Univ Serials Dept Electronic (162.129.250.015) on March 28, 2021. [Article]
- Mutation affecting the conserved acidic WNK1 motif causes inherited hyperkalemic hyperchloremic acidosis.
J Clin Invest. 2020 Dec 1;130(12):6379-6394. doi: 10.1172/JCI94171. [Article]
- Distal convoluted tubule sexual dimorphism revealed by advanced 3D imaging.
Ebrahim Tahaei, Richard Coleman, Turgay Saritas, David H. Ellison, and Paul A Welling. AJP Renal. 2020 Sep 14;doi.org/10.1152/ajprenal.00441.2020 Online ahead of print. [Article]
- The single-cell transcriptomic landscape of early human diabetic nephropathy
Wilson PC, Wu H, Kirita Y, Uchimura K, Ledru N, Rennke HG, Welling PA, Waikar SS, Humphreys BD. Proc Natl Acad Sci U S A. 2019 Sep 24;116(39):19619-19625. doi: 10.1073/pnas.1908706116. Epub 2019 Sep 10. PMID: 31506348 [Article]
- Optical Clearing in the Kidney Reveals Potassium-Mediated Tubule Remodeling.
Saritas T, Puelles VG, Su XT, McCormick JA, Welling PA, Ellison DH. Cell Rep. 2018 Dec 4;25(10):2668-2675.e3. doi: 10.1016/j.celrep.2018.11.021. PMID: 30517856 [Article]
- Mechanism of Hyperkalemia-Induced Metabolic Acidosis
Harris AN, Grimm PR, Lee HW, Delpire E, Fang L, Verlander JW, Welling PA, Weiner ID. J Am Soc Nephrol. 2018 May;29(5):1411-1425. doi: 10.1681/ASN.2017111163. Epub 2018 Feb 26. PMID: 29483157 [Article]
- Constitutively Active SPAK Causes Hyperkalemia by Activating NCC and Remodeling Distal Tubules
Grimm PR, Coleman R, Delpire E, Welling PA. J Am Soc Nephrol. 2017 Sep;28(9):2597-2606. doi: 10.1681/ASN.2016090948. Epub 2017 Apr 25. PMID: 28442491 [Article]
- A Common Signal Patch Drives AP-1 Protein-dependent Golgi Export of Inwardly Rectifying Potassium Channel
Li X, Ortega B, Kim B, Welling PA. J Biol Chem. 2016 Jul 15;291(29):14963-72. doi: 10.1074/jbc.M116.729822. Epub 2016 May 23. PMID: 27226616 [Article]
- Roles and Regulation of Renal K Channels
Welling PA.Annu Rev Physiol. 2016;78:415-35. doi: 10.1146/annurev-physiol-021115-105423. Epub 2015 Dec 11. PMID: 26654186 Review. [Article]
- Integrated compensatory network is activated in the absence of NCC phosphorylation
Grimm PR, Lazo-Fernandez Y, Delpire E, Wall SM, Dorsey SG, Weinman EJ, Coleman R, Wade JB, Welling PA. J Clin Invest. 2015 May;125(5):2136-50. doi: 10.1172/JCI78558. Epub 2015 Apr 20. PMID: 25893600 [Article]