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Bruns A. Watts, III, Ph.D.
Assistant Professor, Division of Nephrology

Bruns A. Watts, III, Ph.D.

Bruns A. Watts, III, Ph.D.
Assistant Professor
Division of Nephrology
Department of Internal Medicine

University of Texas Medical Branch
301 University Blvd.
Galveston, TX 77555-0562
Phone: 409.772.8616
Fax: 409.772.5451


Degree/Training Completed Year Name & Location
B.A. 1984 University of Dallas, Irving, TX
Ph.D. 1994 University of Texas Medical Branch
Department of Cellular Physiology & Molecular Biophysics, Galveston, TX
Postdoctoral 2000 University of Texas Medical Branch
Department of Internal Medicine,
Division of Nephrology, Galveston, TX


Dr. Watts' research focuses on the regulation of renal electrolyte and acid-base transport. His major areas of interest are the cellular and molecular mechanisms that regulate apical and basolateral membrane Na+/H+ exchangers and the functional interaction between these two transporters. Current projects examine the regulation of renal tubule intracellular signaling pathways by immune and inflammatory responses. Ongoing collaborative studies investigate therapeutic agents that prevent sepsis-induced renal dysfunction and seek to identify the cellular mechanisms that are responsible for the protective effects. In addition, Dr. Watts is interested in the effects of neurotrophins on renal transport and the cellular mechanisms by which neurotrophins regulate renal function.

Selected Publications

Good, D.W., T. George, and B.A. Watts, III. Basolateral membrane Na+/H+ exchange enhances HCO3- absorption in rat medullary thick ascending limb: Evidence for functional coupling between basolateral and apical membrane Na+/H+ exchangers. Proc. Natl. Acad. Sci. USA 92: 12525-12529,1995.

Watts, III, B.A., T. George, and D.W. Good. Nerve growth factor inhibits HCO3- absorption through inhibition of basolateral membrane Na+/H+ exchange. J. Biol. Chem. 274: 7841-7847, 1999.

Watts, III, B.A., T. George, and D.W. Good. The basolateral NHE1 Na+ /H+ exchanger regulates transepithelial HCO-3 absorption through actin cytoskeleton remodeling in renal thick ascending limb. J. Biol. Chem. 280: 11439-11447, 2005.

Good, D.W., T. George, and B.A. Watts, III. Nerve growth factor inhibits Na+/H+ exchange and HCO-3 absorption through parallel phosphatidylinositol 3-kinase-mTOR and ERK pathways in thick ascending limb. J Biol. Chem. 283: 26602-26611, 2008.

Good, D.W., T. George, and B.A. Watts, III. Lipopolysaccharide directly alters renal tubule transport through distinct TLR4-dependent pathways in basolateral and apical membranes. Am. J. Physiol. Renal Physiol. 297: F866-F874, 2009.

Good, D.W., T. George, and B.A. Watts, III. Toll-like receptor 2 mediates inhibition of HCO3- absorption by bacterial lipoprotein in medullary thick ascending limb. Am. J. Physiol. Renal Physiol. 299: F536-F544, 2010.

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»Curriculum Vitae

The department of internal medicine is developing evidence based clinical protocols which will be available in EPIC (as order sets) for use when admitting patients with these diagnoses. Their AIM is to standardize care and decrease length of stay and readmission rates.

Currently available protocols are:
  • CAP - Community Acquired Pneumonia Order set
  • Congestive Heart Failure (CHF)
  • Chronic Obstructive Pulmonary Disease (COPD)
  • Diabetic Ketoacidosis Adult, ICU
  • General Medicine Admission
  • Immunodeficiency Flow Panel
  • MICU/CCU Admission Order Set
  • Oral Analgesic Medications
  • Parenteral Opioids
  • Sepsis, Adult ICU
  • 111 - Stroke Alert
  • 112 - Stroke Activation
  • 300086 - Stroke Floor Admission
  • 3000000001 -  Stroke Critical care without tPA
  • 300088 Stroke - Transfer from Critical care to floor
  • 3004002 - Stroke Discharge

All protocols can be found in the EPIC order set section.

» For more information

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The department of Internal Medicine has a large role in the Meaningful Use Initiative. Our participation is key for the success of the initiative. Please visit the meaningful use website for important communication and updates from the Meaningful Use Initiative.

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