Residency:  Internal Medicine, Oregon Health and Science University, Portland, OR 06/2020 - Present

Before beginning my studies at KU Medical Center, my love for basic research developed in the laboratories of Dr. David Ellison and Dr. Jim McCormick at Oregon Health and Science University (OHSU). My research projects concerned the regulation of salt excretion in the kidneys and the role of electroneutral ion transport in essential hypertension, or high blood pressure with no known cause. During my time at OHSU, I was exposed to a spectrum of clinical, translational, and basic science research, working with patients as well as animal, cell, and molecular models to investigate human disease.

I was drawn to KU due to the outstanding reputation and collaborative tradition of the Jared Grantham Kidney Institute. During my first summer, I worked with Dr. Gustavo Blanco on a project concerning autosomal dominant polycystic kidney disease (ADPKD). ADPKD is a common inherited disorder characterized by numerous fluid-filled cysts found primarily in the kidneys. The disorder results from mutations in either of the two genes Pkd1 or Pkd2, which code for the proteins polycystin-1 and polycystin-2, respectively.

In the summer of 2013, I joined the lab of Alan Yu. The Yu lab focuses on paracellular transport of solutes and water in the kidney. This transport is largely passive, mediated by a family of proteins known as claudins found at the tight junction between epithelial cells. The expression of claudins is an important determinant of the selectivity of the paracellular pathway. There are 27 known claudin isoforms. My dissertation work focused on claudin-2, a protein found in the leaky epithelia of the small intestine and renal proximal tubule. The proximal tubule is responsible for the majority of calcium reabsorption in the kidney, the bulk of which appears to occur passively through the paracellular pathway. Mice with global loss of claudin-2 exhibit an increase in the calcium excreted by the kidneys. My work investigated the cause of increased calcium excretion in these mice in order to expand upon our current understanding of calcium homeostasis and renal physiology.

Mentor:  Alan Yu, M.B., B.Chir.