Dr. Ko is a dedicated physiologist and teacher who studies sodium and calcium transport in the kidney, especially as they pertain to kidney stone disease. His integrated approach to scholarship and investigation spans basic science and translational research, with a focus on understanding the molecular mechanisms of renal tubular transport of cations in humans. Using urinary exosomal analyses, small but discrete packages of transporter proteins extruded from the epithelial cell into the urinary space, and a variety of molecular and biochemical techniques he is able to characterize the complex regulation of sodium and calcium homeostasis. His current projects include an examination the molecular mechanisms underlying calcium kidney stone formation and determining the hormonal regulators of the sodium chloride co-transporter. Dr. Ko has been heavily involved for a number of years in medical education including pre-med, medical, resident and fellow trainees. He is a fellow of the Academy of Distinguished Medical Educators and the co-director of the Tissues, Cell and Organ Physiology Course at the Pritzker School of Medicine. Nationally, he serves as the director for the American Society of Nephrology’s Tutored Research and Education of Kidney Scholars (TREKS) program at the University of Chicago.
The University of Chicago Medical Center
Chicago, IL
- Nephrology
2009
Yale New Haven Hospital
New Haven, CT
- Internal Medicine
2004
University of Illinois
Chicago, IL
M.D. - Medicine
2001
University of Illinois
Urbana, IL
B.S. - Chemical Engineering
1997
Contribution of thick ascending limb and distal convoluted tubule to glucose-induced hypercalciuria in healthy controls.
Contribution of thick ascending limb and distal convoluted tubule to glucose-induced hypercalciuria in healthy controls. Am J Physiol Renal Physiol. 2023 12 01; 325(6):F811-F816.
PMID: 37823200
Nephrology Trainee Education Needs Assessment: Five Years and a Pandemic Later.
Nephrology Trainee Education Needs Assessment: Five Years and a Pandemic Later. Kidney Med. 2022 Nov; 4(11):100548.
PMID: 36275043
Interleukin 6 mediated activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron.
Interleukin 6 mediated activation of the mineralocorticoid receptor in the aldosterone-sensitive distal nephron. Am J Physiol Cell Physiol. 2022 11 01; 323(5):C1512-C1523.
PMID: 35912993
The IFN?-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension.
The IFN?-PDL1 Pathway Enhances CD8T-DCT Interaction to Promote Hypertension. Circ Res. 2022 05 13; 130(10):1550-1564.
PMID: 35430873
The Pharmacological Inhibition of CaMKII Regulates Sodium Chloride Cotransporter Activity in mDCT15 Cells.
The Pharmacological Inhibition of CaMKII Regulates Sodium Chloride Cotransporter Activity in mDCT15 Cells. Biology (Basel). 2021 Dec 16; 10(12).
PMID: 34943250
Mechanisms for falling urine pH with age in stone formers.
Mechanisms for falling urine pH with age in stone formers. Am J Physiol Renal Physiol. 2019 07 01; 317(7):F65-F72.
PMID: 31017011
Zinc deficiency induces hypertension by promoting renal Na+ reabsorption.
Zinc deficiency induces hypertension by promoting renal Na+ reabsorption. Am J Physiol Renal Physiol. 2019 04 01; 316(4):F646-F653.
PMID: 30649891
The complexities of lithium.
The complexities of lithium. Physiol Rep. 2017 11; 5(21).
PMID: 29138355
Parathyroid hormone and the regulation of renal tubular calcium transport.
Parathyroid hormone and the regulation of renal tubular calcium transport. Curr Opin Nephrol Hypertens. 2017 09; 26(5):405-410.
PMID: 28614116
CD8+ T cells stimulate Na-Cl co-transporter NCC in distal convoluted tubules leading to salt-sensitive hypertension.
CD8+ T cells stimulate Na-Cl co-transporter NCC in distal convoluted tubules leading to salt-sensitive hypertension. Nat Commun. 2017 01 09; 8:14037.
PMID: 28067240