- Research Fellow/Staff Scientist, NIDDK, NIH, 2001-present
- Visiting Scientist, Massachusetts Institute of Technology, 2000-2001
- Assistant Professor, University of Tennessee, 1994-2001
- HHMI Associate/Assistant Instructor, Vanderbilt University/University of Texas Southwestern Medical Center, 1989-1994
- Ph.D., University of Minnesota, 1989
We seek mechanism-based tools to identify, classify, treat, and monitor kidney disease. Our short-term goal is to improve the quantity and quality of clinical trials. Our long-term goal is to adjust therapies in individual patients to maximize efficacy and minimize toxicity.
We leverage the synergy between pathophysiology, therapeutics, and biomarkers to advance our understanding of acute and chronic kidney disease. We refine animal models to mimic disease characteristics identified in the clinic, especially by epidemiological studies.
Applying our Research
Kidney disease is a major health burden, costing billions of dollars annually and affecting hundreds of thousands of people. Acute kidney injury is a major risk factor for death in hospitalized patients, especially those with sepsis. Only one therapeutic has been approved in the last 30 years for sepsis (with or without kidney injury), but it was withdrawn from the market.
An estimated one in 15 adults has some form of chronic kidney disease (see https://www.niddk.nih.gov/health-information/health-statistics/kidney-disease). Although we have several therapies available, many patients do not respond to any therapy. We need new therapies to treat these individuals, but they should be based on our understanding of the disease, which is incomplete. Our work will help increase our understanding and may lead to better treatments.
Need for Further Study
Our current understanding of the series of events that drive chronic kidney disease and acute kidney injury comes from animal models, but their ability to predict how well therapies will work in human patients is limited. In the animal models, we can get very detailed information about the disease that is not possible in patients. Noninvasive biomarkers may be the simplest bridge between animal models and patients, and they need to be developed and validated extensively. Recently, some nephrologists are increasing their use of kidney biopsies, which are a very rich source of information about kidney disease, as new DNA/RNA sequencing technologies can identify how complex changes are orchestrated at the resolution of a single cell.
- Experimental models of acute kidney injury for translational research.
- Hukriede NA, Soranno DE, Sander V, Perreau T, Starr MC, Yuen PST, Siskind LJ, Hutchens MP, Davidson AJ, Burmeister DM, Faubel S, de Caestecker MP.
- Nat Rev Nephrol (2022 May) 18:277-293. Abstract/Full Text
- Cell-free DNA maps COVID-19 tissue injury and risk of death and can cause tissue injury.
- Andargie TE, Tsuji N, Seifuddin F, Jang MK, Yuen PS, Kong H, Tunc I, Singh K, Charya A, Wilkins K, Nathan S, Cox A, Pirooznia M, Star RA, Agbor-Enoh S.
- JCI Insight (2021 Apr 8) 6. Abstract/Full Text
Research in Plain Language
Kidneys help clear toxins from the blood and help control blood pressure and your body’s response to infection and injury. We study steps that cause kidney failure, a condition that can happen quickly or after a slow decline. Kidney failure may be life-threatening itself, and can make many other diseases worse.