Acute kidney injury is the rapid deterioration of kidney function, most commonly due to low blood pressure, sepsis, and nephrotoxins. In addition to our work on biomarkers to enhance diagnosis, we are interested to identify biomarkers that may suggest therapeutic targets. For example, we have studied dysregulated mineral metabolism and iron toxicity as potential therapeutic areas in AKI prevention and treatment.
SELECTED PAPERS FROM OUR RESEARCH INCLUDE:
- A Genome-Wide Association Study to Identify Single-Nucleotide Polymorphisms for Acute Kidney Injury
- End Points for Clinical Trials in Acute Kidney Injury
- Fibroblast Growth Factor 23 Levels Associate with AKI and Death in Critical Illness
- Length Polymorphisms in Heme Oxygenase-1 and AKI after Cardiac Surgery
- Detection of Drug-Induced Acute Kidney Injury in Humans Using Urinary KIM-1, miR-21, -200c, and -423
- Fibroblast growth factor 23 levels are elevated and associated with severe AKI and death following cardiac surgery
- Intraoperative High-Dose Dexamethasone and Severe AKI after Cardiac Surgery
- Increased plasma catalytic iron in patients may mediate acute kidney injury and death following cardiac surgery
