Acute kidney injury (AKI) dramatically increases morbidity and mortality and is one of the most common forms of organ failure in perioperative and critically ill patients. Unresolved AKI leads to ongoing renal injury, fibrosis, and subsequent chronic kidney disease (CKD), which is a major risk factor for future cardiovascular events. Although AKI is not always preventable, interventions designed to promote renal healing and prevent CKD can improve long-term renal and cardiovascular health. My long-term goal is to develop targeted immunomodulatory therapies for acute kidney injury (AKI) to prevent its transition to chronic kidney disease (CKD) and induction of remote organ failure. Currently, we study mechanisms of injury and repair in mouse models of AKI. We use a variety of genetically floxed mice in order to explore the mechanisms by which cytokines, chemokines, and specific immune cells modulate kidney injury and remote organ dysfunction. Current projects include:
Examining the role of IL-1 receptor signaling in toxic AKI
Deciphering how IL-1 receptor signaling in renal macrophages contributes to renal injury and healing
Elucidating the role of dendritic cells in renal injury and repair.
