Jamie Rae Privratsky

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 and mitochondrial protective therapies for acute kidney injury (AKI) to prevent its transition to chronic kidney disease (CKD). Currently, we study mechanisms of injury and repair in mouse models of ischemic and septic AKI. We use a variety of genetically floxed mice in order to explore the mechanisms by which cytokines, immune cells, and metabolic pathways modulate kidney injury. We are also undertaking translational studies on humans to better understand mechanisms of post-surgical and critical illness AKI. For these studies we use patient medical and epidemiological data to better understand contributors to post-surgical AKI.