What causes the sudden loss of kidney function, also called acute kidney injury (AKI), is often unclear when treating patients. Sian Piret, from the Renaissance School of Medicine at Stony Brook University, researches the molecular and cellular changes that occur in AKI. She has received a $1.4 million grant from the National Institutes of Health’s National Institute of Diabetes and Digestive and Kidney Diseases to investigate a certain metabolic process that is known to occur with AKI, but its exact role with AKI remains unknown.
Her project will aim to understand the role of branched chain amino acid (BCAA) catabolism, or the breakdown of complex molecules into even smaller ones, in AKI as well as in chronic kidney disease (CKD). BCAA catabolism is downregulated in AKI and CKD but its relevance and contribution to kidney injury and repair have not previously been studied.
“Defective BCAA catabolism may have two consequences: loss of energy production by the kidney, and stimulation of cellular pathways that exacerbate injury,” explains Piret, an assistant professor in the Department of Medicine’s Division of Nephrology and Hypertension. “We will study the contributions of these two consequences to the processes of AKI and CKD, with the aim of developing therapeutics to restore BCAA catabolism.”
She adds that the research will help to determine if BCAA is a driver of AKI and/or CKD, or just a correlation that occurs during these conditions.
AKI occurs during other disease or infection processes such as sepsis or toxic exposures, whereas CKD is brought on by other long-term diseases such as diabetes or high blood pressure. However, just one episode of AKI can increase the risk of developing CKD later in life. There are currently no drugs to treat AKI.
For more about the research, visit the Piret lab webpage.