Hospital-acquired acute kidney injury (AKI) accounts for 22% of all cases worldwide, and an estimated 50% of critically ill inpatients are estimated to suffer from AKI. AKI is associated with high rates of morbidity and mortality and causes 2 million deaths per year. Patients who recover are at a higher risk for subsequently developing chronically kidney disease (CKD); other times, the injury is so severe that it leads to end stage renal disease (ESRD). There are no definitive or effective treatments for AKI, nor are there available interventions to decrease the risk of progression to CKD after AKI.
Description
One of the hallmarks of AKI is damage to renal microvasculature, which alters endothelial function and contributes to hypoxic and inflammatory injury to the renal parenchyma. In AKI, some miRNAs appear to act pathogenically by promoting inflammation, apoptosis, and fibrosis, while others may confer protective benefits. Researchers have obtained preliminary data indicating that the absence of the miR-17~92 cluster makes cells are more susceptible to renal ischemia-reperfusion injury while miR-18a and miR-19b protects against renal IRI, providing evidence for a potential novel therapeutic approach for the treatment of acute kidney injury.
Applications
· Treating acute kidney injury
Advantages
· Novel approach to treating acute kidney injury
Invention Readiness
In vivo data in mice using mimics
IP Status
https://patents.google.com/patent/US20230323347A1
