Acute kidney injury (AKI) is a common critical condition with high morbidity and mortality. Not only can AKI cause death in the acute phase, but also can it be associated with the development of chronic kidney disease (CKD) or the progression of CKD. Galectins are members of a lectin family widely expressed in vertebrates, among which galectin-3 (Gal3) is the most studied one. The level of circulating Gal3 largely depends on renal function, so it is elevated in patients with AKI or CKD; elevated Gal3 also aggravates the progression of CKD after the onset of AKI. The proinflammatory and profibrotic properties of Gal3 may render it to be one of the key molecules mediating AKI, CKD, and cardiorenal syndrome. However, the mechanisms of AKI differ from different etiologies, and the process and extent of levels of Gal3 may be also different, so its predictive value in prognosis may vary in different types of AKI. In critically ill patients, AKI is a common complication of sepsis, and sepsis is the most common trigger of AKI. In this prospective observational study, the investigators will explore the differences of Gal3 levels among septic AKI, non-septic AKI, and non-AKI patients and its correlation with prognosis, inflammation, and disease severity in the ICU.
Acute kidney injury (AKI) is a common critical condition with high morbidity and mortality. The level of circulating Galectin-3 (Gal3) largely depends on renal function, so it is elevated in patients with AKI or CKD; elevated Gal3 also aggravates the progression of CKD after the onset of AKI. The proinflammatory and profibrotic properties of Gal3 may render it to be one of the key molecules mediating AKI, CKD, and cardiorenal syndrome. In this prospective observational study, the investigators will explore the differences of Gal3 levels among septic AKI, non-septic AKI, and non-AKI patients and its correlation with prognosis, inflammation, and disease severity in the ICU.