It is typical for acute kidney injury (AKI) to develop and progress to chronic kidney disease (CKD), and both conditions are linked with high rates of morbidity and mortality. There is evidence that the profibrotic and inflammatory characteristics of the beta-galactoside binding protein gal3 (Gal3) contribute to the progression of both acute kidney injury (AKI) and chronic kidney disease (CKD). Patients with AKI and CKD have higher serum Gal3 levels, and this heightened level is linked to the worsening of CKD. Furthermore, AKI is more common in critically sick people who have Gal3 blocked, and both the prevalence and mortality of AKI in murine models of sepsis and ischemia-reperfusion injury are dramatically reduced. We discuss the possible therapeutic benefits of targeting Gal3 and its function in the pathogenesis of acute kidney injury (AKI) and chronic kidney disease (CKD).