TNNI3 and acute kidney injury: The mechanism of cardiac injury involves adenosine triphosphate (ATP) depletion, calcium overload, and the release of cardiac troponin I (cTnI) in myocardial cells due to hypoxia, leading to circulatory system disorders characterized by anuria, severe metabolic acidosis, unstable blood pressure, and acute kidney injury (AKI), manifesting as neonatal shock and renal failure (16, 17).