Acute kidney injury (AKI), previously known as acute renal failure, represents a medical emergency and encompasses a wide range of damage to the kidneys
(AKI) occurs when kidney function rapidly deteriorates, leading to an inability to maintain fluid, electrolyte, and acid-base balance. It contributes to increased morbidity and mortality. The severity of AKI results in significant healthcare costs. Consequently, there is a heightened focus on identifying new biomarkers for AKI. Detecting AKI earlier would ultimately preserve lives, improve patients' quality of life globally, and reduce healthcare system expenses
What is Acute Kidney Injury (AKI) ?
In AKI, the underlying pathophysiology features a complex interaction between predisposing chronic illnesses, haemodynamic disturbances, nephrotoxic insults, and inflammatory responses, resulting in tubular cell injury and, ultimately, a reduction in glomerular filtration rate. Cardiovascular disease associates acute kidney injury (AKI) with heightened morbidity and mortality. In 2005, a landmark study of 71 children undergoing cardiac surgery showed that urine Neutrophile Gelatinase-Associated Lipocalin (uNGAL) and plasma NGAL (pNGAL), assessed 2 hours after cardiopulmonary bypass, had a high diagnostic accuracy for AKI (defined as a ≥50% increase in creatinine from baseline).
uNGAL’s sensitivity was 100% with an area under the receiver-operating characteristic curve (AUC) of 0.998, and pNGAL’s sensitivity was 70% with an AUC of 0.906. These promising results led to further studies of NGAL in cardiogenic shock, contrast induced nephropathy (CIN), heart failure (HF), sepsis, and critical illness. In critical illness, septic patients face a significantly heightened risk of AKI. In a multicenter study that included patients presenting to the emergency department with suspected sepsis, pNGAL (plasma neutrophil gelatinase-associated lipocalin) exhibited a strong predictive capacity for AKI with an AUC of 0.82, surpassing the AUC of 0.73 observed for creatinine
