Current Definitions, Biomarkers, and Treatments for Acute Kidney Injury

An unexpected reduction in renal function during the first seven days after a triggering event is known as acute kidney injury (AKI). AKI is diagnosed when serum creatinine increases by 0.3 mg/dL in 48 h, or an increase ≥ 50% in the first seven days of follow-up or a urinary volume < 0.5 mL/kg/h for six hours. AKI affects between 7% and 20% of hospitalized patients, and the incidence in the community is estimated to be between 20 and 200 per million inhabitants. Among critically ill patients, the incidence of AKI varies between 30% and 70%. AKI is multifactorial and can develop in a heterogeneous population in terms of genetics, age, previous renal function, and different comorbidities. The limitations in classifying and diagnosing AKI lie in the scarce variable specificity since serum creatinine and urine output do not always represent the severity of damage and are only markers of excretory function. Hence, owing to a lack of evidence of kidney damage in some cases (patients who did not present increased creatinine or decreased urine volume at the time of evaluation) and despite patients meeting the criteria for AKI, timely detection of functional changes with more precise and effective biomarkers is urgently needed.

Keywords: ADQI, Acid-base balance, Glomerular filtration rate, KDIGO, Metabolic acidosis.