How to detect Acute Kidney Injury (AKI)?

From the Guidelines

Acute Kidney Injury (AKI) should be detected through a combination of laboratory tests, urine output monitoring, and clinical assessment, with the primary method involving measuring serum creatinine levels and urine output, as recommended by the most recent guidelines 1. The detection of AKI involves several key components, including:

• Measuring serum creatinine levels, with an increase of 0.3 mg/dL within 48 hours or a 50% increase from baseline within 7 days indicating possible AKI 1
• Monitoring urine output, with output less than 0.5 mL/kg/hour for 6 hours suggesting kidney dysfunction 1
• Using a complete metabolic panel including BUN, electrolytes, and estimated GFR to provide additional information about kidney function
• Performing urinalysis to reveal abnormalities like proteinuria, hematuria, or casts that suggest kidney damage
• Considering imaging studies such as renal ultrasound to rule out obstruction in some cases
• Emerging tools like biomarkers (e.g., NGAL and KIM-1) for earlier detection, although not yet standard practice 1 AKI is classified using the KDIGO criteria into three stages based on creatinine elevation and urine output reduction, with higher stages indicating more severe injury 1. It is essential to individualize the frequency and duration of monitoring based on patient risk and clinical course, as suggested by the KDIGO practice guideline 1. Early detection is crucial as AKI can progress rapidly and lead to permanent kidney damage if not addressed promptly. The most recent guidelines emphasize the importance of using a combination of damage and functional biomarkers, along with clinical information, to improve the diagnostic accuracy of AKI 1.

From the Research

Detection of Acute Kidney Injury (AKI)

To detect AKI, several biomarkers and methods can be used, including:

• Serum creatinine (SCr) and urine output, which are traditional markers but have limitations such as being affected by muscle mass and fluid overload 2
• Novel biomarkers like KIM-1 and NGAL, which are considered excellent for early prediction of AKI 2
• Cycle arrest biomarkers, such as urine TIMP-2 and IGFBP7, which have been shown to perform better than other biomarkers for predicting moderate or severe AKI 2
• Cystatin C, which is sensitive to early and mild changes in kidney function and has been proposed as a filtration marker for the early detection of AKI 3, 4, 5
• Neutrophil gelatinase-associated lipocalin (NGAL), which is expressed early after injury and has value in predicting AKI after kidney transplant and cardiopulmonary bypass 3
• Interleukin-18, which has been detected early in AKI after kidney transplant, cardiopulmonary bypass, and sepsis 3
• Kidney injury molecule-1 (KIM-1), which is upregulated after ischemic/toxic injury and can predict the need for renal replacement therapy and mortality 3

Biomarker Combinations

Combining different biomarkers can increase diagnostic accuracy in an acute setting:

• Combining cystatin C and SCr has been shown to perform better than using either alone, especially in situations where CKD needs to be confirmed 2
• Combining creatinine, cystatin C, and urine albumin to creatinine ratio can improve risk stratification for kidney disease progression and mortality 2
• Using a panel of biomarkers, including cystatin C, NGAL, and KIM-1, may aid in detecting, classifying, and predicting the clinical course of AKI 3

Clinical Settings

The detection of AKI can be applied in various clinical settings, including:

• Emergency departments, where serum cystatin C has been shown to be an early predictive biomarker of AKI 4
• Critically ill patients, where early detection of AKI is crucial for timely interventions 6
• Patients after cardiac surgery, pediatric patients, and critically ill patients, where cystatin C has been proposed as a filtration marker for the early detection of AKI 5