What labs should be checked to differentiate between prerenal and intrinsic causes of Acute Kidney Injury (AKI)?

From the Guidelines

To differentiate between prerenal and intrinsic causes of Acute Kidney Injury (AKI), checking the fractional excretion of urea (FEUrea) is recommended, as it may better discriminate between the two, with a FEUrea of <28.16% suggesting prerenal causes 1. When evaluating a patient with AKI, several laboratory tests can help differentiate between prerenal and intrinsic causes.

• Blood urea nitrogen (BUN) to creatinine ratio: typically elevated in prerenal AKI (>20:1) and normal in intrinsic AKI (10-15:1)
• Urine sodium concentration: low in prerenal AKI (<20 mEq/L) and elevated in intrinsic AKI (>40 mEq/L)
• Fractional excretion of sodium (FENa): less than 1% in prerenal AKI and greater than 2% in intrinsic AKI
• Urine osmolality: high in prerenal AKI (>500 mOsm/kg) and low in intrinsic AKI (<350 mOsm/kg)
• Urine sediment examination: may reveal muddy brown granular casts in intrinsic AKI and hyaline casts or normal sediment in prerenal AKI However, according to the most recent study 1, FEUrea may be a more reliable indicator, with a sensitivity of 75% and specificity of 83% in separating hepatorenal syndrome (a type of prerenal AKI) from non-hepatorenal syndrome AKI. The choice of tests should be guided by the clinical context and the need to rapidly identify the cause of AKI to initiate appropriate treatment, as AKI has a significant impact on patient morbidity and mortality, with increased healthcare costs 1. In clinical practice, it is essential to consider the patient's overall clinical picture, including history, physical examination, and laboratory results, to make an accurate diagnosis and provide timely and effective treatment.

From the Research

Laboratory Evaluation for Prerenal vs Intrinsic Acute Kidney Injury (AKI)

To differentiate between prerenal and intrinsic causes of Acute Kidney Injury (AKI), several laboratory tests can be utilized:

• Serum creatinine level: This is a crucial initial test to assess kidney function 2, 3.
• Complete blood count: Helps in identifying underlying conditions that may contribute to AKI 2.
• Urinalysis: Provides information on the presence of blood, protein, or casts in the urine, which can indicate intrinsic renal damage 2, 3.
• Fractional excretion of sodium (FENa): Useful in differentiating prerenal from intrinsic AKI, although its validity may be limited in certain situations, such as in patients taking diuretics 2, 4.
• Fractional excretion of urea (FEU): May be used as an alternative to FENa, especially when FENa's validity is questionable 4.
• Urinary biomarkers: Such as L-type fatty acid-binding protein (L-FABP), neutrophil gelatinase-associated lipocalin (NGAL), interleukin-18 (IL-18), N-acetyl-β-D-glucosaminidase (NAG), and albumin, which can detect mild renal tubular damage in prerenal AKI and improve the diagnosis of intrinsic AKI 5, 6.
• Calprotectin: Has been shown to be an independent risk factor for intrinsic AKI and, when combined with NGAL, can predict intrinsic AKI with a high degree of accuracy 6.

Additional Diagnostic Tools

In addition to laboratory tests, other diagnostic tools may be employed to help differentiate between prerenal and intrinsic AKI:

• Ultrasonography of the kidneys: To rule out obstruction, particularly in older men 2.
• Patient history and physical examination: To identify underlying conditions, such as nephrotoxic medication use, systemic illnesses, or poor renal perfusion 2, 3.