What labs should be ordered to assess Acute Kidney Injury (AKI)?

Laboratory Assessment for Acute Kidney Injury

Order serum creatinine, blood urea nitrogen (BUN), complete blood count with differential, comprehensive metabolic panel (electrolytes, bicarbonate), and urinalysis with microscopy as your core laboratory panel to assess AKI. 1

Essential Laboratory Tests

Primary Diagnostic Markers

• Serum creatinine is the primary diagnostic marker—AKI is defined as an increase ≥0.3 mg/dL within 48 hours or ≥50% from baseline within 7 days 1, 2
• Blood urea nitrogen (BUN) should be measured alongside creatinine to help differentiate prerenal from intrarenal causes 1
• Complete blood count with differential identifies underlying causes such as infection, hemolysis, or thrombotic microangiopathy 1
• Serum electrolytes (sodium, potassium, chloride, bicarbonate) are essential to assess for metabolic complications and guide management 1

Urinalysis and Microscopy

• Urinalysis with microscopy is critical for narrowing the differential diagnosis 1, 3
• Hematuria (>50 RBCs per high-power field) suggests glomerular disease 1
• Proteinuria (>500 mg/day) indicates glomerular disease 1
• Renal tubular epithelial cell casts suggest acute tubular necrosis 1
• Urine chemistry should include sodium and creatinine for calculating fractional excretion indices 1

Calculated Indices for Etiology Determination

• Fractional excretion of sodium (FENa): FENa <1% suggests prerenal AKI; FENa >2% suggests acute tubular necrosis 1
• Fractional excretion of urea (FEUrea) can be used when diuretics confound FENa interpretation 1

Establishing Baseline Creatinine

• Use the most recent known creatinine value from the patient's medical record as baseline—this is superior to imputation methods 1
• If no baseline exists, back-calculate using the MDRD equation assuming GFR of 75 mL/min/1.73 m² 1

Critical caveat: Do not wait for creatinine to reach 1.5 mg/dL before diagnosing AKI, as this outdated threshold often indicates GFR has already fallen to ~30 mL/min 1

Emerging Biomarkers (When Available)

While not yet standard of care, several novel biomarkers show promise for earlier detection and prognostication:

• Neutrophil gelatinase-associated lipocalin (NGAL) can distinguish acute tubular necrosis from hepatorenal syndrome in cirrhotic patients 1, 2
• Kidney injury molecule-1 (KIM-1) may diagnose AKI before creatinine changes occur 1, 2
• TIMP-2 and IGFBP7 combination predicts progression to severe AKI 1, 2
• Urinary TIMP-2 × IGFBP7 >0.3 (ng/mL)²/1000 is associated with death or kidney replacement therapy (hazard ratio 2.16) 4

The 2020 Acute Disease Quality Initiative consensus recommends that damage biomarkers may be used to diagnose AKI even in the absence of serum creatinine changes in appropriate clinical contexts 2

Special Considerations

Volume Status Assessment

• Serum creatinine is a concentration and can be diluted by massive fluid resuscitation, potentially masking significant GFR reduction 1
• Consider adjusting creatinine for volume accumulation in cases of significant fluid resuscitation 1

Cirrhotic Patients

• Focus exclusively on serum creatinine changes rather than urine output, as cirrhotic patients with ascites are frequently oliguric with avid sodium retention yet maintain relatively normal GFR 1
• Diuretic therapy further confounds urine output interpretation in this population 1

Limitations of Standard Markers

• Serum creatinine significantly overestimates actual kidney function in patients with muscle wasting, increased tubular secretion of creatinine, volume expansion, or hyperbilirubinemia 1
• Hyperbilirubinemia can result in inaccurate measurement of serum creatinine by colorimetric methods 1

Additional Testing Based on Clinical Context

• Renal ultrasound is appropriate when obstruction is suspected, or to assess kidney size and rule out chronic kidney disease 1, 2
• Serum phosphorus and parathyroid hormone are indicated when eGFR <60 mL/min/1.73 m² to assess for CKD complications 1

Monitoring Strategy

• Monitor temporal changes in serum creatinine at 48-hour intervals to detect the 0.3 mg/dL threshold 1
• Small increases in creatinine (≥0.3 mg/dL) are independently associated with approximately four-fold increase in hospital mortality 1
• Progression through AKI stages strongly correlates with increased mortality 1