Laboratory Assessment of Acute Kidney Injury
When assessing AKI, order serum creatinine, blood urea nitrogen (BUN), complete blood count, urinalysis with microscopy, and urine chemistry (including urine sodium, urine creatinine, and fractional excretion of sodium). 1, 2, 3
Essential Initial Laboratory Panel
Serum Tests
- Serum creatinine is the cornerstone diagnostic test, with AKI defined as an increase ≥0.3 mg/dL within 48 hours or ≥50% from baseline within 7 days 1, 2, 3
- Blood urea nitrogen (BUN) helps assess severity and distinguish prerenal from intrarenal causes 2, 3
- Complete blood count with differential identifies infection, anemia, or other systemic processes contributing to AKI 2
- Electrolytes (sodium, potassium, bicarbonate, chloride) assess for complications and metabolic derangements 4
Urine Studies
- Urinalysis with microscopy is critical for differentiating AKI etiology—look for cellular casts (particularly renal tubular epithelial cell casts suggesting acute tubular necrosis), hematuria (>50 RBCs/hpf suggesting glomerular disease), and proteinuria (>500 mg/day suggesting glomerular disease) 1, 2
- Urine sodium (UNa) shows high specificity (>85%) for prerenal AKI when low (<20 mEq/L) and high sensitivity for acute tubular necrosis when elevated 5
- Urine specific gravity (USG) demonstrates high specificity (>85%) for prerenal AKI when elevated 5
- Spot urine creatinine enables calculation of fractional excretion indices 5
Calculated Urine Indices
High-Yield Indices
- Fractional excretion of sodium (FENa) = (UNa × PCr)/(PNa × UCr) × 100, where FENa <1% suggests prerenal AKI and >2% suggests intrarenal AKI 5, 3
- Renal failure index (RFI) = UNa/(UCr/PCr) shows high specificity for both prerenal AKI and acute tubular necrosis 5
- Fractional excretion of urea (FEUrea) may be more reliable than FENa in patients on diuretics 5
Important Caveat
These traditional urine indices (UNa, FENa, USG, RFI) are not confounded by loop diuretics, ACE inhibitors/ARBs, or pre-existing chronic kidney disease, contrary to common teaching 5
Emerging Biomarkers (Not Yet Standard of Care)
The 2020 ADQI consensus recommends that novel damage biomarkers may be used to diagnose AKI even in the absence of serum creatinine changes or oliguria in appropriate clinical contexts 6, 7. However, these are not yet routinely available in most clinical settings:
- Neutrophil gelatinase-associated lipocalin (NGAL) can distinguish acute tubular necrosis from other causes 2, 8, 7
- Kidney injury molecule-1 (KIM-1) shows promise for early detection 6, 7
- Tissue inhibitor metalloproteinase-2 (TIMP-2) × insulin-like growth factor-binding protein 7 (IGFBP7) predicts progression to severe AKI 6
- Interleukin-18 (IL-18) and liver-type fatty acid binding protein (L-FABP) are additional promising markers 8, 7
Special Considerations
Limitations of Serum Creatinine
- Serum creatinine significantly overestimates kidney function in patients with muscle wasting, volume expansion, or hyperbilirubinemia 1
- Hyperbilirubinemia can cause inaccurate creatinine measurement by colorimetric methods 1
- In cirrhotic patients, focus primarily on creatinine changes rather than urine output, as oliguria may occur despite normal GFR 1
When to Add Imaging
- Renal ultrasound should be ordered to evaluate kidney size (normal size suggests AKI rather than chronic kidney disease) and rule out obstruction 6, 1, 2
- Ultrasound is particularly indicated with history of stones, obstruction, frequent UTIs, or family history of polycystic kidney disease 6
Monitoring After Initial Assessment
Recheck serum creatinine within 3-7 days of initial diagnosis to establish trajectory and detect early non-recovery 4. Patients at higher risk (heart failure, cirrhosis, malignancy, higher KDIGO stage) require earlier and more frequent surveillance 4.