Laboratory Findings of Acute Kidney Injury (AKI)
The primary laboratory findings of AKI include an increase in serum creatinine of ≥0.3 mg/dL within 48 hours, or an increase of ≥50% from baseline within 7 days, or a reduction in urine output to <0.5 mL/kg/h for 6 hours or more. 1, 2
Diagnostic Criteria
- AKI is defined by the Kidney Disease Improving Global Outcomes (KDIGO) criteria as an abrupt decrease in kidney function occurring over 7 days or less 1
- The diagnosis requires at least one of the following criteria:
AKI Staging Based on Laboratory Findings
Stage 1:
Stage 2:
Stage 3:
Urinalysis Findings
- Urinalysis can help differentiate the etiology of AKI 3:
- Normal or "bland" sediment may suggest prerenal causes 4
- Presence of hematuria (>50 RBCs per high-power field) may indicate glomerular disease 3
- Presence of proteinuria (>500 mg/day) may suggest glomerular disease 3
- Presence of cellular casts, particularly renal tubular epithelial cell casts, suggests acute tubular necrosis 3
Urine Biochemistry
Fractional excretion of sodium (FENa):
Urine sodium concentration:
Fractional excretion of urea (FEUrea):
Factors Affecting Laboratory Interpretation
Serum creatinine has important limitations as a marker of AKI 3:
- Affected by muscle mass, age, sex, and nutritional status 3
- May underestimate severity of renal function reduction in patients with cirrhosis due to impaired hepatic production of creatine 3
- Hyperbilirubinemia can result in inaccurate measurement by colorimetric methods 3
- Changes in creatinine lag behind actual kidney injury 3
Small increases in serum creatinine (≥0.3 mg/dL) are independently associated with approximately fourfold increase in hospital mortality 1, 2
Novel Biomarkers
- While not yet part of routine diagnostic criteria, several biomarkers are being studied for earlier detection of AKI 3:
- Neutrophil gelatinase-associated lipocalin (NGAL) in serum or urine 3, 5
- Kidney injury molecule-1 (KIM-1) 3, 5
- Tissue inhibitor metalloproteinase-2 (TIMP-2) and insulin-like growth factor-binding protein 7 (IGFBP7) 3
- Cystatin C may predict need for chronic dialysis after AKI 3, 5
- Interleukin-18, liver-type fatty acid-binding protein, and calprotectin 5
Common Pitfalls in Laboratory Interpretation
- Relying solely on serum creatinine without considering urine output may miss cases of AKI 1
- Failure to establish an accurate baseline creatinine can lead to misclassification 1
- Not accounting for biological and analytical variability in creatinine measurements 3
- Small absolute increases in creatinine in patients with pre-existing chronic kidney disease represent smaller percentage increases, potentially leading to underdiagnosis 3
- Not recognizing that AKI can occur in both hospital and community settings 1
Imaging Findings
- Renal ultrasound is recommended to evaluate kidney size and rule out obstruction 3, 4
- Normal kidney size suggests AKI rather than chronic kidney disease 4
- New imaging techniques such as contrast-enhanced ultrasound, doppler ultrasound, and functional MRI are being studied but their role in changing outcomes is yet to be determined 3