What labs should be ordered to assess for Acute Kidney Injury (AKI) in a patient, particularly in those with a history of kidney disease or at high risk for AKI, such as the elderly or those with diabetes?

Laboratory Assessment for Acute Kidney Injury

Order serum creatinine, blood urea nitrogen (BUN), complete blood count with differential, urinalysis with microscopy, and urine chemistry (including urine sodium, urine creatinine) as the core laboratory panel to assess for AKI. 1

Essential Laboratory Tests

Blood Tests

• Serum creatinine is the primary diagnostic marker, with AKI 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 helps identify 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

Urine Tests

• Urinalysis with microscopy is critical to differentiate AKI etiology—look for cellular casts (suggesting acute tubular necrosis), hematuria (>50 RBCs/hpf suggesting glomerular disease), or proteinuria (>500 mg/day suggesting glomerular pathology) 1, 2
• Urine sodium (UNa) has high specificity (>85%) for prerenal AKI when low (<20 mEq/L) and high sensitivity for acute tubular necrosis when elevated 3
• Urine specific gravity (USG) shows high specificity (>85%) for prerenal AKI when elevated 3
• Spot urine creatinine to calculate fractional excretion of sodium (FENa) and urine-to-plasma creatinine ratio 1, 3

Calculated Indices for Etiology Determination

Use urine sodium, urine specific gravity, and renal failure index as first-line parameters to differentiate prerenal from intrarenal AKI, as these are highly specific, easily obtained from spot urine, and not confounded by diuretics or pre-existing CKD. 3

• Fractional excretion of sodium (FENa): FENa <1% suggests prerenal AKI; FENa >2% suggests acute tubular necrosis 1
• Renal failure index (RFI): Shows high specificity for both prerenal AKI and acute tubular necrosis 3
• Fractional excretion of urea (FEUrea) can be used when diuretics confound FENa interpretation 1

Important Caveats

Baseline Creatinine Determination

• Use the most recent known creatinine value from the medical record as baseline—this is superior to imputation methods 1, 2
• If no baseline exists, back-calculate using the MDRD equation assuming GFR of 75 mL/min/1.73 m² 1, 2
• Be aware this back-calculation method may overestimate AKI incidence in populations with high CKD prevalence 1

Special Population Considerations

• In cirrhotic patients with ascites, focus exclusively on serum creatinine changes rather than urine output, as these patients are frequently oliguric despite normal GFR 2
• Hyperbilirubinemia can cause inaccurate creatinine measurement by colorimetric methods 2
• Muscle wasting, volume expansion, or increased tubular secretion can cause creatinine to overestimate actual kidney function 2
• Massive fluid resuscitation can dilute serum creatinine, potentially masking significant GFR reduction 2

Monitoring Frequency

During Hospitalization

• Monitor serum creatinine at 48-hour intervals to detect the 0.3 mg/dL threshold for AKI diagnosis 2
• Reassess patients with persistent AKI daily for volume status and medication adjustments 1

Post-Discharge Surveillance

• Measure serum creatinine within 3-7 days of discharge after AKI 4
• Continue monitoring at 2-4 weeks, then at 1,2,3,4, and 6 months if kidney function remains stable 4
• For dialysis-dependent AKI, assess weekly pre-dialysis creatinine and residual kidney function with 24-hour urine collection 4

Emerging Biomarkers

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

• Neutrophil gelatinase-associated lipocalin (NGAL) can distinguish acute tubular necrosis from hepatorenal syndrome in cirrhotic patients 1, 5
• Kidney injury molecule-1 (KIM-1) may diagnose AKI before creatinine changes occur 1, 5
• TIMP-2 and IGFBP7 combination predicts progression to severe AKI 1, 5

These biomarkers are not yet routinely recommended but may be considered in high-risk patients or research settings 1.

Additional Testing Based on Clinical Context

• Renal ultrasound is appropriate when obstruction is suspected (history of stones, frequent UTIs, family history of polycystic kidney disease) or to assess kidney size 1, 5
• Quantitative proteinuria (albumin-to-creatinine ratio) should be measured for CKD risk stratification, though this is often underutilized in practice 6
• Serum phosphorus and parathyroid hormone are indicated when eGFR <60 mL/min/1.73 m² to assess for CKD complications 1, 6