What are the lab findings of Acute Kidney Injury (AKI)?

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Last updated: October 29, 2025View editorial policy

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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:
    • Increase in serum creatinine by ≥0.3 mg/dL (26.5 μmol/L) within 48 hours 3, 1
    • Increase in serum creatinine to ≥1.5 times baseline within the previous 7 days 3, 2
    • Urine volume <0.5 mL/kg/h for 6 consecutive hours 3, 2

AKI Staging Based on Laboratory Findings

  • Stage 1:

    • Serum creatinine increase ≥0.3 mg/dL within 48 hours or 50-99% from baseline within 7 days 2
    • Urine output <0.5 mL/kg/h for >6 hours 2
  • Stage 2:

    • Serum creatinine increase of 100-199% from baseline within 7 days 2
    • Urine output <0.5 mL/kg/h for >12 hours 2
  • Stage 3:

    • Serum creatinine increase ≥200% from baseline within 7 days 2
    • Serum creatinine ≥4.0 mg/dL with an acute increase of at least 0.3 mg/dL 2
    • Initiation of renal replacement therapy 2
    • Urine output <0.3 mL/kg/h for 24 hours or anuria for 12 hours 2

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):

    • FENa <1% suggests prerenal causes (increased sodium reabsorption) 4
    • FENa >1% suggests intrinsic renal causes (tubular damage) 4
    • Note: The value of urine biochemistry has been questioned, especially in sepsis 3, 4
  • Urine sodium concentration:

    • <10 mEq/L typically seen in prerenal AKI 4
    • 20 mEq/L often seen in intrinsic renal causes 4

  • Fractional excretion of urea (FEUrea):

    • <28.16% may be indicative of hepatorenal syndrome with sensitivity of 75% and specificity of 83% 4
    • May be more reliable than FENa in certain settings such as diuretic use 4

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

References

Guideline

Acute Kidney Injury Definition and Diagnosis

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Diagnóstico y Estadificación de Lesión Renal Aguda

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Guideline

Guideline Directed Topic Overview

Dr.Oracle Medical Advisory Board & Editors, 2025

Guideline

Diferenciación de Insuficiencia Renal Aguda

Praxis Medical Insights: Practical Summaries of Clinical Guidelines, 2025

Professional Medical Disclaimer

This information is intended for healthcare professionals. Any medical decision-making should rely on clinical judgment and independently verified information. The content provided herein does not replace professional discretion and should be considered supplementary to established clinical guidelines. Healthcare providers should verify all information against primary literature and current practice standards before application in patient care. Dr.Oracle assumes no liability for clinical decisions based on this content.

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