How to Diagnose Acute Kidney Injury (AKI)
Diagnose AKI when serum creatinine increases by ≥0.3 mg/dL within 48 hours OR increases ≥50% from baseline within 7 days OR when urine output falls below 0.5 mL/kg/h for more than 6 hours. 1, 2, 3
Diagnostic Criteria
The KDIGO criteria define AKI using either creatinine changes or urine output thresholds—meeting either criterion is sufficient for diagnosis 2, 3:
Serum Creatinine Criteria:
- Absolute increase ≥0.3 mg/dL within 48 hours 1, 2
- Relative increase ≥50% (1.5 times baseline) within 7 days 1, 2, 3
Urine Output Criteria:
Establishing Baseline Creatinine
Use a serum creatinine value from the previous 3 months when available; if multiple values exist, use the one closest to admission time. 1 If no prior value exists, use the creatinine on admission as baseline 1. This approach captures both community-acquired AKI (present on arrival) and hospital-acquired AKI (developing after admission) 1.
Staging AKI Severity
Once diagnosed, stage the severity to guide prognosis and management 2, 3:
Stage 1:
- Creatinine increase ≥0.3 mg/dL OR 1.5-1.9 times baseline 1, 2
- Urine output <0.5 mL/kg/h for 6-12 hours 2
Stage 2:
Stage 3:
- Creatinine increase ≥3.0 times baseline OR ≥4.0 mg/dL with acute rise ≥0.3 mg/dL OR initiation of dialysis 1, 2
- Urine output <0.3 mL/kg/h for ≥24 hours OR anuria for ≥12 hours 2
Higher stages correlate strongly with increased mortality—even small creatinine increases of 0.3 mg/dL independently increase hospital mortality approximately fourfold. 2
Essential Diagnostic Workup
After diagnosing AKI, determine the underlying cause through systematic evaluation 1, 3:
Laboratory Assessment:
- Serial creatinine measurements to track progression 3
- Urinalysis with microscopy: RBC casts suggest glomerulonephritis; WBC casts suggest interstitial nephritis; muddy brown casts suggest acute tubular necrosis 3
- Urine chemistry including sodium and urea to calculate fractional excretion of sodium 1, 4
- Complete blood count 4
Imaging:
- Renal ultrasound to rule out obstruction (especially in older men) and assess kidney size—normal size suggests AKI rather than chronic kidney disease 2, 3
Clinical Evaluation:
- Review all medications for nephrotoxins (NSAIDs, aminoglycosides, contrast agents) 1, 4
- Assess volume status through physical examination 1, 4
- Search rigorously for infection: diagnostic paracentesis for spontaneous bacterial peritonitis in cirrhotic patients, blood and urine cultures, chest radiograph 1
Critical Caveats for Special Populations
In patients with cirrhosis and ascites, rely exclusively on serum creatinine changes—do NOT use urine output criteria. 1, 2 These patients are frequently oliguric with avid sodium retention despite maintaining relatively normal GFR, and diuretics further confound interpretation 1. Additionally, serum creatinine underestimates kidney dysfunction in cirrhosis due to decreased muscle mass, increased tubular creatinine secretion, and dilution by ascites 1, 2, 3.
Do not wait for creatinine to reach 1.5 mg/dL before diagnosing AKI—this outdated threshold indicates GFR has already fallen to approximately 30 mL/min. 2 Monitor temporal changes at 48-hour intervals to detect the critical 0.3 mg/dL threshold 2.
Pitfalls to Avoid
- Hyperbilirubinemia can cause inaccurate creatinine measurement by colorimetric methods 2
- Muscle wasting, age, sex, and nutritional status affect creatinine levels and may underestimate severity 2, 5
- Diuretic therapy makes urine output unreliable as a diagnostic criterion 2
- Neither creatinine nor urine output are kidney-specific markers—clinical context is essential 5
When to Refer to Nephrology
Emergently refer for Stage 2 or 3 AKI, or Stage 1 AKI with concomitant decompensated conditions. 3 Urgent referral is warranted if AKI does not improve with treatment or if glomerulonephritis is suspected 6.