What is the definition of acute kidney injury (AKI) based on serum creatinine criteria?

AKI Definition Based on Serum Creatinine Criteria

Acute kidney injury is diagnosed when serum creatinine rises by ≥0.3 mg/dL within 48 hours OR increases to ≥1.5 times baseline within 7 days, according to the KDIGO criteria. 1

Core Diagnostic Thresholds

The KDIGO framework defines AKI using two distinct serum creatinine criteria, and meeting either one is sufficient for diagnosis:

• Absolute criterion: Serum creatinine increase of ≥0.3 mg/dL within any 48-hour period 1, 2
• Relative criterion: Serum creatinine rise to ≥1.5 times (≥50% increase from) the baseline value within the preceding 7 days 1, 2

Even the modest 0.3 mg/dL threshold is clinically critical—this small absolute rise independently predicts approximately a 4-fold increase in hospital mortality. 1, 2

KDIGO Staging by Serum Creatinine

Once AKI is diagnosed, severity is staged using the magnitude of creatinine elevation:

Stage	Creatinine Criterion
Stage 1	1.5–1.9 × baseline OR increase ≥0.3 mg/dL [1]
Stage 2	2.0–2.9 × baseline [1]
Stage 3	≥3.0 × baseline OR increase to ≥4.0 mg/dL with acute rise ≥0.3 mg/dL OR initiation of renal replacement therapy [1]

• Progression through stages correlates strongly with mortality risk—higher stages predict worse outcomes in a dose-dependent fashion. 1
• Patients are assigned the worst criterion met among creatinine or urine output when determining stage. 3

Establishing Baseline Creatinine

Use the most recent measured creatinine from the patient's medical record within the prior 3 months—this approach is superior to any imputation method. 1, 2

• Search aggressively for prior values in outpatient labs, emergency-department visits, pre-operative assessments, and prior admissions. 2
• If no baseline exists, the admission creatinine serves as baseline. 1
• Avoid back-calculating baseline creatinine using MDRD equations (assuming eGFR of 75 mL/min/1.73 m²) in patients with cirrhosis or populations with high CKD prevalence, as this overestimates AKI incidence. 1, 2

Critical Caveats and Pitfalls

Factors That Confound Creatinine Interpretation

Serum creatinine is a concentration and can be diluted by massive fluid resuscitation, potentially masking significant GFR reduction. 1

• When cumulative fluid gain exceeds 5–10% of baseline body weight, measured creatinine should be corrected for volume expansion to avoid underestimating AKI severity. 1
• In critically ill patients receiving large-volume crystalloid, stage 1 AKI may be present despite "stable" creatinine due to dilution. 1

Creatinine generation is reduced in patients with low muscle mass, which blunts any rise with AKI:

• Old age, female sex, muscle-wasting conditions, amputation, malnutrition, and critical illness all lower baseline creatinine. 4
• In cirrhotic patients, baseline creatinine underestimates true GFR because of reduced muscle mass; even a small absolute rise (≥0.3 mg/dL) signals clinically important kidney injury. 1

Laboratory interferences can falsely elevate or lower creatinine:

• Hyperbilirubinemia interferes with Jaffe assays (falsely elevates creatinine) and enzymatic assays (falsely lowers creatinine). 4, 1
• Trimethoprim and cimetidine reduce tubular secretion of creatinine, causing falsely elevated values. 4

Time-Dependent Kinetics

The time required to reach diagnostic thresholds depends heavily on baseline kidney function. 5

• After a 90% reduction in creatinine clearance, patients with normal baseline kidney function reach a 50% creatinine increase in only 4 hours, whereas those with stage 4 CKD require 27 hours. 5
• By contrast, the time to reach a 0.5 mg/dL absolute increase is nearly identical (regardless of baseline) after moderate-to-severe AKI. 5
• Small absolute creatinine rises on a background of CKD represent progressively smaller percentage increases as baseline creatinine rises, making the probability that small rises are random variation considerable. 4

Special Populations

In cirrhotic patients with ascites, focus exclusively on serum creatinine changes rather than urine output:

• These patients are frequently oliguric with avid sodium retention yet maintain relatively normal GFR, making urine output unreliable. 1, 2
• Diuretic therapy further confounds urine-output interpretation. 1, 2
• A serum creatinine threshold of ≥1.5 mg/dL predicts AKI progression and worse prognosis in this population. 1

Do not wait for creatinine to reach 1.5 mg/dL before diagnosing AKI—this outdated threshold often indicates GFR has already fallen to ~30 mL/min. 1

• Instead, monitor temporal changes in creatinine at 48-hour intervals to detect the 0.3 mg/dL threshold. 1

Algorithmic Approach to Diagnosis

1. Obtain current serum creatinine and search medical records for any creatinine measured within the prior 3 months. 1, 2
2. Compare current value to baseline:
   • If rise ≥0.3 mg/dL occurred within any 48-hour window → AKI diagnosed 1
   • If rise to ≥1.5 × baseline occurred within 7 days → AKI diagnosed 1
3. Assess for confounders:
   • Calculate cumulative fluid balance; if >5–10% body weight gained, adjust creatinine for dilution 1
   • Review medications (trimethoprim, cimetidine) and laboratory flags (hemolysis, icterus) 4
4. Stage the AKI using the worst creatinine criterion met (Stage 1,2, or 3). 1
5. In cirrhotic patients, ignore urine output and focus solely on creatinine changes. 1, 2

Relationship to Urine Output Criteria

Although this question focuses on creatinine, AKI is diagnosed when either creatinine OR urine output criteria are met—you do not need both. 1, 2

• Urine output <0.5 mL/kg/h for ≥6 consecutive hours also defines AKI (Stage 1). 1
• However, urine output alone is insufficient in patients on diuretics or with cirrhosis and ascites. 1

Temporal Framework Beyond AKI

• 0–7 days of kidney dysfunction = AKI 2
• 7–90 days = Acute Kidney Disease (AKD), which includes persistent AKI or subacute injury not meeting strict AKI thresholds 2
• >90 days = Chronic Kidney Disease (CKD) 2

4, 1, 2, 5