KDIGO Criteria for Acute Kidney Injury
Diagnostic Criteria
AKI is diagnosed when any one of the following three criteria is met: serum creatinine increase ≥0.3 mg/dL (26.5 μmol/L) within 48 hours, OR serum creatinine increase to ≥1.5 times baseline within 7 days, OR urine output <0.5 mL/kg/hour for 6 hours. 1, 2
The KDIGO criteria represent the universally accepted standard for AKI diagnosis, having harmonized the older RIFLE and AKIN classifications into a single, validated framework. 2
Staging System
Stage 1:
- Serum creatinine: Rise of ≥0.3 mg/dL (26 μmol/L) within 48 hours OR 1.5-1.9 times baseline within 7 days 1
- Urine output: <0.5 mL/kg/hour for more than 6 hours 1
Stage 2:
- Serum creatinine: 2.0-2.9 times baseline within 7 days 1
- Urine output: <0.5 mL/kg/hour for more than 12 hours 1
Stage 3:
- Serum creatinine: ≥3.0 times baseline within 7 days OR creatinine ≥354 μmol/L (4.0 mg/dL) with either a rise of ≥26 μmol/L or >50% increase from baseline OR any requirement for renal replacement therapy 1
- Urine output: <0.3 mL/kg/hour for 24 hours or anuria for 12 hours 1
Patients are classified according to the highest stage criterion met, whether by creatinine rise or urine output. 1
Clinical Application and Prognostic Significance
The KDIGO criteria have been independently validated across multiple patient populations, with AKI occurring in approximately 50% of critically ill patients admitted to intensive care units. 2, 3 A stepwise increase in mortality is associated with increasing KDIGO stages, with even small creatinine rises (≥0.3 mg/dL) independently associated with approximately fourfold increased hospital mortality. 1
Important Nuances in Stage 1 AKI
Recent evidence suggests that Stage 1 AKI encompasses patients with disparate outcomes. 4 Patients whose peak creatinine does not exceed 1.5 mg/dL (133 μmol/L) have mortality similar to those without AKI, while those whose peak creatinine exceeds 1.5 mg/dL have significantly higher mortality. 1, 4 This 1.5 mg/dL threshold remains clinically important for predicting AKI progression and prognosis. 1
Urine Output Criteria Considerations
Urine output criteria are generally applicable only in intensive care settings where accurate monitoring is feasible; ascertainment of AKI from serum creatinine changes alone is acceptable in other clinical settings. 2
There is emerging evidence that urine output criteria may overclassify AKI severity, particularly after cardiac surgery, where patients meeting only urine output criteria for AKI often do not demonstrate elevated kidney biomarkers or worse clinical outcomes compared to those meeting both creatinine and urine output criteria. 5, 6 Patients meeting both creatinine and urine output criteria have significantly worse short-term and mid-term outcomes than those meeting only one criterion. 5
Management Framework
Immediate Assessment
When AKI is diagnosed, immediately discontinue all nephrotoxic medications including NSAIDs, ACE inhibitors, ARBs, and diuretics. 7, 8
Assess volume status through physical examination looking specifically for poor skin turgor, dry mucous membranes, orthostatic hypotension, tachycardia, decreased jugular venous pressure (prerenal), versus peripheral edema, pulmonary congestion, and weight gain (volume overload). 8
Obtain kidney ultrasound immediately to rule out obstructive uropathy, particularly in older men with prostatic hypertrophy, history of nephrolithiasis, pelvic malignancy, or single functioning kidney. 7, 8
Diagnostic Workup
Perform urinalysis with microscopy to detect hematuria, proteinuria, or abnormal urinary sediment to exclude structural renal diseases. 7, 8
Calculate fractional excretion of sodium (FeNa): FeNa <1% suggests prerenal azotemia, while FeNa >2% suggests intrinsic renal disease. 8 A BUN:creatinine ratio >20:1 indicates prerenal azotemia from volume depletion, while ratio <20:1 typically indicates intrinsic renal injury such as acute tubular necrosis. 8
Treatment Based on Etiology
For prerenal AKI (FeNa <1%, BUN:Cr >20:1, clinical hypovolemia):
- Initiate fluid resuscitation with isotonic fluids 7, 8
- Withdraw nephrotoxic drugs 8
- Hold or reduce diuretics 8
For intrinsic renal AKI (BUN:Cr <20:1, muddy brown casts, FeNa >2%):
- Avoid aggressive fluid resuscitation 8
- Achieve euvolemia 8
- Adjust all medication doses based on reduced GFR 7, 8
Indications for Renal Replacement Therapy
Urgent RRT is indicated for: severe oliguria unresponsive to fluid resuscitation, severe metabolic derangements, uremic symptoms, and fluid overload. 7
Nephrology Consultation
Obtain nephrology consultation for: Stage 2 or 3 AKI, Stage 1 AKI with concomitant decompensated condition, unclear etiology despite workup, no improvement with supportive treatment, suspected glomerulonephritis, or preexisting stage 4 or higher chronic kidney disease. 8, 9
Monitoring and Follow-Up
Monitor serum electrolytes, BUN, and creatinine every 4-6 hours initially during acute phase. 7 Track fluid balance with strict input/output measurements. 7
Close follow-up is mandatory for all AKI patients, with creatinine checks every 2-4 days during hospitalization and every 2-4 weeks for 6 months post-discharge. 8
Critical Pitfalls to Avoid
Never continue nephrotoxic medications during AKI recovery phase, as this leads to continued kidney damage. 7 The "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs more than doubles AKI risk and must be avoided. 7
Avoid overly aggressive fluid administration in non-hypovolemic patients, which worsens outcomes and can lead to fluid overload. 7, 8 Conversely, delaying RRT when clear indications exist increases mortality. 7
Do not neglect to adjust medication dosages dynamically as kidney function changes during recovery. 7 Reassess frequently based on current estimated GFR. 7