BUN/Creatinine Ratio in Acute Kidney Injury
The BUN/creatinine ratio has limited clinical utility in diagnosing or managing AKI and should not be used as a reliable tool to distinguish prerenal from intrinsic AKI, particularly in critically ill patients. 1, 2
Why the BUN/Cr Ratio Fails in AKI
The traditional teaching that a BUN/Cr ratio >20:1 indicates prerenal azotemia is not supported by modern evidence:
In the largest study examining this question (1,103 ED patients with AKI), the BUN/Cr ratio showed no capacity to discriminate between prerenal and intrinsic AKI, with an area under the ROC curve of 0.5 (equivalent to a coin flip). 1
In critically ill patients (N=10,228), a BUN/Cr ratio >20 was paradoxically associated with increased mortality rather than the better prognosis traditionally expected with "prerenal" disease. 2
The ratio is heavily influenced by non-renal factors including protein intake, gastrointestinal bleeding, corticosteroid use, and catabolic states, limiting its diagnostic utility. 3
What Actually Works: The Correct Diagnostic Approach
Primary Diagnostic Criteria for AKI
AKI is defined by absolute changes in serum creatinine, not ratios: 4
- Increase in sCr ≥0.3 mg/dL (≥26.5 μmol/L) within 48 hours, OR
- Percentage increase in sCr ≥50% from baseline within 7 days
Establishing Baseline Creatinine
Use the most recent creatinine value within the previous 3 months as baseline when available. 4
- If multiple values exist within 3 months, use the one closest to admission time. 4
- If no prior value exists, use admission creatinine as baseline. 4
- Do not use reverse MDRD calculations to estimate baseline, as this formula is inaccurate in cirrhosis and adds further bias. 4
Superior Diagnostic Tools for Prerenal vs Intrinsic AKI
Fractional excretion of sodium (FeNa) is more useful than BUN/Cr ratio, though still imperfect: 3
- FeNa <1% suggests prerenal causes (100% sensitivity but only 14% specificity in cirrhosis). 3
- FeNa of 0.8% supports prerenal etiology, though borderline. 3
- FeNa is falsely elevated by diuretics, so interpret cautiously if patient recently received loop or thiazide diuretics. 3
Fractional excretion of urea (FEUrea) performs better in specific populations: 3
- FEUrea <28% has 75% sensitivity and 83% specificity for hepatorenal syndrome versus other AKI causes. 3
- More reliable than FeNa when diuretics have been administered. 3
Urine microscopy should be performed routinely in all AKI cases, as it can definitively establish diagnosis: 3, 5
- Muddy brown granular casts are pathognomonic for acute tubular necrosis. 3
- RBC casts indicate glomerulonephritis or vasculitis requiring immediate nephrology consultation. 3
- Hyaline casts or bland sediment support prerenal etiology. 3
Management Algorithm for AKI (Regardless of BUN/Cr Ratio)
Immediate Actions for All AKI Patients
Withdraw all nephrotoxic medications immediately: 4, 3, 5
- NSAIDs, ACE inhibitors, ARBs, aminoglycosides, contrast agents. 4, 3, 5
- Review all medications including over-the-counter drugs. 4
- Hold or reduce diuretics. 4, 3
Volume Assessment and Resuscitation
The critical decision is distinguishing true hypovolemia from volume overload, as indiscriminate fluid administration worsens outcomes: 5
- Clinical signs of hypovolemia: hypotension, tachycardia, poor skin turgor, recent vomiting/diarrhea/hemorrhage. 3, 5
- Clinical signs of volume overload: jugular venous distension, pulmonary edema, peripheral edema. 5
For clinically suspected hypovolemia, give albumin 1 g/kg/day (maximum 100 g/day) for 2 consecutive days: 3
- Monitor closely for volume overload and pulmonary edema. 3
- Alternatively, use balanced crystalloids or blood products if hemorrhage present. 4
Staging and Monitoring
Stage AKI to guide intensity of management: 4
- Stage 1: sCr increase ≥0.3 mg/dL or 1.5-2× baseline
- Stage 2: sCr increase >2-3× baseline
- Stage 3: sCr increase >3× baseline OR sCr ≥4.0 mg/dL with acute increase ≥0.3 mg/dL OR initiation of RRT
Monitor creatinine every 2-4 days during hospitalization. 3, 5
Check daily for life-threatening complications: 3, 5
- Potassium >6.0 mEq/L (most immediately dangerous). 3, 5
- Severe metabolic acidosis. 3
- Oliguria (<0.5 mL/kg/h for >6 hours). 5
Critical Pitfalls to Avoid
Do not rely on BUN/Cr ratio alone to guide management decisions. 1, 2
Do not use eGFR for medication dosing in AKI—it overestimates true renal function in non-steady state conditions. 5
Do not assume "prerenal" AKI has a benign prognosis—even patients who respond to volume expansion remain at increased long-term risk for recurrent AKI, CKD progression, cardiovascular events, and mortality. 3, 5
Post-Discharge Follow-Up
All AKI patients require close follow-up regardless of apparent recovery: 3, 5