What is the diagnosis and management for a patient with Acute Kidney Injury (AKI) with a Fractional Excretion of Sodium (FeNa) of 0.8%, Blood Urea Nitrogen (BUN) of 57, and creatinine of 3.36?

Diagnosis: Prerenal Acute Kidney Injury

Based on your FeNa of 0.8%, BUN:Cr ratio of 17:1, and elevated creatinine, this presentation is most consistent with prerenal AKI (volume depletion or decreased effective arterial blood volume), though the FeNa is borderline and requires careful clinical correlation. 1, 2

Interpretation of Laboratory Values

FeNa Analysis

• Your FeNa of 0.8% falls just below the traditional 1% cutoff for prerenal AKI 1, 2
• FeNa <1% suggests prerenal causes including volume depletion, with the kidney appropriately conserving sodium in response to decreased perfusion 1, 2
• However, FeNa has important limitations: in cirrhosis, FeNa <1% has 100% sensitivity but only 14% specificity for prerenal causes, meaning many patients with intrinsic kidney disease can also have low FeNa 1
• If the patient has received diuretics, FeNa becomes unreliable - diuretics increase urinary sodium excretion and can falsely elevate FeNa even in prerenal states 3, 4

BUN:Creatinine Ratio

• Your BUN:Cr ratio of 17:1 (57÷3.36) is at the lower end of what typically suggests prerenal azotemia 2
• Classic prerenal AKI usually shows BUN:Cr ratio >20:1, though this can be affected by protein intake, GI bleeding, and catabolic states 2
• The relatively modest elevation suggests either early prerenal AKI or a mixed picture 2

Consider Fractional Excretion of Urea (FEUrea)

• FEUrea is superior to FeNa if diuretics have been administered 3, 4
• FEUrea <35% indicates prerenal AKI with 89% sensitivity in diuretic-treated patients, compared to only 48% for FeNa <1% 3
• FEUrea remains low in prerenal states (typically 25-28%) regardless of diuretic use, while it rises to >50% in acute tubular necrosis 3, 4
• If diuretics were given, obtain FEUrea immediately to clarify the diagnosis 3, 4

Differential Diagnosis Based on Your Values

Most Likely: Prerenal AKI (Volume Depletion)

• FeNa 0.8% supports this, though borderline 1, 2
• Look for: recent diuretic use, poor oral intake, vomiting, diarrhea, hemorrhage, third-spacing (cirrhosis, heart failure, sepsis) 1
• Should respond to volume expansion with return of creatinine to within 0.3 mg/dL of baseline 1

Alternative: Early Acute Tubular Necrosis (ATN)

• Low FeNa can occur in early ATN if tested within 1-2 days of onset - 39% of ATN patients have FeNa <1% when tested early 5
• FeNa typically converts to >1% on repeat testing as ATN evolves 5
• Look for: nephrotoxin exposure (NSAIDs, aminoglycosides, contrast), prolonged hypotension, sepsis 6
• Urine microscopy showing muddy brown casts or renal tubular epithelial cells strongly suggests ATN 6

Consider: Hepatorenal Syndrome (if cirrhosis present)

• HRS-AKI typically shows FeNa <1% but FeNa has very poor specificity (14%) in cirrhotic patients 1
• FEUrea <28% has better discrimination (75% sensitivity, 83% specificity) for HRS versus non-HRS causes 1
• Requires exclusion of volume depletion, nephrotoxins, and structural kidney disease 1

Immediate Management Algorithm

Step 1: Remove Risk Factors (All AKI Patients)

• Withdraw all nephrotoxic drugs immediately: NSAIDs, ACE inhibitors, ARBs, aminoglycosides, contrast agents 1
• Hold or reduce diuretics 1
• Review all medications including over-the-counter drugs 1

Step 2: Assess Volume Status and Expand if Indicated

• If clinical hypovolemia suspected, give albumin 1 g/kg/day (maximum 100 g/day) for 2 consecutive days 1
• Alternative: crystalloids or blood products if hemorrhage present 1
• Monitor carefully for volume overload and pulmonary edema - this is a critical complication of albumin therapy 1

Step 3: Rule Out Infection

• Obtain cultures (blood, urine) and chest X-ray 1
• If cirrhosis: perform diagnostic paracentesis to exclude spontaneous bacterial peritonitis 1
• Start empiric antibiotics if infection strongly suspected 1

Step 4: Obtain Urine Microscopy

• Muddy brown casts or renal tubular epithelial cells indicate ATN 6
• Bland sediment supports prerenal AKI or HRS 1
• Microscopy significantly improves prognostic accuracy beyond clinical assessment alone 6

Step 5: Assess Response at 48 Hours

• Full response: creatinine returns to within 0.3 mg/dL of baseline - confirms prerenal AKI 1
• No response or progression: suggests ATN, HRS, or other intrinsic kidney disease 1
• If no response and creatinine ≥1.5 mg/dL in cirrhosis, consider vasoconstrictor therapy (terlipressin or norepinephrine) plus albumin for HRS-AKI 1

Critical Pitfalls to Avoid

• Do not rely solely on FeNa if diuretics were given - obtain FEUrea instead 3, 4
• Do not assume low FeNa always means prerenal - early ATN and HRS can also show FeNa <1% 1, 5
• Do not overlook timing - FeNa measured early in AKI course may be falsely low and convert to high values within days 5
• Do not give excessive albumin without monitoring - pulmonary edema is a life-threatening complication 1
• In cirrhosis, do not use FeNa alone for diagnosis - it has poor specificity and FEUrea is superior 1

Prognosis

• Patients with prerenal AKI who respond to volume expansion have better outcomes than those with ATN 6
• Even after "recovery," all AKI survivors remain at increased long-term risk for recurrent AKI, CKD progression, cardiovascular events, and mortality 1
• Close follow-up is mandatory: check creatinine every 2-4 days during hospitalization and every 2-4 weeks for 6 months post-discharge 1