Workup of Acute Kidney Injury
Begin with immediate confirmation of AKI using KDIGO criteria: serum creatinine increase ≥0.3 mg/dL within 48 hours OR ≥50% increase within 7 days OR urine output <0.5 mL/kg/h for 6 hours, then rapidly categorize the etiology as prerenal, intrinsic renal, or postrenal to guide targeted intervention. 1
Initial Diagnostic Steps
Establish Baseline and Stage AKI
- Obtain baseline creatinine: Use a value from the previous 3 months when available; if multiple values exist, use the one closest to admission 1
- If no prior creatinine available: Use admission creatinine as baseline, recognizing this may underdiagnose community-acquired AKI 1
- Stage the AKI immediately using KDIGO criteria 1:
- Stage 1: SCr increase 1.5-1.9× baseline OR ≥0.3 mg/dL increase OR urine output <0.5 mL/kg/h for 6-12 hours
- Stage 2: SCr increase 2.0-2.9× baseline OR urine output <0.5 mL/kg/h for ≥12 hours
- Stage 3: SCr increase ≥3.0× baseline OR SCr ≥4.0 mg/dL with acute rise ≥0.3 mg/dL OR initiation of RRT OR urine output <0.3 mL/kg/h for ≥24 hours or anuria for ≥12 hours
Focused History
- Identify nephrotoxic exposures: NSAIDs, ACE inhibitors/ARBs, aminoglycosides, contrast agents, chemotherapy agents 1
- Recent procedures: Cardiac catheterization, surgery (especially cardiac), imaging with contrast 1, 2
- Volume status indicators: Vomiting, diarrhea, bleeding, decreased oral intake, diuretic use 3, 4
- Systemic illness symptoms: Fever, rash, joint pain, hematuria suggesting glomerulonephritis or vasculitis 3
- Obstructive symptoms: Hesitancy, decreased stream, suprapubic pain, known prostatic disease in older men 2, 3
Physical Examination Priorities
- Volume assessment: Jugular venous pressure, mucous membranes, skin turgor, orthostatic vital signs, peripheral edema 3, 4
- Hemodynamic status: Blood pressure, heart rate, signs of shock or sepsis 2
- Skin examination: Rashes suggesting vasculitis, livedo reticularis indicating atheroembolic disease 3
- Bladder palpation: Assess for urinary retention 2
Laboratory Workup
Essential Initial Tests
- Complete metabolic panel including creatinine, BUN, electrolytes
- Complete blood count
- Calculate BUN/creatinine ratio (>20:1 suggests prerenal etiology)
Urinalysis with microscopy 2, 3:
- Prerenal: Hyaline casts, high specific gravity (>1.020)
- Acute tubular necrosis: Muddy brown granular casts, renal tubular epithelial cells
- Glomerulonephritis: Dysmorphic RBCs, RBC casts, proteinuria
- Interstitial nephritis: WBCs, WBC casts, eosinophiluria
Fractional excretion of sodium (FENa) 3:
- FENa <1% suggests prerenal azotemia (if not on diuretics)
- FENa >2% suggests intrinsic renal disease
- Use fractional excretion of urea if patient is on diuretics
Additional Testing Based on Clinical Context
Renal ultrasonography: Perform in most patients, particularly older men, to exclude obstruction; assess kidney size and echogenicity 2, 3
For suspected glomerulonephritis or vasculitis 2:
- Complement levels (C3, C4)
- Antinuclear antibody, anti-dsDNA
- ANCA panel
- Anti-GBM antibodies
- Serum and urine protein electrophoresis
For suspected rhabdomyolysis: Creatine kinase, urine myoglobin 2
Categorization of AKI Etiology
Prerenal (Hypoperfusion)
- Clinical indicators: Volume depletion, heart failure, cirrhosis, sepsis 3, 4
- Laboratory findings: BUN/Cr >20:1, FENa <1%, concentrated urine 3
- Management priority: Fluid resuscitation with isotonic crystalloid; avoid nephrotoxins 2
Intrinsic Renal
- Acute tubular necrosis: Most common in hospitalized patients; history of ischemia, sepsis, or nephrotoxin exposure 2, 3
- Acute interstitial nephritis: Recent medication exposure (especially antibiotics, PPIs, NSAIDs); fever, rash, eosinophiluria 3
- Glomerulonephritis: Hematuria with RBC casts, significant proteinuria 3
- Vascular: Atheroembolic disease after vascular procedure, thrombotic microangiopathy 2
Postrenal (Obstruction)
- Risk factors: Older male with prostatic hypertrophy, known malignancy, nephrolithiasis, single functioning kidney 2, 3
- Diagnosis: Renal ultrasonography showing hydronephrosis 2
- Management: Urgent urological consultation for relief of obstruction 2
Critical Management Considerations
Nephrotoxin Management
Discontinue immediately if causal 1:
- NSAIDs
- Aminoglycosides
- Non-essential nephrotoxic agents
Hold ACE inhibitors/ARBs during acute phase 1:
- Restart only after GFR stabilizes and volume status optimized
- Failure to restart post-operatively associated with increased 30-day mortality from hypertensive rebound 1
Adjust all medication doses for renal function 1
Minimize duration and dose of necessary nephrotoxins 1
When to Consult Nephrology
Immediate consultation indicated for 2:
- Stage 3 AKI or inadequate response to initial management
- AKI without clear etiology despite workup
- Preexisting stage 4 or higher CKD
- Need for renal replacement therapy consideration
- Suspected glomerulonephritis requiring biopsy
- Electrolyte abnormalities refractory to treatment (hyperkalemia >6.5 mEq/L, severe acidosis)
Monitoring During AKI Episode
- Measure serum creatinine at appropriate intervals based on clinical context and AKI stage 1
- Monitor for progression through AKI stages, as this strongly correlates with mortality 1
- Assess for recovery: Regression to lower stage or return of creatinine to within 0.3 mg/dL of baseline 1
- Consider fluid status: Fluid overload affects creatinine distribution and is associated with increased mortality 1
Common Pitfalls
- Using estimated GFR alone: Creatinine changes are more sensitive for acute changes; eGFR formulas are inaccurate in AKI 1
- Ignoring urine output criteria: When creatinine unavailable, urine output criteria should be used for diagnosis 1
- Assuming "prerenal" is benign: Volume-unresponsive "prerenal" AKI has similar mortality to intrinsic AKI 4
- Delaying obstruction evaluation: Renal ultrasound should be performed early, especially in high-risk patients 2, 3
- Continuing nephrotoxins unnecessarily: Drugs account for 20-25% of AKI cases; systematic review and discontinuation is essential 1