What is the initial workup and management for a patient presenting with Acute Kidney Injury (AKI)?

Initial Workup and Management of Acute Kidney Injury (AKI)

The initial workup for AKI should include serum creatinine, blood urea nitrogen, complete blood count, electrolytes with anion gap, urinalysis with microscopy, and urine chemistry, followed by immediate management steps including discontinuation of nephrotoxic medications, diuretics, and appropriate volume expansion based on the underlying cause. 1

Definition and Diagnosis of AKI

AKI is diagnosed when one of the following criteria is met:

• Increase in serum creatinine by ≥0.3 mg/dL within 48 hours
• Increase in serum creatinine by ≥50% from baseline within 7 days
• Urine output reduced below 0.5 mL/kg/h for >6 hours 2, 1

AKI Staging

Stage	Creatinine Increase	Urine Output
1	≥0.3 mg/dL or 1.5-1.9× baseline	<0.5 mL/kg/h for 6-12h
2	2.0-2.9× baseline	<0.5 mL/kg/h for ≥12h
3	≥3.0× baseline or creatinine >4 mg/dL	<0.3 mL/kg/h for ≥24h or anuria for ≥12h

Initial Laboratory Workup

1. Essential laboratory tests:

   • Serum creatinine and blood urea nitrogen (BUN)
   • Complete blood count with differential
   • Serum electrolytes with calculated anion gap
   • Urinalysis with microscopy
   • Urine chemistry (sodium, creatinine, urea) 1

2. Imaging:

   • Renal ultrasound to rule out obstruction 1

3. Additional tests based on clinical suspicion:

   • Blood cultures if infection suspected
   • Diagnostic paracentesis in patients with cirrhosis to rule out spontaneous bacterial peritonitis 2

Classification of AKI Types

Determine the type of AKI based on clinical presentation and laboratory findings:

1. Pre-renal AKI (most common):

   • Urine Na+ <20 mEq/L
   • FENa <1%
   • Urine osmolality >500 mOsm/kg
   • Bland urinary sediment 1

2. Intrinsic AKI:

   • Acute tubular necrosis (ATN): muddy brown casts, renal tubular epithelial cells
   • Acute interstitial nephritis: white cell casts, eosinophiluria
   • Glomerulonephritis: red cell casts, dysmorphic RBCs 1

3. Post-renal AKI:

   • Hydronephrosis on ultrasound
   • Uncommon in general population, rare in cirrhotic patients 2

4. Hepatorenal syndrome (HRS-AKI) in cirrhotic patients:

   • Functional renal failure that persists despite volume repletion
   • No response to albumin challenge
   • Absence of shock, nephrotoxic drugs, or intrinsic kidney disease 2

Immediate Management Steps

1. Remove precipitating factors:

   • Discontinue all nephrotoxic medications (NSAIDs, aminoglycosides, contrast agents) 2, 1
   • Hold diuretics and adjust or discontinue beta-blockers 2
   • Hold ACE inhibitors and ARBs 1

2. Volume assessment and management:

   • For hypovolemia: Use isotonic crystalloids rather than colloids for initial volume expansion 2
   • For AKI Stage 2-3: Consider volume expansion with albumin (1g/kg) for 48 hours 1
   • For patients with cirrhosis and AKI: Administer albumin 1 g/kg/day (maximum 100 g) for two consecutive days 2

3. Treat underlying infections:

   • Perform thorough infection workup (blood cultures, urine cultures, chest X-ray)
   • Start appropriate antibiotics when infection is suspected 2

4. Hemodynamic support:

   • Use vasopressors in conjunction with fluids in patients with vasomotor shock 2
   • Target protocol-based management of hemodynamic parameters 2

5. Monitoring:

   • Daily serum creatinine and electrolytes
   • Strict intake and output monitoring
   • Daily weights 1

Special Considerations for Cirrhotic Patients

For patients with cirrhosis and AKI:

1. Stage 1 AKI:

   • Close monitoring
   • Remove risk factors (nephrotoxic drugs, vasodilators, NSAIDs)
   • Reduce/withdraw diuretics
   • Treat infections when diagnosed
   • Plasma volume expansion for hypovolemia 2

2. Stage 2-3 AKI:

   • Withdraw diuretics completely
   • Volume expansion with albumin (1 g/kg) for 2 days
   • If no response and HRS-AKI is diagnosed, consider vasoconstrictors with albumin 2

Indications for Renal Replacement Therapy

Consider RRT for:

• Refractory hyperkalemia
• Volume overload unresponsive to diuretics
• Severe metabolic acidosis
• Uremic symptoms
• Certain toxin ingestions 1

Follow-up and Monitoring

• Evaluate kidney function 3 months after AKI episode
• Monitor for development of chronic kidney disease
• Adjust medications as kidney function recovers 1, 3

Common Pitfalls to Avoid

• Excessive fluid administration without proper assessment of volume status can lead to pulmonary edema 1
• Delayed recognition of specific AKI phenotypes (e.g., hepatorenal syndrome) can lead to inadequate treatment 1
• Failure to discontinue nephrotoxic medications can worsen kidney injury 1

By following this systematic approach to AKI diagnosis and management, you can improve outcomes and reduce the risk of progression to chronic kidney disease.