What is the definition and treatment of Acute Kidney Injury (AKI)?

Definition and Treatment of Acute Kidney Injury (AKI)

Definition of AKI

Acute kidney injury (AKI) is defined as an increase in serum creatinine ≥0.3 mg/dL within 48 hours, or an increase in serum creatinine ≥1.5 times baseline within 7 days, or urine output <0.5 mL/kg/h for 6 hours or more, according to the KDIGO criteria. 1

AKI is staged according to severity:

Stage	Serum Creatinine Criterion	Urine Output Criterion
1	Increase ≥0.3 mg/dL within 48h or 1.5-1.9 times baseline	<0.5 mL/kg/h for 6-12h
2	2.0-2.9 times baseline	<0.5 mL/kg/h for ≥12h
3	≥3.0 times baseline or ≥4.0 mg/dL or RRT initiation	<0.3 mL/kg/h for ≥24h or anuria for ≥12h

It's important to note that AKI represents a continuum with acute kidney disease (AKD), which is defined as kidney damage persisting between 7 and 90 days after an AKI initiating event 2. Persistent AKI is characterized by the continuance of AKI beyond 48 hours from onset, while complete reversal within 48 hours characterizes rapid reversal of AKI 2.

Classification of AKI

AKI can be classified into three main categories based on the underlying pathophysiology:

1. Prerenal AKI: Caused by decreased kidney perfusion (hypovolemia, heart failure, sepsis)
2. Intrinsic renal AKI: Direct damage to kidney structures (acute tubular necrosis, glomerulonephritis)
3. Postrenal AKI: Obstruction to urinary flow (stones, tumors, prostatic hypertrophy)

Treatment of AKI

1. Initial Management

• Remove risk factors: Immediately withdraw nephrotoxic drugs, vasodilators, and NSAIDs 2, 1
• Reduce or withdraw diuretics in all AKI patients 2, 1
• Fluid resuscitation: Use isotonic crystalloids rather than colloids for initial volume expansion 1
  • Normal saline or balanced crystalloid solutions are preferred first-line options
  • Avoid hydroxyethyl starches which increase AKI incidence
  • Consider albumin 1 g/kg/day for two consecutive days in specific subgroups (e.g., cirrhosis with ascites) 2, 1

2. Hemodynamic Support

• Vasopressors: Use in conjunction with fluids in patients with vasomotor shock
  • Norepinephrine is preferred over dopamine as first-line vasopressor 1
• Monitor fluid status closely to avoid pulmonary edema risk 2
• Target blood pressure: Higher blood pressure targets are often needed in AKI

3. Supportive Care

• Nutrition: Provide 20-30 kcal/kg/day total energy intake 1
  • Protein recommendations: 0.8-1.0 g/kg/day in noncatabolic patients without dialysis
  • 1.0-1.5 g/kg/day in patients on renal replacement therapy (RRT)
  • Up to 1.7 g/kg/day in patients on continuous RRT and hypercatabolic patients
• Prefer enteral nutrition when possible 1
• Medication management: Adjust doses based on estimated GFR 1

4. Monitoring

• Daily monitoring of serum creatinine, BUN, electrolytes, fluid balance, and hemodynamic parameters 1
• Closer monitoring for patients with heart failure or cirrhosis 1
• Monitor for signs of renal recovery: Increasing urine output, decreasing serum creatinine, improved electrolyte balance

5. Renal Replacement Therapy (RRT)

RRT should be considered when 1:

• Severe metabolic acidosis persists
• Hyperkalemia is refractory to medical management
• Volume overload remains unresponsive to conservative measures
• Uremic symptoms develop

The optimal timing of RRT initiation remains unclear and is an area of active investigation 3. The decision should be individualized based on the clinical context.

6. Special Considerations for AKI in Cirrhosis

For patients with cirrhosis and AKI, follow this algorithmic approach 2:

1. Stage 1 AKI:

   • Review medications, withdraw diuretics and nephrotoxic drugs
   • Plasma volume expansion with albumin 1 g/kg for two consecutive days

2. Stage 2-3 AKI or progression from Stage 1:

   • Continue albumin
   • If no response after 2 days and patient meets hepatorenal syndrome (HRS) criteria, initiate vasoconstrictors with albumin

3. Monitor response:

   • Complete response: Return of serum creatinine to <0.3 mg above baseline
   • Partial response: Reduction in serum creatinine but still >0.3 mg above baseline

Prevention of AKI

• Risk factor identification: Recognize high-risk patients (older age, sepsis, hypovolemia, contrast exposure, diabetes, pre-existing CKD)
• Avoid nephrotoxins: Discontinue potentially nephrotoxic medications
• Optimize volume status: Ensure adequate hydration, especially before contrast procedures
• Monitor renal function: Regular assessment of serum creatinine in high-risk patients

Long-term Follow-up

Even a single episode of AKI increases the risk of cardiovascular disease, chronic kidney disease, and death 4. Therefore, patients who have experienced AKI should receive appropriate follow-up care based on AKI severity and risk factors for progression to chronic kidney disease 1.

Common Pitfalls to Avoid

1. Overreliance on serum creatinine: In patients with cirrhosis, serum creatinine often overestimates GFR due to decreased muscle mass, increased tubular secretion, and dilution effects 2

2. Excessive fluid administration: Volume overload in AKI is associated with adverse outcomes; balance the need for adequate perfusion against the risk of fluid overload 1

3. Delayed recognition of AKI: Early identification and management are critical for improving outcomes; monitor high-risk patients closely

4. Failure to identify and address the underlying cause: AKI is often multifactorial; a thorough evaluation of potential causes is essential for effective management

5. Inappropriate continuation of nephrotoxic medications: Promptly review and adjust medication regimens in patients with AKI