What is Acute Kidney Injury (AKI)?

Acute Kidney Injury (AKI) Definition

Acute kidney injury (AKI) is defined by the Kidney Disease Improving Global Outcomes (KDIGO) guidelines as an increase in serum creatinine of ≥0.3 mg/dL within 48 hours, or an increase in serum creatinine ≥1.5 times the baseline value within 7 days, or a decrease in urine output <0.5 mL/kg/hour for >6 hours. 1

AKI Staging System

AKI is classified into three stages based on severity:

Stage	Creatinine Criterion	Urine Output Criterion
1	Increase ≥0.3 mg/dL in 48h or increase of 1.5-1.9 times baseline in 7 days	<0.5 mL/kg/h for >6h
2	Increase of 2.0-2.9 times baseline	<0.5 mL/kg/h for >12h
3	Increase ≥3.0 times baseline, or increase to ≥4.0 mg/dL, or initiation of renal replacement therapy	<0.3 mL/kg/h for ≥24h or anuria for ≥12h

Pathophysiology and Classification

AKI represents a sudden loss of excretory kidney function 2 and can be conceptually classified into three categories:

1. Prerenal AKI: Caused by decreased renal perfusion (e.g., hypovolemia, hypotension)
2. Intrarenal AKI: Direct damage to kidney parenchyma
3. Postrenal AKI: Urinary tract obstruction

The most common intrarenal cause is acute tubular necrosis (ATN), which can result from:

• Ischemia
• Nephrotoxic medications
• Contrast agents
• Sepsis

Distinguishing Features

AKI is part of a spectrum of kidney dysfunction:

• AKI: Abrupt decrease in kidney function occurring over 7 days or less 3
• Acute Kidney Disease (AKD): Kidney damage or GFR <60 ml/min per 1.73 m² for <3 months 3
• Chronic Kidney Disease (CKD): Kidney damage or GFR <60 ml/min per 1.73 m² for >3 months 3

Clinical Significance and Outcomes

AKI is not merely a temporary condition but has significant implications:

• Occurs in approximately 7-18% of hospitalized patients and up to 50% of ICU patients 3
• Associated with increased mortality (particularly with higher AKI stages) 1
• Significantly increases risk of developing CKD 2
• Increases risk of cardiovascular events and future mortality 1

Evaluation of Suspected AKI

Initial laboratory workup should include:

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

Imaging:

• Renal ultrasound to rule out obstruction 1

Management Principles

1. Identify and remove potential causes:

   • Discontinue nephrotoxic medications (NSAIDs, aminoglycosides, ACE inhibitors/ARBs) 1
   • Treat underlying conditions (infections, GI bleeding, etc.)

2. Volume management:

   • For hypovolemic patients: administer isotonic crystalloids rather than colloids 1
   • Avoid excessive fluid administration in euvolemic or hypervolemic patients 1

3. Maintain adequate renal perfusion:

   • Ensure adequate mean arterial pressure 1

4. Consider renal replacement therapy for:

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

Follow-up and Monitoring

• Evaluate kidney function 3 months after an AKI episode to screen for development of CKD 1
• Adjust medications as kidney function recovers
• Higher risk patients (Stage 3 AKI, baseline CKD, incomplete recovery) require closer follow-up 1

Common Pitfalls to Avoid

1. Relying solely on serum creatinine: Creatinine is a late marker of kidney injury and may not rise until significant kidney function is lost.

2. Delayed recognition: Early identification of AKI is crucial for preventing progression and complications.

3. Inadequate drug dosing adjustment: Failure to adjust medication doses in AKI can lead to toxicity.

4. Overlooking drug-induced AKI: Many commonly used medications can cause or worsen AKI, including NSAIDs, aminoglycosides, and contrast agents 3.

5. Inappropriate fluid management: Both under-resuscitation and fluid overload can worsen outcomes in AKI.