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

Initial Workup for Suspected Acute Kidney Injury (AKI)

The initial workup for suspected AKI should include assessment of the underlying etiology (prerenal, intrinsic renal, or postrenal), measurement of serum creatinine, urinalysis, evaluation of volume status, and identification of potential nephrotoxic exposures to guide appropriate management and prevent further kidney damage. 1, 2

Definition and Classification

• AKI is characterized by a sudden decrease in kidney function, manifested by an increase in serum creatinine level with or without reduced urine output 2
• According to the Acute Disease Quality Initiative (ADQI), persistent AKI is characterized by the continuance of AKI beyond 48 hours from onset, while complete reversal within 48 hours indicates rapid reversal 1
• AKI that persists for ≥7 days progresses to acute kidney disease (AKD), which represents the continuum between AKI and chronic kidney disease (CKD) 1

Initial Laboratory Evaluation

• Serum creatinine measurement to establish baseline and current kidney function 2
• Complete blood count to assess for evidence of hemolysis, infection, or other systemic conditions 2
• Comprehensive urinalysis with microscopic examination to identify hematuria, proteinuria, casts, or crystals that may indicate specific etiologies 2
• Calculation of fractional excretion of sodium (FENa) to help differentiate between prerenal and intrinsic causes 2
• Assessment of electrolytes, particularly potassium, to identify life-threatening abnormalities requiring immediate intervention 2

Imaging Studies

• Renal ultrasonography should be performed in most patients with AKI, particularly in older men, to rule out urinary tract obstruction (postrenal causes) 2
• Ultrasound can also assess kidney size, echogenicity, and identify structural abnormalities 2

Etiologic Classification and Focused Assessment

Prerenal Causes

• Review medication history for diuretics, ACE inhibitors, ARBs, NSAIDs, and other potentially nephrotoxic drugs 1
• Assess volume status through physical examination (skin turgor, mucous membranes, jugular venous pressure, edema) 2
• Evaluate for conditions causing decreased renal perfusion (heart failure, liver disease, sepsis) 1

Intrinsic Renal Causes

• Assess for exposure to nephrotoxic medications or contrast media 2
• Evaluate for systemic conditions that can cause glomerulonephritis or vasculitis 2
• Consider rhabdomyolysis by checking creatine kinase levels if appropriate 3

Postrenal Causes

• Assess for symptoms of urinary obstruction (decreased urine output, distended bladder) 2
• Ultrasonography to identify hydronephrosis or hydroureter 2

Special Considerations for Cirrhotic Patients

• In patients with cirrhosis and ascites, a specific algorithm should be followed based on AKI staging 1:
  • Stage 1 AKI: Review medications, withdraw nephrotoxic drugs and diuretics, expand plasma volume if hypovolemic, and treat infections if present 1
  • Stages 2-3 AKI: Withdraw diuretics and administer albumin (1 g/kg for 2 days, maximum 100g/day) 1

Initial Management

• Remove potential nephrotoxic agents and avoid further exposure to nephrotoxins 1
• Optimize hemodynamics and ensure adequate renal perfusion 1
• Use isotonic crystalloids rather than colloids for initial volume expansion in hypovolemic patients 1
• Identify and treat underlying causes (infections, obstruction) 1
• Monitor for complications such as fluid overload, acidosis, and hyperkalemia that may require renal replacement therapy 1
• Consider nephrology consultation if etiology is unclear or specialized care is needed 1

Monitoring and Follow-up

• Close monitoring of kidney function, urine output, and electrolytes during the acute phase 1
• For patients who recover from AKI, follow-up is recommended to assess for development of CKD, particularly in high-risk patients (severe AKI requiring RRT or persistent dysfunction at discharge) 1

Common Pitfalls to Avoid

• Relying solely on serum creatinine for diagnosis, as it may lag behind actual kidney injury 4
• Failing to recognize and discontinue nephrotoxic medications promptly 1
• Overlooking postrenal causes that may be readily reversible with decompression 2
• Assuming a single etiology when AKI is often multifactorial 3
• Delaying appropriate volume resuscitation in hypovolemic patients 1