What is the management approach for a patient with Acute Kidney Injury (AKI)?

Management of Acute Kidney Injury

Immediately discontinue all nephrotoxic medications (NSAIDs, ACE inhibitors, ARBs, aminoglycosides, diuretics), assess volume status, identify and treat the underlying cause, and monitor serum creatinine and electrolytes closely. 1, 2, 3

Diagnosis and Staging

• Define AKI using KDIGO criteria: serum creatinine increase ≥0.3 mg/dL within 48 hours, increase ≥50% from baseline within 7 days, or urine output <0.5 mL/kg/hour for 6 hours 4, 1, 3
• Stage the severity (Stage 1-3) using KDIGO criteria, with Stage 3 being most severe and requiring intensive intervention 1, 3

Determine the Underlying Cause

Classify AKI as prerenal (volume responsive), intrinsic renal (acute tubular necrosis), or postrenal (obstructive) through systematic evaluation 4, 2, 3

Diagnostic Workup

• Obtain detailed history focusing on recent medication exposures (NSAIDs, aminoglycosides, contrast agents), volume losses (vomiting, diarrhea, bleeding), and systemic illnesses (sepsis, heart failure) 2, 3
• Perform urinalysis with microscopy to differentiate causes: muddy brown casts suggest acute tubular necrosis, red cell casts indicate glomerulonephritis, white cell casts suggest interstitial nephritis 2, 3
• Check urine chemistry: fractional excretion of sodium <1% suggests prerenal AKI, while >2% indicates intrinsic renal disease 2, 3
• Obtain renal ultrasound immediately to rule out obstructive uropathy, especially in older males with prostatic symptoms 2, 3
• Conduct rigorous infection search in all patients: blood cultures, urine cultures, chest radiograph, and diagnostic paracentesis if ascites present 4, 2, 3

Immediate Interventions (All Stages)

Medication Management

• Stop all nephrotoxic agents immediately: NSAIDs, aminoglycosides, contrast agents 1, 2, 3
• Hold ACE inhibitors, ARBs, and diuretics until volume status is optimized 4, 2, 3
• Discontinue or adjust nonselective beta-blockers in cirrhotic patients 4, 3
• Adjust all medication dosages based on current estimated GFR to prevent toxicity 2, 3

Volume and Hemodynamic Management

• Assess volume status clinically: examine for jugular venous distension, peripheral edema, pulmonary crackles, orthostatic hypotension 2, 3
• For hypovolemic/prerenal AKI: administer isotonic crystalloids (normal saline or lactated Ringer's) with close monitoring; avoid colloids 1, 2, 5
• Maintain mean arterial pressure >65 mmHg to ensure adequate renal perfusion using vasopressors if needed 1
• Monitor strict input/output and avoid volume overload, which is associated with worse outcomes 2, 5

Stage-Specific Management

Stage 1 AKI

• Monitor serum creatinine and electrolytes daily 2, 3
• Continue nephrotoxic medication avoidance and volume optimization 3
• Reassess medication dosing requirements as renal function changes 3

Stage 2 AKI

• Intensify monitoring to every 4-6 hours for creatinine, BUN, and electrolytes 1, 2, 3
• Increase frequency of clinical assessments for signs of fluid overload (peripheral edema, pulmonary congestion) 2, 3
• Prepare for potential need for renal replacement therapy 3

Stage 3 AKI

• Monitor electrolytes, BUN, and creatinine every 4-6 hours 1, 2, 3
• Initiate urgent renal replacement therapy (RRT) for: severe oliguria unresponsive to fluid resuscitation, refractory hyperkalemia, severe metabolic acidosis (pH <7.1), volume overload unresponsive to diuretics, uremic complications (encephalopathy, pericarditis), or certain toxin ingestions 1, 3
• Reassess need for continued RRT daily 1, 2

Special Considerations for Cirrhosis Patients

Cirrhotic patients with AKI require specific management due to high risk of hepatorenal syndrome 4, 3

• Perform diagnostic paracentesis in all cirrhotic patients with AKI to evaluate for spontaneous bacterial peritonitis 4, 2, 3
• Hold diuretics and nonselective beta-blockers 4, 3
• Administer albumin 1 g/kg/day (maximum 100 g/day) for 2 days if serum creatinine doubles from baseline 4, 1, 2, 3
• For hepatorenal syndrome-AKI (HRS-AKI): give albumin 1 g/kg IV on day 1, then 20-40 g daily, plus vasoactive agents (terlipressin preferred; or octreotide plus midodrine; or norepinephrine if others unavailable) 1, 2, 3
• Start broad-spectrum antibiotics whenever infection is strongly suspected 4, 2

Prevention Strategies

Identify high-risk patients: advanced age, pre-existing chronic kidney disease, diabetes mellitus, heart failure, sepsis, recent contrast exposure 3, 6

• Avoid NSAIDs entirely in at-risk patients 4, 3
• Avoid excessive or unmonitored diuretic use 4, 3
• Provide albumin replacement (8 g per liter removed) with large-volume paracentesis in cirrhotic patients 4, 3
• Ensure adequate hydration before contrast procedures 1, 3
• Implement pharmacist-led medication review programs to identify nephrotoxic exposures 3

Monitoring and Complications Management

• Monitor for hyperkalemia: obtain ECG if potassium >6.0 mEq/L and treat urgently with calcium gluconate, insulin/dextrose, and sodium polystyrene sulfonate 1, 2
• Watch for metabolic acidosis: consider sodium bicarbonate if pH <7.2 and bicarbonate <15 mEq/L 1
• Avoid overly rapid correction of hyponatremia (no more than 8-10 mEq/L in 24 hours) to prevent osmotic demyelination syndrome 2
• Monitor for fluid overload: assess for peripheral edema, pulmonary congestion, and rising jugular venous pressure 2, 3

Follow-Up After AKI

• Schedule close clinical evaluation within 3 months for patients with Stage 2-3 AKI to assess for resolution, new-onset chronic kidney disease, or worsening of pre-existing chronic kidney disease 4, 2, 3
• Risk stratify based on AKI severity to guide timing of nephrology follow-up 4, 2, 3
• Provide patient education on avoiding over-the-counter NSAIDs and recognizing symptoms of worsening kidney function 2, 3
• Continue adjusting medication dosages as kidney function changes during recovery 3

Critical Pitfalls to Avoid

• Do not delay RRT when clear indications exist (refractory hyperkalemia, severe acidosis, uremic complications), as delay increases mortality 1
• Do not continue nephrotoxic medications during AKI recovery 1
• Do not assume AKI is self-limited: even one episode increases risk of chronic kidney disease, cardiovascular disease, and death 5
• Do not use hydroxyethyl starches for volume resuscitation, as they worsen outcomes 5
• Do not overlook infection as a precipitating cause, especially in cirrhotic patients 4, 2