What is the initial management of acute kidney injury in an adult patient?

Initial Management of Acute Kidney Injury in Adults

Immediately discontinue all nephrotoxic medications—including ACE inhibitors, ARBs, NSAIDs, and diuretics—as soon as AKI is diagnosed, then identify and treat the underlying cause while optimizing volume status and monitoring for life-threatening complications. 1, 2

Immediate Actions Upon AKI Diagnosis

Stop Nephrotoxic Medications

• Discontinue ACE inhibitors, ARBs, NSAIDs, and diuretics immediately upon recognizing AKI to prevent further renal injury 1, 2, 3
• Hold beta-blockers in cirrhotic patients with AKI 2
• Avoid the "triple whammy" combination of NSAIDs, diuretics, and ACE inhibitors/ARBs, which more than doubles AKI risk 2, 4
• Review all medications and adjust dosages based on reduced GFR, as kidney function changes dynamically during AKI 1, 2, 4

Assess Volume Status and Hemodynamics

• Perform focused clinical examination to determine intravascular volume: assess jugular venous pressure, check for peripheral edema, auscultate lungs for crackles, and obtain daily weights 1, 4
• Consider central venous pressure monitoring when volume status is unclear 1, 2
• For hypovolemic patients, provide fluid resuscitation with isotonic crystalloids (not colloids) to restore renal perfusion 1, 3, 5
• Maintain mean arterial pressure >65 mmHg with vasopressors if needed to ensure adequate renal perfusion 1

Identify the Underlying Cause

• Classify AKI as prerenal, intrinsic renal, or postrenal through systematic evaluation 3, 5, 6
• Obtain kidney ultrasound immediately to rule out obstructive uropathy, especially in older men with prostatic hypertrophy 2, 5, 6
• Perform urinalysis with microscopy to identify casts: muddy-brown casts suggest acute tubular necrosis, red-cell casts indicate glomerulonephritis, white-cell casts suggest interstitial nephritis 1
• Measure urine sodium and fractional excretion of sodium (FENa): urine sodium <20 mEq/L or FENa <1% favors prerenal azotemia; urine sodium >40 mEq/L or FENa >2% suggests intrinsic renal injury 1

Search for Infection

• Obtain blood cultures, urine cultures, and chest radiograph when infection is suspected 1
• In cirrhotic patients, perform diagnostic paracentesis to rule out spontaneous bacterial peritonitis 1, 2
• Start broad-spectrum antibiotics promptly when infection is strongly suspected, without awaiting culture results 1

Initial Laboratory Monitoring

• Measure serum creatinine, BUN, and complete metabolic panel (sodium, potassium, calcium, magnesium, chloride, bicarbonate) immediately to identify life-threatening electrolyte abnormalities 1
• Repeat serum creatinine and electrolytes every 4–6 hours during the initial phase of severe AKI (KDIGO Stage 2–3) to track progression and detect complications 1, 2
• Obtain complete blood count to screen for anemia and thrombocytopenia 1
• Track strict fluid balance with input/output measurements 2

Management of Complications

Hyperkalemia

• Correct severe hyperkalemia urgently with calcium gluconate (for cardiac membrane stabilization), insulin with dextrose, and sodium bicarbonate 1
• Consider dialysis for refractory hyperkalemia 5, 6

Metabolic Acidosis

• Treat severe metabolic acidosis; consider sodium bicarbonate in patients with AKI and metabolic acidosis 7
• Dialysis may be required for intractable acidosis 5, 6

Fluid Overload

• Monitor for signs of fluid overload: peripheral edema, pulmonary congestion, weight gain, respiratory distress 2, 4
• Implement fluid restriction and consider diuretics cautiously in volume-overloaded patients 2
• Avoid overly aggressive fluid administration in non-hypovolemic patients, which worsens outcomes 2, 4

Indications for Urgent Renal Replacement Therapy

Initiate RRT emergently when any of the following are present: 1, 2, 5, 6

• Severe oliguria or anuria unresponsive to fluid resuscitation

• Refractory hyperkalemia

• Severe metabolic acidosis

• Volume overload causing pulmonary edema or respiratory compromise

• Uremic complications (encephalopathy, pericarditis, pleuritis)

• Certain toxin ingestions requiring removal

• Reassess the need for continued RRT daily as kidney function may recover 1, 2, 4

Special Considerations for Cirrhotic Patients

• Administer albumin 1 g/kg/day (maximum 100 g) for two consecutive days when serum creatinine has doubled from baseline to support intravascular volume 1, 2
• Use ICA-AKI criteria (creatinine rise ≥0.3 mg/dL within 48 hours or ≥50% from baseline) without a fixed 1.5 mg/dL threshold, because baseline creatinine underestimates true GFR in cirrhosis due to reduced muscle mass 1
• When hepatorenal syndrome criteria are met, add vasoactive therapy—preferably terlipressin, or alternatively norepinephrine, or midodrine plus octreotide 1, 2

Nephrology Consultation

• Consider nephrology consultation when: 7, 6
  • The etiology of AKI is unclear
  • AKI persists beyond 48 hours despite initial management
  • Stage 3 AKI is present
  • Pre-existing stage 4 or higher CKD exists
  • Subspecialist expertise is needed (e.g., glomerulonephritis, vasculitis)
  • RRT is being considered

Common Pitfalls to Avoid

• Delaying RRT when clear indications exist increases mortality; do not wait for "one more lab" when urgent indications are present 1, 2, 4
• Failing to identify and address the underlying cause leads to continued kidney damage and poor outcomes 1, 2
• Continuing nephrotoxic medications during AKI causes ongoing renal injury and delays recovery 2, 4
• Overly aggressive fluid administration in non-hypovolemic patients worsens outcomes and can precipitate pulmonary edema 2, 4
• Neglecting to adjust medication dosages as kidney function changes during recovery leads to drug toxicity or underdosing 2, 4
• Dismissing modest absolute creatinine rises (≥0.3 mg/dL) in CKD patients as "insignificant" when they actually represent clinically important AKI associated with four-fold higher mortality 1