What are the steps to manage Acute Kidney Injury (AKI)?

Management of Acute Kidney Injury: Step-by-Step Approach

Immediately discontinue all nephrotoxic medications (NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides) and assess volume status to guide fluid resuscitation with isotonic crystalloids, while simultaneously searching for and treating reversible causes. 1

Step 1: Diagnose and Stage AKI

• Diagnose AKI when serum creatinine increases ≥0.3 mg/dL within 48 hours, increases ≥50% from baseline within 7 days, or urine output decreases to <0.5 mL/kg/hour for >6 hours 1, 2, 3
• Stage the severity using KDIGO criteria (Stage 1,2, or 3) based on degree of creatinine elevation or urine output reduction 2
• Obtain baseline creatinine from prior records; if unavailable, use the initial hospital value as baseline 1

Step 2: Immediate Medication Review and Discontinuation

• Stop all nephrotoxic drugs immediately: NSAIDs, ACE inhibitors, ARBs, aminoglycosides, contrast agents, and vasodilators 1, 3
• Hold diuretics and beta-blockers in all patients with AKI 1
• Review all medications including over-the-counter drugs for potential nephrotoxicity 1, 3

Step 3: Assess Volume Status and Determine AKI Etiology

• Perform focused physical examination looking for signs of hypovolemia (dry mucous membranes, decreased skin turgor, orthostatic hypotension) or volume overload (pulmonary edema, peripheral edema, elevated JVP) 2, 3
• Obtain urinalysis with microscopy to detect hematuria, proteinuria (>500 mg/day), or abnormal sediment that suggests structural kidney disease 1, 3
• Check urine chemistry: fractional excretion of sodium and urea to differentiate prerenal from intrinsic causes 1, 3
• Perform renal ultrasound to exclude obstruction and assess kidney structure 1
• Classify AKI type: hypovolemic (most common), acute tubular necrosis, hepatorenal syndrome, or postrenal 1

Step 4: Search for and Treat Underlying Causes

• Rigorously search for infection in all patients: obtain blood cultures, urine cultures, chest radiograph 1, 3
• Perform diagnostic paracentesis in cirrhotic patients to evaluate for spontaneous bacterial peritonitis 1, 3
• Start broad-spectrum antibiotics when infection is strongly suspected; do not use prophylactic antibiotics routinely 1
• Treat specific precipitants: gastrointestinal bleeding, diarrhea, excessive lactulose use 1

Step 5: Fluid Management Based on Volume Status

For Hypovolemic Patients:

• Administer isotonic crystalloids (normal saline or balanced crystalloids) rather than colloids for initial volume expansion 1, 2
• Avoid starch-containing fluids as they are associated with harm 1
• In cirrhotic patients with AKI: give albumin 1 g/kg/day (maximum 100 g/day) for 2 consecutive days 1, 3

For Euvolemic/Hypervolemic Patients:

• Restrict fluids and monitor closely for volume overload 2, 3
• Do not use diuretics to treat AKI except for managing volume overload 1, 2

Step 6: Hemodynamic Support

• Use vasopressors in conjunction with fluids for patients with vasomotor shock 1, 2
• Target mean arterial pressure >65 mmHg to ensure adequate renal perfusion; higher targets (>75 mmHg) may be needed in patients with preexisting hypertension 2, 4
• Implement protocol-based hemodynamic management in perioperative and septic shock settings 1

Step 7: Special Management for Hepatorenal Syndrome (HRS-AKI)

If serum creatinine remains >2 times baseline after 48 hours of diuretic withdrawal and albumin administration, and HRS criteria are met:

• Initiate vasoconstrictor therapy with albumin 1 g/kg IV on day 1, then 20-40 g daily 1, 3
• First-line vasoconstrictor: Terlipressin 1 mg IV every 4-6 hours (total 4-6 mg/day); increase to 2 mg every 4-6 hours (maximum 12 mg/day) if creatinine doesn't decrease by 25% at day 3 1
• Alternative regimen: Continuous terlipressin infusion starting at 2 mg/day, titrating up to 12 mg/day 1
• If terlipressin unavailable: Use midodrine 7.5-12.5 mg PO three times daily plus octreotide 100-200 mcg SC three times daily 1
• Alternative: Norepinephrine 0.5 mg/hour IV, increase by 0.5 mg/hour every 4 hours to maximum 3 mg/hour, targeting MAP increase ≥10 mmHg 1
• Continue treatment until creatinine returns to ≤0.3 mg/dL above baseline for 2 consecutive days or for maximum 14 days 1

Step 8: Monitor for Complications

• Check electrolytes, BUN, creatinine every 4-6 hours initially 2, 3
• Monitor for hyperkalemia and treat urgently if severe 2
• Watch for pulmonary edema when administering albumin, especially in cirrhotic patients 1
• Monitor for ischemic complications with vasoconstrictors (angina, digital ischemia, intestinal ischemia) 1
• Track urine output hourly and adjust fluid management accordingly 1, 3

Step 9: Nutritional Management

• Provide 20-30 kcal/kg/day total energy intake 1
• Protein intake: 0.8-1.0 g/kg/day in non-catabolic AKI without dialysis; 1.0-1.5 g/kg/day in patients on RRT; up to 1.7 g/kg/day in hypercatabolic patients on CRRT 1
• Do not restrict protein to prevent or delay dialysis initiation 1
• Use enteral nutrition preferentially over parenteral 1
• Target glucose 110-149 mg/dL with insulin therapy in critically ill patients 1

Step 10: Indications for Renal Replacement Therapy

Initiate RRT for:

• Severe oliguria unresponsive to fluid resuscitation 2, 3
• Severe metabolic acidosis 2
• Uremic complications (pericarditis, encephalopathy, bleeding) 2
• Refractory hyperkalemia 2
• Fluid overload unresponsive to diuretics 2
• In cirrhotic patients: Consider RRT for acute tubular necrosis or HRS-AKI in liver transplant candidates 1, 3

Critical Pitfalls to Avoid

• Never continue nephrotoxic medications during AKI recovery 2, 3
• Never delay RRT when clear indications exist, as this increases mortality 2
• Never use low-dose dopamine to prevent or treat AKI (proven ineffective) 1
• Never use diuretics to prevent AKI or treat it except for volume overload 1, 2
• Never administer excessive albumin without monitoring for pulmonary edema 1
• Never use terlipressin if creatinine ≥5 mg/dL or oxygen saturation <90% 1
• Never fail to identify and treat infection, the most common reversible cause 1, 3