What is the recommended initial management for acute kidney injury?

Initial Management of Acute Kidney Injury

Immediately discontinue all nephrotoxic medications (NSAIDs, ACE inhibitors, ARBs, diuretics, aminoglycosides, contrast media) and assess volume status to guide fluid resuscitation with isotonic crystalloids. 1, 2, 3

Immediate Universal Actions (First 30 Minutes)

Stop all potentially harmful medications immediately:

• Discontinue diuretics, NSAIDs, ACE inhibitors, ARBs, and beta-blockers 1, 2, 3
• Hold aminoglycosides and any nephrotoxic agents 1, 2
• Review all medications including over-the-counter drugs 3
• The "triple whammy" combination (NSAIDs + diuretics + ACE-I/ARB) dramatically increases AKI risk and must be avoided 2, 3

Assess volume status clinically:

• Look for signs of hypovolemia (dry mucous membranes, tachycardia, orthostatic hypotension) or volume overload (pulmonary edema, peripheral edema, elevated JVP) 1, 2, 3
• Consider central venous pressure monitoring in critically ill patients 1, 2

Initial Diagnostic Workup

Obtain essential laboratory tests:

• Serum creatinine, BUN, comprehensive metabolic panel (sodium, potassium, calcium, magnesium, chloride, bicarbonate) every 4-6 hours initially 1, 2
• Complete blood count to assess for anemia or thrombocytopenia 2
• 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
• Urine sodium and fractional excretion of sodium (FENa): FENa <1% suggests prerenal azotemia; FENa >2% indicates intrinsic renal injury 1, 4

Classify AKI by KDIGO criteria:

• Stage 1: Creatinine rise ≥0.3 mg/dL within 48 hours OR 1.5-1.9× baseline OR urine output <0.5 mL/kg/h for >6 hours 1
• Stage 2: Creatinine 2.0-2.9× baseline OR urine output <0.5 mL/kg/h for >12 hours 1
• Stage 3: Creatinine ≥3.0× baseline OR ≥4.0 mg/dL OR urine output <0.3 mL/kg/h for ≥24 hours OR initiation of RRT 1

Determine the underlying cause:

• Prerenal (volume depletion, hypotension, heart failure, hepatorenal syndrome) 4
• Intrinsic renal (acute tubular necrosis, glomerulonephritis, acute interstitial nephritis, atheroembolic disease) 5, 4
• Postrenal (urinary obstruction—obtain renal ultrasound in all patients, especially older men) 4

Fluid Management Strategy

For hypovolemic patients (prerenal AKI):

• Administer isotonic crystalloids (normal saline or lactated Ringer's) rather than colloids for initial volume expansion 5, 1, 3
• Avoid hydroxyethyl starch solutions—they cause harm in AKI 5, 3
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 1, 2, 3
• Use vasopressors (norepinephrine preferred over dopamine) in conjunction with fluids if hypotension persists despite volume resuscitation 5, 1, 3

Special albumin protocol for unclear etiology (Stage >1A):

• If no obvious cause identified and AKI is beyond Stage 1A, administer 20% albumin 1 g/kg/day for 2 consecutive days (maximum 100 g/day) 1, 3
• This serves both diagnostic and therapeutic purposes: prerenal AKI responds within 48 hours with creatinine improvement; intrinsic AKI does not respond 3

For cirrhotic patients with AKI:

• Give albumin 1 g/kg on day 1 (maximum 100 g), then 20-40 g daily 1
• Perform diagnostic paracentesis to rule out spontaneous bacterial peritonitis 1
• If hepatorenal syndrome is diagnosed, add vasoactive agents (terlipressin preferred; alternatively norepinephrine or midodrine plus octreotide) 1, 3

Avoid over-resuscitation:

• Volume overload worsens AKI outcomes 3
• Monitor strict input/output and daily weights 2

Hemodynamic Optimization

• Maintain mean arterial pressure ≥65 mmHg 1, 2, 3
• Use norepinephrine as first-line vasopressor if fluid resuscitation fails 3
• Do not use dopamine—it does not prevent or treat AKI 5, 3
• Do not use diuretics to prevent or treat AKI—they are ineffective and potentially harmful 5

Management of Complications

Monitor and correct electrolyte abnormalities:

• Check potassium, bicarbonate, calcium, and phosphate every 4-6 hours in severe AKI 1, 2
• Treat hyperkalemia urgently if present (calcium gluconate for cardiac protection, insulin/glucose, sodium bicarbonate if acidotic, dialysis if refractory) 1
• Administer intravenous sodium bicarbonate for severe metabolic acidosis; consider dialysis if refractory 1

Indications for Urgent Renal Replacement Therapy

Initiate RRT for:

• Refractory hyperkalemia despite medical management 1, 4
• Severe volume overload unresponsive to diuretics 1, 4, 6
• Intractable metabolic acidosis 1, 4, 6
• Uremic complications (encephalopathy, pericarditis, pleuritis) 1, 4
• Severe oliguria/anuria unresponsive to fluid resuscitation 1, 2
• Certain toxin removal 4

Reassess need for RRT daily 1, 2

Monitoring During First 48-72 Hours

• Measure serum creatinine and electrolytes every 4-6 hours 1, 2
• Track urine output hourly 2, 3
• Assess fluid balance with strict input/output measurements 2
• Persistent AKI is defined as continuation beyond 48 hours despite initial management 5, 2, 3
• Complete reversal within 48 hours typically indicates prerenal etiology 5, 3

When to Consult Nephrology

Obtain nephrology consultation if:

• Underlying cause cannot be identified after initial evaluation 1
• AKI persists >48 hours despite appropriate management 1
• Stage 3 AKI or pre-existing CKD Stage 4-5 1
• Glomerulonephritis, vasculitis, or rapidly progressive AKI suspected 5

Critical Pitfalls to Avoid

• Do not continue nephrotoxic medications during evaluation—each additional nephrotoxin increases AKI odds by 53% 3
• Do not delay RRT when clear indications exist—this increases mortality 1, 2
• Do not use eGFR equations during acute changes—they require steady-state creatinine and are invalid in AKI 2
• Do not dismiss small creatinine rises in CKD patients—a 0.3 mg/dL increase carries a four-fold mortality risk regardless of baseline 1
• Do not use albumin in traumatic brain injury—it causes harm in this setting 5
• Do not fail to adjust medication dosages as kidney function changes during recovery 2

Special Populations

Cirrhotic patients:

• Use ICA-AKI criteria (≥0.3 mg/dL rise within 48h or ≥50% from baseline) without fixed 1.5 mg/dL threshold because baseline creatinine underestimates GFR 1
• Urine output is unreliable due to diuretic use and altered sodium handling 1
• Screen aggressively for infection—it is a common precipitant 1, 3

Patients with baseline CKD:

• Higher risk for developing AKI and worse outcomes when it occurs 2
• Absolute 0.3 mg/dL criterion is crucial because percentage-based criteria under-diagnose AKI in advanced CKD 1
• Consider nephrology consultation early 1, 2

Evidence Quality Note

The KDOQI and Canadian Society of Nephrology commentaries 5 emphasize that management should be based on overall clinical status, specific cause, trends in kidney function, comorbidities, volume status, and electrolyte disturbances—not solely on KDIGO stage. The stage-based approach proposed in KDIGO lacks sufficient validation for clinical management, though the definition itself is useful for recognition and research 5.