Management of Acute Kidney Injury
Manage AKI by first identifying and correcting the underlying cause, optimizing hemodynamics with balanced crystalloids (not saline or colloids), avoiding nephrotoxins, and initiating renal replacement therapy emergently only for life-threatening complications—not based on arbitrary creatinine thresholds. 1, 2
Initial Diagnostic Approach
Determine the etiology immediately by categorizing AKI as prerenal, intrinsic renal, or postrenal through focused evaluation 2, 3, 4:
- History: Identify nephrotoxic medication exposure (NSAIDs, aminoglycosides, contrast agents, ACE-inhibitors), recent hypotensive episodes, sepsis, or urinary symptoms 2, 3
- Physical examination: Assess for hypovolemia (tachycardia, hypotension, dry mucous membranes) versus hypervolemia (peripheral edema, pulmonary crackles, elevated JVP) 5, 3
- Laboratory evaluation: Measure serum creatinine, complete blood count, urinalysis with microscopy, and fractional excretion of sodium (FENa <1% suggests prerenal, >2% suggests intrinsic renal) 3, 4
- Imaging: Perform renal ultrasonography in all older men and any patient with risk factors for obstruction to rule out postrenal causes 3, 4
Hemodynamic Management and Fluid Strategy
Use balanced crystalloids (lactated Ringer's) exclusively for volume resuscitation—avoid 0.9% saline and all colloids 5, 2:
- Fluid challenge protocol (only if hypovolemic): Administer 500-1000 mL of balanced crystalloid over 30-60 minutes, reassess hemodynamics after each bolus using dynamic indices (passive leg raise, pulse pressure variation), and stop immediately once euvolemia is achieved 5
- Critical safety threshold: Volume overload >10-15% of body weight is associated with adverse outcomes, delayed renal recovery, and increased mortality 5, 2
- Avoid synthetic colloids (hydroxyethyl starches): These increase mortality and worsen AKI based on high-quality evidence 5, 2
- Vasopressor support: Use vasopressors (norepinephrine preferred) along with fluids in vasodilatory shock, targeting MAP ≥65 mmHg, rather than excessive fluid administration 1, 5
Common Pitfall to Avoid
Do not interpret all AKI as "hypovolemic" requiring aggressive fluid resuscitation—established oliguric AKI without hemodynamic instability does not require fluid administration and may cause harm 5. Clinical context and timing of insult are critical when deciding on fluid therapy 5.
Medication Management
Immediately discontinue or avoid all nephrotoxic agents 2, 4:
- Stop: NSAIDs, aminoglycosides, vancomycin (unless essential with dose adjustment), ACE-inhibitors/ARBs (temporarily), contrast agents 1, 2
- Adjust dosing: Modify all renally cleared medications according to current GFR 2
- Do NOT use low-dose dopamine—it does not prevent or treat AKI 2, 6
- Do NOT use diuretics to prevent AKI—consider them only for managing established volume overload, not for prevention 2
Metabolic and Nutritional Support
Provide adequate nutrition and maintain metabolic control 2:
- Energy intake: 20-30 kcal/kg/day 2
- Protein intake: 0.8-1.0 g/kg/day in non-catabolic AKI without dialysis; do NOT restrict protein to delay dialysis initiation 2
- Glycemic control: Maintain blood glucose 110-149 mg/dL (6.1-8.3 mmol/L) 2
Management of Persistent AKI
When AKI persists beyond 48-72 hours, initiate extended evaluation 1:
- Reassess etiology: Consider multifactorial causes (sepsis, shock, nephrotoxins) and rare causes requiring specialty consultation (tumor lysis syndrome, thrombotic thrombocytopenic purpura, cholesterol embolization) 1
- Additional testing: Evaluate urine sediment for casts, measure proteinuria, consider biomarker assessment, and obtain renal imaging 1
- Monitor recovery pattern: Stuttering versus prompt recovery patterns are linked to morbidity and mortality—interventions that alter recovery patterns may improve outcomes 1
Renal Replacement Therapy Indications
Initiate RRT emergently only for life-threatening complications 1, 7:
Absolute Indications
- Severe hyperkalemia with ECG changes (peaked T-waves, widened QRS) 1, 7
- Refractory volume overload causing pulmonary edema unresponsive to diuretics 1, 7
- Severe metabolic acidosis with impaired respiratory compensation 1, 7
- Uremic complications: Encephalopathy, pericarditis, or uremic bleeding 1, 7
- Intractable fluid overload causing respiratory compromise 1, 7
Modality Selection
- Continuous RRT (CRRT): Preferred for hemodynamically unstable patients requiring vasopressor support 1, 7
- Intermittent hemodialysis: Preferred for hemodynamically stable patients requiring rapid correction of severe hyperkalemia 1, 7
- Vascular access: Use uncuffed non-tunneled catheter; first choice is right internal jugular vein or femoral vein (avoid femoral in obese patients) 1
Transition Strategy
Transition from CRRT to intermittent hemodialysis when vasopressor support is discontinued, hemodynamic stability is achieved, and positive fluid balance can be controlled 1, 7.
Special Scenario: Polyuric Phase Management
During the polyuric recovery phase, replace 80-100% of measured urine losses with balanced crystalloids to prevent dehydration 5, 7:
- Monitor electrolytes every 48 hours or more frequently if clinically indicated 5, 7
- Potassium replacement: Typically requires 1-3 mmol/kg/day 5, 7
- Watch for volume depletion: Tachycardia, hypotension, decreased urine output, or worsening renal function indicate inadequate replacement 5
Post-Discharge Follow-Up
All patients with AKI require clinical follow-up, especially those with severe AKI (stage 3) or persistent renal dysfunction at discharge 2: