What is the treatment for acute kidney injury?

Treatment for Acute Kidney Injury

The cornerstone of AKI treatment is identifying and eliminating the underlying cause while providing meticulous supportive care focused on fluid management, hemodynamic optimization, medication adjustment, and timely renal replacement therapy when indicated. 1

Immediate Assessment and Causative Factor Management

Stop all nephrotoxic medications immediately when AKI is identified, including NSAIDs, aminoglycosides, and contrast agents. 1 This single intervention can prevent progression in many cases. 2

For patients with cirrhosis and AKI, hold diuretics and nonselective beta-blockers immediately upon diagnosis. 1

Rule out urinary obstruction with renal ultrasonography, particularly in older men, as this represents a reversible cause requiring urgent intervention. 2

Fluid Management Strategy

Initial Volume Assessment and Resuscitation

Use balanced crystalloids (lactated Ringer's solution) as first-line fluid therapy rather than 0.9% saline, as balanced solutions prevent metabolic acidosis and hyperchloremia that worsen kidney injury. 3, 1

Administer 500-1000 mL of balanced crystalloid over 30-60 minutes when hypovolemia is suspected, reassessing hemodynamics after each bolus using dynamic indices. 3

Stop fluid administration once euvolemia is achieved—continuing beyond this point causes harm. 3 Volume overload greater than 10-15% of body weight is associated with adverse outcomes and delayed renal recovery. 3

Specific Clinical Contexts

For hypovolemic AKI in cirrhosis: Administer albumin 1 g/kg (maximum 100 g/day), expecting creatinine reduction to within 0.3 mg/dL of baseline. 3 If serum creatinine shows doubling from baseline, give albumin 1 g/kg/day for 2 days. 1

For septic shock: Target mean arterial pressure ≥65 mmHg with initial crystalloid bolus of 30 mL/kg, but consider earlier vasopressor use rather than excessive fluid administration. 3

Avoid synthetic colloids (hydroxyethyl starches) entirely—they increase mortality and worsen AKI based on high-quality evidence. 3, 1

Polyuric Phase Management

During the polyuric recovery phase, replace 80-100% of measured urine losses with balanced crystalloids to prevent dehydration while avoiding volume overload. 3

Monitor for signs of volume depletion (tachycardia, hypotension, decreased urine output) that indicate inadequate replacement. 3

Hemodynamic Optimization

Target mean arterial pressure ≥65 mmHg through fluid resuscitation first, then vasopressors if needed. 3

Use vasopressors earlier rather than administering excessive fluids in patients who remain hypotensive after initial volume resuscitation. 1

Implement protocol-based hemodynamic management in high-risk patients, particularly in perioperative settings or septic shock. 1

Medication Management

Medications to Avoid

Do not use diuretics for prevention or treatment of AKI unless specifically treating volume overload—they do not improve kidney outcomes. 1

Avoid dopamine and recombinant human IGF-1 for AKI prevention or treatment. 1

Medication Dosing Adjustments

Implement therapeutic drug monitoring for potentially nephrotoxic medications that cannot be avoided. 1

Adjust all medication doses based on changing renal function and dialysis support to prevent both toxicities and underdosing. 4

Metabolic and Nutritional Management

Target plasma glucose 110-149 mg/dL in critically ill patients. 1

Provide total energy intake of 20-30 kcal/kg/day via the enteral route when possible. 1

Protein administration should be:

• 0.8-1.0 g/kg/day in noncatabolic AKI patients without dialysis 1
• 1.0-1.5 g/kg/day in patients on RRT 1
• Up to 1.7 g/kg/day in patients on CRRT and hypercatabolic patients 1

Renal Replacement Therapy (RRT)

Indications for RRT Initiation

Initiate RRT for the following absolute indications:

• Refractory hyperkalemia unresponsive to medical management 1
• Severe metabolic acidosis 1
• Volume overload unresponsive to diuretics 1
• Uremic complications (encephalopathy, pericarditis, pleuritis) 1, 2
• Removal of certain dialyzable toxins 2

The optimal timing for RRT beyond these absolute indications remains controversial, but consider initiation when metabolic and fluid demands exceed the kidney's capacity. 1

Do not use biomarkers alone when deciding whether to initiate RRT—clinical context is paramount. 1

RRT Modality Selection

For hemodynamically unstable patients, use continuous RRT (CRRT) rather than intermittent hemodialysis, as it is more physiologically appropriate despite lack of mortality benefit in RCTs. 1

For patients on ECMO, CRRT is the most appropriate modality due to hemodynamic instability and sensitivity to fluid overload. 5 Earlier RRT initiation may be required in ECMO patients specifically for preventing and managing fluid overload. 5

RRT Dosing

For intermittent or extended RRT: Deliver a Kt/V of at least 1.2 per treatment 3 times per week. 6

For continuous RRT: Deliver an effluent volume of 20-25 ml/kg per hour, which may require higher prescription to achieve target delivery. 6, 5

Anticoagulation

Use regional citrate anticoagulation for CRRT in patients without contraindications. 1

For patients on ECMO with concurrent RRT, anticoagulation is not standardized and depends on patient bleeding risk, circuit setup, and institutional protocols. 5 RRT circuits can run without dedicated heparin unless excessive clotting occurs. 6

RRT Discontinuation

Discontinue RRT when kidney function has recovered or when RRT becomes inconsistent with shared care goals. 6, 1

Transition from CRRT to intermittent hemodialysis when:

• Vasopressor support has been stopped 6
• Intracranial hypertension has resolved 6
• Positive fluid balance can be controlled by intermittent hemodialysis 6

Special Considerations for Hepatorenal Syndrome

For hepatorenal syndrome with AKI, initiate albumin with vasoactive agents. 1

Consider RRT for AKI secondary to acute tubular necrosis or hepatorenal syndrome-AKI in potential liver transplant candidates. 1

Post-AKI Follow-Up

Target follow-up to high-risk populations: patients with baseline CKD, severe AKI, or incomplete recovery of kidney function at discharge. 1

Monitor for proteinuria, which is associated with worse long-term outcomes and future loss of kidney function after AKI. 6, 1

Assess for development or progression of chronic kidney disease, as approximately 33.6% of AKI patients develop acute kidney disease. 7

Critical Pitfalls to Avoid

Do not interpret all AKI as "hypovolemic" requiring aggressive fluid resuscitation—clinical context and timing of insult are critical. 3

Excessive fluid administration worsens outcomes; volume overload and venous congestion have adverse effects on kidney function. 1

Avoid attempting to "reverse" established AKI with fluids, which results in harmful fluid overload. 6

Oliguria has multiple etiologies beyond hypovolemia—do not reflexively administer fluids for all cases of reduced urine output. 6