What is the treatment for acute kidney injury (AKI)?

Treatment of Acute Kidney Injury

The cornerstone of AKI treatment is immediately identifying and reversing the underlying cause while discontinuing all nephrotoxic medications—this takes absolute priority over all other interventions. 1

Immediate Medication Management

Stop all nephrotoxic drugs immediately, including NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics (in most cases), beta-blockers, vasodilators, and iodinated contrast media. 1 The "triple whammy" combination of NSAIDs + diuretics + ACE inhibitors/ARBs is particularly dangerous and must be discontinued urgently. 1 Each additional nephrotoxin increases AKI odds by 53%, making polypharmacy review critical. 1

Critical pitfall: Never use furosemide or other diuretics in hemodynamically unstable patients with prerenal AKI—this worsens volume depletion and reduces renal perfusion. 1 Diuretics should only be used after adequate renal perfusion is restored and only for managing volume overload. 2, 3

Fluid Resuscitation Strategy

Use isotonic crystalloids as first-line therapy for volume expansion, preferentially choosing balanced crystalloids (lactated Ringer's) over 0.9% saline to prevent metabolic acidosis and hyperchloremia. 1, 2, 3 The evidence from large multicenter trials now clearly favors physiological crystalloids over saline. 4

Avoid hydroxyethyl starches completely—they increase the risk of worsening AKI and mortality, particularly in critically ill patients with sepsis. 1, 2

Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion. 1 Use dynamic indices (passive leg-raising test, pulse/stroke volume variation, echocardiography) rather than static measurements to guide fluid therapy and prevent both under-resuscitation and fluid overload. 1, 4

Consider earlier use of vasoactive medications instead of excessive fluid administration for hypotension, as volume overload and venous congestion worsen kidney function and outcomes. 4, 3

Monitoring Protocol

Measure serum creatinine and electrolytes every 12-24 hours during acute management in the first 48-72 hours. 1 Monitor urine output continuously, as oliguria is associated with poor prognosis. 2 Use echocardiography or CVP when indicated to assess volume status and prevent fluid overload. 1

Special Population: Cirrhotic Patients

In cirrhotic patients with AKI, discontinue BOTH diuretics AND beta-blockers (not just diuretics alone). 1, 2 Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from hepatorenal syndrome. 1, 2 For hepatorenal syndrome-AKI, initiate vasoconstrictors and albumin earlier, as higher creatinine at treatment initiation leads to lower response rates. 2

Metabolic Management

Target plasma glucose of 110-149 mg/dL in critically ill patients. 2, 3 Provide total energy intake of 20-30 kcal/kg/day. 2, 3 Administer protein at 0.8-1.0 g/kg/day in noncatabolic AKI patients without dialysis, 1.0-1.5 g/kg/day in patients on RRT, and up to 1.7 g/kg/day in patients on CRRT and hypercatabolic patients. 2, 3 Provide nutrition preferentially via the enteral route. 2, 3

Renal Replacement Therapy Indications

Consider RRT for severe metabolic derangements: refractory hyperkalemia, severe acidosis unresponsive to medical management, volume overload unresponsive to diuretics, or uremic complications (encephalopathy, pericarditis, pleuritis). 2, 3 The optimal timing remains controversial, but individualize based on overall clinical condition rather than specific creatinine or BUN thresholds. 1, 3

For hemodynamically unstable patients, continuous RRT is more physiologically appropriate than intermittent hemodialysis. 3 When using intermittent or extended RRT, deliver a Kt/V of at least 1.2 per treatment 3 times weekly. 3 For continuous RRT, deliver an effluent volume of 20-25 ml/kg per hour. 3 Use regional citrate anticoagulation for continuous RRT in patients without contraindications. 3

What Does NOT Work (High-Quality Evidence)

Do not use dopamine, diuretics (for AKI treatment), N-acetylcysteine, or recombinant human insulin-like growth factor 1 for AKI prevention or treatment—these have level 1A/B evidence showing lack of efficacy. 1, 2, 3

Critical Pitfalls to Avoid

• Do not use eGFR equations designed for CKD to assess renal function in AKI—they are inaccurate in this acute setting. 1
• Do not delay fluid resuscitation in truly hypovolemic patients. 1
• Avoid excessive fluid administration that leads to volume overload, as fluid overload >10-15% body weight is associated with adverse outcomes. 4
• Remember that nephrotoxin avoidance is not always possible when treating certain infections requiring potentially nephrotoxic antimicrobials; in these cases, implement therapeutic drug monitoring. 2, 3

Follow-Up After AKI

Target follow-up to high-risk populations: neonatal/pediatric patients, individuals with baseline CKD, and patients with severe AKI or incomplete recovery of kidney function at hospital discharge. 2, 3 Monitor for development or progression of chronic kidney disease, as even patients with complete recovery remain at increased risk of progressive CKD. 4, 2