What is the immediate treatment for acute kidney injury?

Treatment of Acute Kidney Injury

Immediate First-Line Actions

The immediate treatment for acute kidney injury requires stopping all nephrotoxic medications first—including NSAIDs, aminoglycosides, ACE inhibitors, ARBs, diuretics, beta-blockers, vasodilators, and contrast media—while simultaneously identifying and reversing the underlying cause. 1

Critical Medication Discontinuation

• Stop the "triple whammy" combination immediately (NSAIDs + diuretics + ACE inhibitors/ARBs), as this combination is particularly dangerous and must be discontinued without delay 1
• Review all prescription and over-the-counter medications to identify hidden nephrotoxins, as each additional nephrotoxic agent increases AKI odds by 53% 1
• In cirrhotic patients specifically, discontinue both diuretics and beta-blockers (not just diuretics as in other populations) 1, 2
• Regular monitoring of renal function is required while on any remaining necessary nephrotoxic medications 3

Fluid Resuscitation Strategy

First-Line Fluid Therapy

• Use isotonic crystalloids as first-line therapy, preferentially choosing balanced crystalloids (lactated Ringer's) over 0.9% saline to prevent metabolic acidosis and hyperchloremia 1, 2
• Avoid hydroxyethyl starches completely—they increase the risk of worsening AKI 1, 4
• Target mean arterial pressure ≥65 mmHg to ensure adequate renal perfusion 1, 2

Dynamic Fluid Assessment

• Use dynamic indices (passive leg-raising test, pulse/stroke volume variation) rather than static measurements to guide fluid therapy 1
• Avoid excessive fluid administration that leads to volume overload, as fluid overload >10-15% body weight is associated with adverse outcomes 1
• Consider earlier use of vasoactive medications instead of excessive fluid administration for hypotension 1

Common Pitfall to Avoid

• Never use furosemide in hemodynamically unstable patients with prerenal AKI—it worsens volume depletion and reduces renal perfusion 1, 2
• Do not use diuretics to treat AKI except for managing volume overload after adequate renal perfusion is restored 1, 2

Special Population: Cirrhotic Patients with AKI

Albumin Protocol for Differentiation

• Administer IV albumin 1 g/kg bodyweight (maximum 100g) for two consecutive days to differentiate prerenal AKI from hepatorenal syndrome or acute tubular necrosis 1, 2
• If serum creatinine falls to within 0.3 mg/dL of baseline after albumin infusion, the diagnosis is prerenal AKI 1
• A favorable creatinine response should be evident within 48 hours; lack of improvement after two days suggests acute tubular necrosis or hepatorenal syndrome 1

Stage-Based Management in Cirrhosis

Stage 1 AKI (creatinine rise >0.3 mg/dL but <2× baseline):

• Remove precipitating factors, provide volume expansion if hypovolemic, and monitor closely 1
• Vasoconstrictors are not indicated unless creatinine reaches ≥1.5 mg/dL 1

Stage 2-3 AKI (creatinine ≥2× baseline or ≥1.5 mg/dL):

• Discontinue diuretics and beta-blockers, give albumin 1 g/kg daily for two days 1, 2
• If no response after 2 days and hepatorenal syndrome criteria are met, start vasoconstrictor therapy (terlipressin, norepinephrine, or midodrine + octreotide) together with albumin 1, 2

Additional Cirrhosis-Specific Interventions

• For tense ascites, perform therapeutic paracentesis combined with albumin infusion to improve renal function 1, 2
• Albumin infusion during spontaneous bacterial peritonitis prevents the development of AKI 1, 2

Vasopressor Therapy

• Use norepinephrine as first-line vasopressor if fluid resuscitation fails to restore adequate blood pressure 1
• Earlier use of vasoactive medications may be appropriate instead of excessive fluid administration for hypotension 1, 2

What Does NOT Work (High-Quality Evidence)

• Do not use dopamine to prevent or treat AKI—it is ineffective based on Level 1A evidence 1
• Do not use N-acetylcysteine (NAC) for AKI treatment based on Level 1A/B evidence 1
• Do not use recombinant human insulin-like growth factor 1 for AKI treatment 1

Monitoring Protocol

Acute Phase (First 48-72 Hours)

• Measure serum creatinine and electrolytes every 12-24 hours during acute management 1
• Monitor urine output, vital signs, and fluid balance closely 1, 2
• Use echocardiography or CVP when indicated to assess volume status and prevent fluid overload 1

Cirrhotic Patients Specifically

• For Stage 1A AKI, check serum creatinine every 2-4 days during hospitalization 1
• After discharge, assess serum creatinine at least every 2-4 weeks for the first 6 months 1

Renal Replacement Therapy Indications

• Consider RRT for persistent AKI despite appropriate interventions, based on the patient's clinical status 1
• Specific indications include:
  • Refractory hyperkalemia
  • Severe, intractable metabolic acidosis
  • Volume overload causing pulmonary edema
  • Uremic complications (encephalopathy, pericarditis) 1
• Intrinsic AKI from crush injury or rhabdomyolysis may require more frequent dialysis due to hypercatabolic state and severe hyperkalemia 1

Critical Diagnostic Pitfall

• Do not use eGFR equations (MDRD, CKD-EPI) designed for CKD to assess renal function in AKI—they require steady-state creatinine and are inaccurate in acute settings 1

Infection Management

• Promptly recognize and treat bacterial infections when diagnosed or strongly suspected 1
• Sepsis is a frequent trigger for both prerenal AKI and acute tubular necrosis; aggressive screening and treatment of infections are essential 1

Obstruction Evaluation

• Rule out urinary tract obstruction through clinical assessment 1
• Avoid indwelling bladder catheterization unless necessary, while measuring urine volume as oliguria is associated with poor prognosis 1

ACE Inhibitor/ARB Considerations

Despite recommendations to routinely stop ACE inhibitors and ARBs during AKI, the evidence is nuanced. Two studies demonstrated increased 30-day mortality when these agents were not restarted after surgery, possibly from hypertensive rebound leading to acute cardiac decompensation 3. However, during the acute phase of AKI, the risk-benefit ratio favors discontinuation, with re-introduction considered when GFR has stabilized and volume status is optimized 3.