How do I manage oliguric Acute Kidney Injury (AKI)?

Management of Oliguric Acute Kidney Injury

The cornerstone of managing oliguric AKI is immediate discontinuation of nephrotoxic agents, aggressive search for infection, fluid resuscitation with isotonic crystalloids to achieve euvolemia, and avoidance of diuretics for the purpose of treating oliguria itself. 1, 2

Immediate Initial Actions

Identify and Treat Precipitating Causes

• Conduct a rigorous search for infection in all patients - obtain blood cultures, urine cultures, chest radiograph, and perform diagnostic paracentesis if ascites is present to evaluate for spontaneous bacterial peritonitis. 1, 2

• Discontinue all nephrotoxic medications immediately unless they are absolutely essential - this includes NSAIDs, aminoglycosides (unless no alternative exists), and ACE inhibitors/ARBs. 1, 2

• Hold diuretics and nonselective beta-blockers when AKI is diagnosed, as these can worsen renal perfusion. 1, 2

• Start broad-spectrum antibiotics if infection is strongly suspected, but avoid routine prophylactic antibiotics. 1

Fluid Management Strategy

• Use isotonic crystalloids (normal saline or balanced crystalloids) as the initial fluid for volume expansion - avoid colloids including hydroxyethyl starches, which are associated with increased AKI incidence and mortality. 1, 2, 3, 4

• Target euvolemia through careful clinical assessment - monitor urine output, vital signs, and fluid balance daily. Use dynamic preload indices (stroke volume variation, pulse pressure variation) rather than static measurements like CVP when available. 2, 3

• Administer albumin 1 g/kg/day for 2 consecutive days if serum creatinine shows doubling from baseline despite initial crystalloid resuscitation. 1, 2

• In patients with tense ascites and AKI, perform therapeutic paracentesis with albumin infusion as this improves renal function. 1

Critical "Don'ts" in Oliguric AKI Management

Do not use diuretics to treat oliguria or prevent AKI progression - despite common practice, particularly in surgical patients, diuretics are ineffective for treating AKI and should only be considered for managing severe fluid overload, not for converting oliguric to non-oliguric AKI. 1, 2 The question of diuretic versus dialysis for severe fluid overload remains unanswered. 1

Avoid the following interventions as they are proven ineffective:

• Dopamine for AKI prevention or treatment 1, 2
• N-acetylcysteine 2, 4
• Recombinant human insulin-like growth factor 1 2

Hemodynamic Optimization

• Use vasopressors in conjunction with fluids if the patient has vasomotor shock or sepsis - norepinephrine is typically first-line, though vasopressin may be added in septic shock. 1, 4

• Implement protocol-based hemodynamic management in high-risk perioperative patients or those with septic shock, targeting tissue oxygenation parameters. 1

Monitoring Requirements

• Measure serum creatinine, urea, and electrolytes at least every 48 hours or more frequently in high-risk patients. 2

• Monitor urine output hourly and assess fluid balance meticulously to avoid both hypovolemia and fluid overload, as both are associated with increased mortality. 5, 3, 6

• Use echocardiography or CVP (if central line already present) when indicated to monitor fluid status and prevent pulmonary edema from excessive albumin administration. 1

Special Consideration: Hepatorenal Syndrome-AKI

If serum creatinine remains >2× baseline despite volume repletion with crystalloids and albumin, initiate treatment for HRS-AKI:

• Albumin 1 g/kg IV on day 1, then 20-40 g daily plus vasoactive agents. 1, 2

• Terlipressin (if available): Start 1 mg IV every 4-6 hours, increase to 2 mg every 4-6 hours if creatinine doesn't decrease by ≥25% at day 3. Maximum 14 days or until creatinine returns to ≤0.3 mg/dL of baseline. Do not use if creatinine ≥5 mg/dL or oxygen saturation <90%. 1

• Alternative: Norepinephrine 0.5 mg/h continuous IV infusion, increase by 0.5 mg/h every 4 hours to maximum 3 mg/h, targeting mean arterial pressure increase ≥10 mmHg. 1

• Alternative: Midodrine plus octreotide - midodrine 7.5-12.5 mg PO three times daily with octreotide 100-200 mcg subcutaneously three times daily. 1

Renal Replacement Therapy Considerations

• Initiate RRT for severe complications including life-threatening hyperkalemia, severe metabolic acidosis, uremic complications, or refractory fluid overload. 2, 4

• Continuous RRT (CRRT) is preferred in hemodynamically unstable patients and those with acute brain injury. 2, 4

• When prescribing ultrafiltration during CRRT, use moderate net ultrafiltration rates (prescribed in mL/kg/h based on body weight) as both very slow and very fast rates are associated with increased mortality and cardiac arrhythmias. 6

Nutritional Support During Oliguric Phase

• Provide 20-30 kcal/kg/day total energy intake. 1, 2

• Protein intake: 0.8-1.0 g/kg/day in non-catabolic patients not on dialysis; increase to 1.0-1.5 g/kg/day if on RRT. 1, 2

• Administer nutrition preferentially via enteral route. 1

• Target plasma glucose 110-149 mg/dL (6.1-8.3 mmol/L) with insulin therapy in critically ill patients. 1

Common Pitfalls to Avoid

• Do not restrict protein intake with the aim of preventing or delaying RRT initiation - this is ineffective and potentially harmful. 1

• Beware of furosemide ototoxicity - the FDA warns that rapid IV injection, severe renal impairment, and high doses increase risk of irreversible hearing loss. If high-dose parenteral therapy is elected, use controlled IV infusion not exceeding 4 mg/min. 7

• Avoid fluid overload - there is a paradigm shift away from liberal fluid strategies; after initial resuscitation, target neutral to slightly negative fluid balance as hypervolemia is detrimental to both renal outcomes and survival. 5, 3

• In cirrhotic patients, sudden alterations in fluid and electrolyte balance may precipitate hepatic coma - strict observation is necessary during diuresis, and therapy is best initiated in the hospital setting. 7