What is the vasopressor of choice for a patient with acute kidney injury (Impaired renal function)?

Vasopressor of Choice for Acute Kidney Injury

The vasopressor of choice for AKI depends critically on the underlying etiology: norepinephrine is first-line for AKI with shock, while terlipressin (or norepinephrine if unavailable) is the treatment of choice specifically for hepatorenal syndrome-AKI (HRS-AKI) in cirrhotic patients without shock. 1

Context-Dependent Approach

For AKI with Septic Shock or Vasodilatory Shock

Norepinephrine is the first-line vasopressor for patients with AKI and hemodynamic instability or shock. 2, 3 The evidence strongly supports that norepinephrine is safe and beneficial in hypotensive vasodilated patients with AKI, as it restores blood pressure within autoregulatory values and improves renal perfusion. 3, 4

• Target MAP of 75 mmHg appears optimal, as increasing MAP from 60 to 75 mmHg improves renal oxygen delivery, glomerular filtration rate, and renal oxygenation in vasodilatory shock with AKI. 4
• Further increases to MAP 90 mmHg show no additional renal benefit. 4
• Vasopressin can be added as adjunctive therapy in septic shock patients with AKI, particularly in less severely ill patients where it may reduce mortality compared to norepinephrine alone. 2

For Hepatorenal Syndrome-AKI (HRS-AKI)

Terlipressin is the vasopressor of choice for HRS-AKI in cirrhotic patients without shock. 1, 2 This represents a fundamentally different clinical scenario than general AKI with shock.

Terlipressin Protocol:

• Starting dose: 1 mg IV every 4-6 hours, titrated up to maximum 12 mg/day based on response. 1
• Duration: Up to 14 days, but discontinue if no response by day 3-4. 1
• Concurrent albumin: 1 g/kg on day 1 (maximum 100 g), then 20-40 g/day. 1, 2
• Continuous infusion alternative: Starting at 2 mg/day, increased every 24-48 hours up to 12 mg/day, achieves similar efficacy with lower total dose and fewer side effects. 1

When Terlipressin is Unavailable (North America):

• Norepinephrine is equally effective as terlipressin for HRS-AKI, though it requires ICU monitoring. 1
  • Starting dose: 0.5 mg/hour, increased every 4 hours by 0.5 mg/hour to maximum 3 mg/hour
  • Goal: Increase MAP by 10 mmHg or urine output >50 mL/hour for at least 4 hours 1
• Midodrine plus octreotide is inferior to terlipressin but may be used when other options unavailable. 1

Critical Distinction: HRS-AKI vs Other AKI in Cirrhosis

Vasoconstrictors should ONLY be used for HRS-AKI, not for other forms of AKI in cirrhotic patients (such as acute tubular necrosis, prerenal AKI, or AKI from other causes). 1, 2 This is because vasoconstrictors work by counteracting the extreme splanchnic vasodilation specific to HRS-AKI pathophysiology. 1

Predictors of Response to Vasoconstrictor Therapy in HRS-AKI:

• Baseline creatinine <5 mg/dL (ideally 2.25-5 mg/dL) 1, 2
• Baseline bilirubin <10 mg/dL 1
• Lower MELD score and Child-Pugh score <13 1
• Sustained increase in MAP by 5-10 mmHg during treatment 1

Important Safety Considerations

Terlipressin Contraindications and Cautions:

• Avoid in patients with: Known ischemic heart disease, peripheral vascular disease, or baseline respiratory compromise. 1
• High-risk population: Patients with ACLF-3 (acute-on-chronic liver failure grade 3) have increased risk of respiratory failure (8% incidence). 1
• Monitor for: Ischemic complications (angina, arrhythmia, digital ischemia), abdominal pain, diarrhea, and pulmonary edema. 1
• Albumin-related risk: Excessive albumin administration can cause pulmonary edema, especially in patients with cirrhotic cardiomyopathy or diastolic dysfunction. 1

General Vasopressor Cautions in AKI:

• Increasing doses of norepinephrine and vasopressin during continuous kidney replacement therapy are associated with higher in-hospital mortality, likely reflecting severity of illness. 5
• Catecholamine vasopressors may exacerbate medullary hypoxia and intrarenal inflammation compared to non-catecholamine vasopressors (vasopressin, angiotensin II). 6

Common Pitfalls to Avoid

• Do not use vasoconstrictors for uncomplicated ascites, after large-volume paracentesis, or in spontaneous bacterial peritonitis without AKI. 1
• Do not continue terlipressin beyond day 4 if no improvement in creatinine, as response is unlikely. 1
• Do not use vasoconstrictors in cirrhotic patients with AKI from acute tubular necrosis or other non-HRS causes. 1, 2
• Avoid terlipressin in patients with severe cardiac or respiratory disease at baseline. 1