Overview
Acute kidney injury (AKI) is a common complication of septic shock and together these conditions carry a high mortality risk. In septic patients who develop severe AKI renal cortical perfusion is deficient despite normal macrovascular organ blood flow. This intra-renal perfusion abnormality may be amenable to pharmacological manipulation, which may offer mechanistic insight into the pathophysiology of septic AKI. The aim of the current study is to investigate the effects of vasopressin and angiotensin II on renal microcirculatory perfusion in a cohort of patients with septic shock.
Eligibility
Inclusion Criteria:
- Within 48 hours of intensive care admission
- Evidence of suspected or confirmed infection
- Sequential Organ Failure (SOFA) score increase of 2 or more (assuming a baseline of 0 if no previous measures)
- Requirement for norepinephrine infusion as the sole vasopressor agent in a dose of >0.1mcg/kg/min
- Lactate >2mmol/L at any stage prior to randomisation
Exclusion Criteria:
- Known intolerance to Sonovueâ„¢ contrast medium, vasopressin or angiotensin II
- Patients receiving other vasoactive drugs in addition to norepinephrine
- Patients with known chronic kidney disease (CKD) stage 4 or 5 (baseline glomerular filtration rate (GFR) <30mls/min)
- Patients receiving extra corporal membrane oxygenation (ECMO)
- Patients with acute occlusive coronary syndromes requiring intervention
- Patients with mesenteric ischaemia
- Patients with a history or presence of aortic dissection or abdominal aortic aneurysm
- Patients with Raynaud's syndrome or acute vaso-occlusive conditions
- Pregnancy