Septic shock is a common and life-threatening condition associated with an in-hospital mortality rate exceeding 40%. The symptomatic management of septic shock relies primarily on vasopressor therapy, particularly norepinephrine. However, the use of high doses of norepinephrine may lead to adverse effects, prompting the search for alternative therapeutic strategies, including angiotensin II, which has recently been investigated as an adjunctive vasopressor.
Indeed, alterations of the renin-angiotensin-aldosterone system (RAAS), particularly a relative deficiency of angiotensin II, have been hypothesized to occur during septic shock. However, to date, no human study has used gold-standard techniques for measuring RAAS peptides to confirm this hypothesis.
Furthermore, it remains unclear whether these alterations are specific to septic shock or may also be observed in less severe infections (sepsis) or in other forms of circulatory failure, such as cardiogenic shock.
Inclusion Criteria:
Adult patients with septic shock:
Adult critically ill control patients with sepsis without circulatory failure:
Adult critically ill control patients with cardiogenic shock:
Adult healthy volunteers:
Exclusion Criteria:
adrien.picod@aphp.fr+33 1 48 95 55 55
Blood samples will be collected at 6, 24, and 72 hours after study inclusion
Critically ill control patients, including patients with sepsis without circulatory failure and patients with cardiogenic shock, will undergo blood sampling at 6, 24, and 72 hours.
blood sampling at inclusion
Renin and Renal Biomarker Response to Angiotensin II
Renin Levels as Prognostic Indicators of Septic Shock Severity and Outcome
Angiotensin in Septic Kidney Injury Trial
Evaluation of Plasma Angiotensin II and Angiotensin II Receptor Levels in Patients With Sepsis and Septic Shock: a Prospective Observational Study.
Monitoring of Septic Shock-induced Immunosuppression
Characterization of Hemostatic Disordres in Septic Shock: Searching for Biological Markers
Mechanistic Assessment of Norepinephrine Therapy vs. Angiotensin-II in Septic Shock
Upregulation of Alpha-1 Receptors Upon Septic Shock?