Therapeutic Plasma Exchange in Sepsis and Organ Dysfunction

Sepsis arises from a dysregulated immune and endothelial response to infection, leading to widespread inflammation, coagulation disturbances and progressive organ dysfunction. Therapeutic plasma exchange (TPE) has emerged as an adjunctive strategy aimed at interrupting this pathological cascade. By removing circulating injurious mediators—such as proinflammatory cytokines, activated complement components and ultralarge von Willebrand factor multimers—and replacing them with donor plasma rich in anticoagulant and barrier-protective factors, TPE may restore haemostatic balance, attenuate endothelial injury and improve microcirculatory flow. Clinical observations suggest rapid reductions in vasopressor requirements and lactate levels, accompanied by improvements in barrier function and organ perfusion. While the optimal timing, dosing and patient selection criteria remain under investigation, TPE holds promise as a modular intervention to complement antimicrobial therapy and organ support in refractory septic shock.

Research from Nature Portfolio

No recent Nature Portfolio content available.

Therapeutic Plasma Exchange in Sepsis and Organ Dysfunction publication trend

The graph below shows the total number of articles in therapeutic plasma exchange in sepsis and organ dysfunction across all publications each year (not limited to Nature Index journals).

Technical terms

Therapeutic Plasma Exchange (TPE): An extracorporeal procedure that removes a patient’s plasma to eliminate pathogenic substances and replaces it with donor plasma to restore deficient proteins.

Proinflammatory cytokines: Small secreted proteins (e.g. interleukin-6, interleukin-1β) that amplify inflammatory signalling and endothelial activation.

Vasopressors: Pharmacological agents (e.g. norepinephrine) that constrict blood vessels to maintain blood pressure in shock states.

ADAMTS-13: A metalloprotease enzyme that cleaves ultralarge von Willebrand factor multimers, preventing pathological microthrombosis.

Angiopoietin-2: An endothelial-derived protein that increases vascular permeability and promotes inflammation when elevated.

References

1. Influence of therapeutic plasma exchange treatment on short-term mortality of critically ill adult patients with sepsis-induced organ dysfunction: a systematic review and meta-analysis. Critical Care (2024).
2. Early therapeutic plasma exchange in septic shock: a prospective open-label nonrandomized pilot study focusing on safety, hemodynamics, vascular barrier function, and biologic markers. Critical Care (2018).
3. Clinical and biochemical endpoints and predictors of response to plasma exchange in septic shock: results from a randomized controlled trial. Critical Care (2022).