Extracorporeal Membrane Oxygenation and the Kidney

Abstract

Background: Extracorporeal membrane oxygenation (ECMO) is an effective therapy for patients with reversible cardiac and/or respiratory failure. Acute kidney injury (AKI) often occurs in patients supported with ECMO; it frequently evolves into chronic kidney damage or end-stage renal disease and is associated with a reported 4-fold increase in mortality rate. Although AKI is generally due to the hemodynamic alterations associated with the baseline disease, ECMO itself may contribute to maintaining kidney dysfunction through several mechanisms.

Summary: AKI may be related to conditions derived from or associated with extracorporeal therapy, leading to a reduction in renal oxygen delivery and/or to inflammatory damage. In particular, during pathological conditions requiring ECMO, the biological defense mechanisms maintaining central perfusion by a reduction of perfusion to peripheral organs (such as the kidney) have been identified as pretreatment and patient-related risk factors for AKI. Hormonal pathways are also impaired in patients supported with ECMO, leading to failures in mechanisms of renal homeostasis and worsening fluid overload. Finally, inflammatory damage, due to the primary disease, heart and lung crosstalk with the kidney or associated with extracorporeal therapy itself, may further increase the susceptibility to AKI. Renal replacement therapy can be integrated into the main extracorporeal circuit during ECMO to provide for optimal fluid management and removal of inflammatory mediators.

Key messages: AKI is frequently observed in patients supported with ECMO. The pathophysiology of the associated AKI is chiefly related to a reduction in renal oxygen delivery and/or to inflammatory damage. Risk factors for AKI are associated with a patient's underlying disease and ECMO-related conditions.

Keywords: Acute kidney injury; Carbon dioxide removal; Extracorporeal membrane oxygenation; Renal replacement therapy; Systemic inflammation.

Fig. 1

Relationship between ECMO and AKI. a Variables directly derived from ECMO therapy may cause AKI; in this hypothesis, ECMO contributes to maintaining kidney dysfunction and causally participates in the development of AKI. b Pretreatment variables or variables which lead to ECMO initiation may also cause AKI development; in this hypothesis, AKI is an epiphenomenon of ECMO and derives from ECMO-independent variables. Theoretically, a third hypothesis may be presented, in which patients with AKI may further require ECMO initiation (e.g. for a cardiorenal syndrome type 3), but this hypothesis is beyond the intention of this review.

Fig. 2

Major hemodynamic factors related to the development of AKI in patients treated with ECMO. CRS 1 = Cardiorenal syndrome type 1; RBF = renal blood flow.

Fig. 3

Major inflammatory factors related to the development of AKI in patients treated with ECMO.