Gianluca Villa1, Nevin Katz2, Claudio Ronco3. 1. Section of Anesthesiology and Intensive Care, Department of Health Sciences, University of Florence, Florence, Vicenza, Italy; Department of Nephrology, Dialysis and Transplantation, International Renal Research Institute, San Bortolo Hospital, Vicenza, Italy. 2. Division of Cardiac Surgery, Johns Hopkins University, Baltimore, Md., USA. 3. Department of Nephrology, Dialysis and Transplantation, International Renal Research Institute, San Bortolo Hospital, Vicenza, Italy.
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.
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.
Authors: Herbert P Wiedemann; Arthur P Wheeler; Gordon R Bernard; B Taylor Thompson; Douglas Hayden; Ben deBoisblanc; Alfred F Connors; R Duncan Hite; Andrea L Harabin Journal: N Engl J Med Date: 2006-05-21 Impact factor: 91.245
Authors: Claudius Diez; Assad Haneya; Frank Brünger; Alois Philipp; Stephan Hirt; Leopold Ruppecht; Reinhard Kobuch; Andreas Keyser; Michael Hilker; Thomas Puehler; Christof Schmid Journal: ASAIO J Date: 2009 Nov-Dec Impact factor: 2.872
Authors: J Graulich; B Walzog; M Marcinkowski; K Bauer; H Kössel; G Fuhrmann; C Bührer; P Gaehtgens; H T Versmold Journal: Pediatr Res Date: 2000-11 Impact factor: 3.756
Authors: David J Askenazi; David T Selewski; Matthew L Paden; David S Cooper; Brian C Bridges; Michael Zappitelli; Geoffrey M Fleming Journal: Clin J Am Soc Nephrol Date: 2012-04-12 Impact factor: 8.237
Authors: Matthieu Schmidt; Vincent Pellegrino; Alain Combes; Carlos Scheinkestel; D Jamie Cooper; Carol Hodgson Journal: Crit Care Date: 2014-01-21 Impact factor: 9.097
Authors: David Andrijevic; Zvonimir Vrselja; Taras Lysyy; Shupei Zhang; Mario Skarica; Ana Spajic; David Dellal; Stephanie L Thorn; Robert B Duckrow; Shaojie Ma; Phan Q Duy; Atagun U Isiktas; Dan Liang; Mingfeng Li; Suel-Kee Kim; Stefano G Daniele; Khadija Banu; Sudhir Perincheri; Madhav C Menon; Anita Huttner; Kevin N Sheth; Kevin T Gobeske; Gregory T Tietjen; Hitten P Zaveri; Stephen R Latham; Albert J Sinusas; Nenad Sestan Journal: Nature Date: 2022-08-03 Impact factor: 69.504
Authors: Murat Sargın; Müge Taşdemir Mete; Sevinç Bayer Erdoğan; Hüseyin Kuplay; Murat Baştopçu; Fatih Bayraktar; Murat Acarel; Serap Aykut Aka Journal: Turk Gogus Kalp Damar Cerrahisi Derg Date: 2019-06-21 Impact factor: 0.332