TY  - JOUR
A1  - Greite, Robert
A1  - Störmer, Johanna
A1  - Gueler, Faikah
A1  - Khalikov, Rasul
A1  - Haverich, Axel
A1  - Kühn, Christian
A1  - Madrahimov, Nodir
A1  - Natanov, Ruslan
T1  - Different acute kidney injury patterns after renal ischemia reperfusion injury and extracorporeal membrane oxygenation in mice
JF  - International Journal of Molecular Sciences
N2  - The use of extracorporeal membrane oxygenation (ECMO) is associated with acute kidney injury (AKI) in thoracic organ transplantation. However, multiple other factors contribute to AKI development after these procedures such as renal ischemia-reperfusion injury (IRI) due to hypo-perfusion of the kidney during surgery. In this study, we aimed to explore the kidney injury patterns in mouse models of ECMO and renal IRI. Kidneys of C57BL/6 mice were examined after moderate (35 min) and severe (45 min) unilateral transient renal pedicle clamping and 2 h of veno-venous ECMO. Renal injury markers, neutrophil infiltration, tubular transport function, pro-inflammatory cytokines, and renal heme oxygenase-1 (HO-1) expression were determined by immunofluorescence and qPCR. Both procedures caused AKI, but with different injury patterns. Severe neutrophil infiltration of the kidney was evident after renal IRI, but not following ECMO. Tubular transport function was severely impaired after renal IRI, but preserved in the ECMO group. Both procedures caused upregulation of pro-inflammatory cytokines in the renal tissue, but with different time kinetics. After ECMO, but not IRI, HO-1 was strongly induced in tubular cells indicating contact with hemolysis-derived proteins. After IRI, HO-1 was expressed on infiltrating myeloid cells in the tubulo-interstitial space. In conclusion, renal IRI and ECMO both caused AKI, but kidney damage after renal IRI was more pronounced including severe neutrophil infiltration and tubular transport impairment. Enhanced HO-1 expression in tubular cells after ECMO encourages limitation of hemolysis as a therapeutic approach to reduce ECMO-associated AKI.
KW  - acute kidney injury
KW  - extracorporeal membrane oxygenation
KW  - heme oxygenase-1
KW  - renal inflammation
Y1  - 2022
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-288282
SN  - 1422-0067
VL  - 23
IS  - 19
ER  - 
TY  - JOUR
A1  - Kredel, Markus
A1  - Kunzmann, Steffen
A1  - Schlegel, Paul-Gerhardt
A1  - Wölfl, Matthias
A1  - Nordbeck, Peter
A1  - Bühler, Christoph
A1  - Lotz, Christopher
A1  - Lepper, Philipp M.
A1  - Wirbelauer, Johannes
A1  - Roewer, Norbert
A1  - Muellenbach, Ralf M.
T1  - Double Peripheral Venous and Arterial Cannulation for Extracorporeal Membrane Oxygenation in Combined Septic and Cardiogenic Shock
JF  - American Journal of Case Reports
N2  - Background: 
The use of venoarterial extracorporeal membrane oxygenation (va-ECMO) via peripheral cannulation for septic shock is limited by blood flow and increased afterload for the left ventricle.

Case Report: 
A 15-year-old girl with acute myelogenous leukemia, suffering from severe septic and cardiogenic shock, was treated by venoarterial extracorporeal membrane oxygenation (va-ECMO). Sufficient extracorporeal blood flow matching the required oxygen demand could only be achieved by peripheral cannulation of both femoral arteries. Venous drainage was performed with a bicaval cannula inserted via the left V. femoralis. To accomplish left ventricular unloading, an additional drainage cannula was placed in the left atrium via percutaneous atrioseptostomy (va-va-ECMO). Cardiac function recovered and the girl was weaned from the ECMO on day 6. Successful allogenic stem cell transplantation took place 2 months later.

Conclusions: 
In patients with vasoplegic septic shock and impaired cardiac contractility, double peripheral venoarterial extracorporeal membrane oxygenation (va-va-ECMO) with transseptal left atrial venting can by a lifesaving option.
KW  - extracorporeal membrane oxygenation
KW  - myeloid
KW  - leukemia
KW  - acute
KW  - shock
KW  - cardiogenic
KW  - septic
Y1  - 2017
U6  - http://nbn-resolving.de/urn/resolver.pl?urn:nbn:de:bvb:20-opus-158193
VL  - 18
ER  -