Intra-graft Coagulation Events in Clinical Renal Transplantation and Delayed Graft Function

NCT ID: NCT02568696

Last Updated: 2018-03-29

Study Results

Results pending

The study team has not published outcome measurements, participant flow, or safety data for this trial yet. Check back later for updates.

Basic Information

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Recruitment Status

UNKNOWN

Total Enrollment

100 participants

Study Classification

OBSERVATIONAL

Study Start Date

2015-06-30

Study Completion Date

2018-12-31

Brief Summary

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The purpose of this study is to investigate local activation of the coagulation system in the kidney graft during organ preservation and during early reperfusion in adult kidney transplantation. Generation of thrombin and fibrin as well as activation and inhibition of fibrinolysis will be investigated. Influence of these events on delayed graft function (DGF) and acute cell-mediated rejection will be evaluated.

Detailed Description

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Background

In clinical kidney transplantation organ retrieval, cold-preservation of the graft as well as restoration of the blood flow to the transplant cause tissue damage (ischemia/reperfusion injury). Clinically these events can manifest themselves as delayed graft function (DGF), which is usually defined as the need for dialysis during first week after transplantation. DGF increases the risk of developing chronic rejection and subsequently loss of the transplant.

Ischaemia/reperfusion injury is biologically characterized by local profound inflammatory response, activation of the coagulation system and endothelial dysfunction in the transplanted organ. After reperfusion activated neutrophils cause tissue damage in the graft by production of reactive oxygen species (ROS) and release of proteolytic enzymes, which lead to plugging of the capillaries by accumulation of thrombocytes and fibrin. Blood flow is further diminished by increased blood viscosity and local vasoconstriction and swelling of the endothelial cells. Disorders of the microcirculation lead to "no-reflow" phenomenon whereby locally tissues remain ischemic, despite of good blood flow in the organ artery and vein.

Coagulation is activated in the renal transplant during reperfusion, when circulating factor VIIa (FVIIa) comes into contact with the tissue factor (TF), which is expressed on the endothelium due to ischaemia. FVII-TF complex activates factor X (FX) and activated FX (FXa) cleaves thrombin (FII) from prothrombin. Thrombin activates thrombocytes, cleaves fibrin from fibrinogen and activates factor XIII( FXIII), which stabilizes fibrin clot. Fibrin has been demonstrated to accumulate in the kidney graft during reperfusion. Fibrin accumulation is aggravated by inhibition of fibrinolysis due to reperfusion.

Furthermore, the investigators conducting this current research project, have previously gained indirect evidence in a small cohort study, that accumulation of fibrin occurs even before reperfusion, during donor care and organ retrieval. Most importantly, specifically this pre-reperfusion fibrin deposition was related to DGF.

Patients and sample size

There were several limitations in investigators previous study concerning intra-graft coagulation events in DGF. It was conducted as a part of a larger trial in renal transplantation and included only 30 patients in two study arms with different immunosuppressant regimens (peri-operative basiliximab and conventional triple therapy). Therefore, a new study, with larger sample size and standardized immunosuppression is warranted.

Therefore, in this current prospective observational study surgical technique, anaesthesia and hemodynamic management, immunosuppressive medications are strictly standardized. Sample size is increased to 100. The investigators prospectively screen all adult patients receiving their first kidney transplant from cadaveric donor. Only patients scheduled to receive local standard triple immunosuppressant therapy with cyclosporine A, mycophenolate mofetil and methylprednisolone are included.

Blood samples and prospective data collection

Blood samples for assessment of intra-graft coagulation events (generation of thrombin and fibrin, activation and inhibition of fibrinolysis) are drawn peri-operatively. Predefined clinical and demographical data are collected preoperatively and prospectively during 3 months after kidney transplantation to assess the influence of these coagulation events on delayed graft function according to Halloran criteria (8) (primary outcome) and acute cell mediated graft rejection (primary outcome).

Conditions

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End Stage Renal Disease Reperfusion Injury Delayed Graft Function Kidney Transplantation

Study Design

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Observational Model Type

CASE_ONLY

Study Time Perspective

PROSPECTIVE

Eligibility Criteria

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Inclusion Criteria

* adult person (over 18 years old)
* cadaveric transplantation
* conventional standard immunosuppression plan (methylprednisolone, cyclosporin A, mycophenolate mofetil)

Exclusion Criteria

* previous kidney transplant
* other than local standard immunosuppression
* panel reactive antibodies (PRA) \>30%
* warfarin therapy
* dual anti-platelet therapy
* use of low molecular weight heparins (LMWH) or fondaparinux during last two weeks before surgery for other indication than hemodialysis
Minimum Eligible Age

18 Years

Eligible Sex

ALL

Accepts Healthy Volunteers

No

Sponsors

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University of Helsinki

OTHER

Sponsor Role collaborator

Helsinki University Central Hospital

OTHER

Sponsor Role lead

Responsible Party

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Arie Passov

MD, Resident in Anaesthesiology and Intensive Care Medicine

Responsibility Role PRINCIPAL_INVESTIGATOR

Principal Investigators

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Eero Pesonen, PhD

Role: STUDY_CHAIR

Helsinki University Central Hospital

Locations

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Helsinki University and Helsinki University Hospital

Helsinki, , Finland

Site Status

Countries

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Finland

References

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Eltzschig HK, Eckle T. Ischemia and reperfusion--from mechanism to translation. Nat Med. 2011 Nov 7;17(11):1391-401. doi: 10.1038/nm.2507.

Reference Type BACKGROUND
PMID: 22064429 (View on PubMed)

Nemeth N, Furka I, Miko I. Hemorheological changes in ischemia-reperfusion: an overview on our experimental surgical data. Clin Hemorheol Microcirc. 2014;57(3):215-25. doi: 10.3233/CH-131648.

Reference Type BACKGROUND
PMID: 23340000 (View on PubMed)

Sevastos J, Kennedy SE, Davis DR, Sam M, Peake PW, Charlesworth JA, Mackman N, Erlich JH. Tissue factor deficiency and PAR-1 deficiency are protective against renal ischemia reperfusion injury. Blood. 2007 Jan 15;109(2):577-83. doi: 10.1182/blood-2006-03-008870. Epub 2006 Sep 21.

Reference Type BACKGROUND
PMID: 16990608 (View on PubMed)

Esmon CT. Targeting factor Xa and thrombin: impact on coagulation and beyond. Thromb Haemost. 2014 Apr 1;111(4):625-33. doi: 10.1160/TH13-09-0730. Epub 2013 Dec 12.

Reference Type BACKGROUND
PMID: 24336942 (View on PubMed)

Sorensen-Zender I, Rong S, Susnik N, Lange J, Gueler F, Degen JL, Melk A, Haller H, Schmitt R. Role of fibrinogen in acute ischemic kidney injury. Am J Physiol Renal Physiol. 2013 Sep 1;305(5):F777-85. doi: 10.1152/ajprenal.00418.2012. Epub 2013 Jun 26.

Reference Type BACKGROUND
PMID: 23804451 (View on PubMed)

Favreau F, Thuillier R, Cau J, Milin S, Manguy E, Mauco G, Zhu X, Lerman LO, Hauet T. Anti-thrombin therapy during warm ischemia and cold preservation prevents chronic kidney graft fibrosis in a DCD model. Am J Transplant. 2010 Jan;10(1):30-9. doi: 10.1111/j.1600-6143.2009.02924.x. Epub 2009 Dec 2.

Reference Type BACKGROUND
PMID: 19958330 (View on PubMed)

Turunen AJ, Lindgren L, Salmela KT, Kyllonen LE, Petaja J, Pesonen EJ. Intragraft coagulation events and delayed graft function in clinical renal transplantation. Transplantation. 2008 Mar 15;85(5):693-9. doi: 10.1097/TP.0b013e31816615d8.

Reference Type BACKGROUND
PMID: 18337662 (View on PubMed)

Halloran PF, Aprile MA, Farewell V, Ludwin D, Smith EK, Tsai SY, Bear RA, Cole EH, Fenton SS, Cattran DC. Early function as the principal correlate of graft survival. A multivariate analysis of 200 cadaveric renal transplants treated with a protocol incorporating antilymphocyte globulin and cyclosporine. Transplantation. 1988 Aug;46(2):223-8.

Reference Type BACKGROUND
PMID: 3043779 (View on PubMed)

Other Identifiers

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Dnro/64/13/03/02/2015

Identifier Type: OTHER

Identifier Source: secondary_id

Dnro/64/13/03/02/2015

Identifier Type: -

Identifier Source: org_study_id

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