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Ischemia reperfusion injury in kidney transplantation: A case report

RATIONALE: Kidney transplantation is considered the best treatment for patients with end stage renal disease. Ischemia- reperfusion injury (IRI) is an evitable event after deceased donor transplantation and influences short term and long term graft outcome. Few data on IRI's histology in the se...

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Detalles Bibliográficos
Autores principales: Philipponnet, Carole, Aniort, Julien, Garrouste, Cyril, Kemeny, Jean-Louis, Heng, Anne-Elisabeth
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Wolters Kluwer Health 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6314654/
https://www.ncbi.nlm.nih.gov/pubmed/30593134
http://dx.doi.org/10.1097/MD.0000000000013650
Descripción
Sumario:RATIONALE: Kidney transplantation is considered the best treatment for patients with end stage renal disease. Ischemia- reperfusion injury (IRI) is an evitable event after deceased donor transplantation and influences short term and long term graft outcome. Few data on IRI's histology in the setting of kidney transplantation are available in the literature despite its frequency and its severity. PATIENT CONCERNS: A 64-year-old patient was admitted for his 1st kidney transplantation. There were no pre-existing immunization. The surgery proceeded without complications; with cold ischemia estimated at 37 h 50 min and warm ischemia at 44 min. The immunosuppression protocol was as follows: induction by thymoglobulins, mycophelonate mofetil, corticosteroids. Few hours after transplantation, the patient remained anuric and the biological assessment highlighted in addition to renal failure, hyperlactatemia at 5 mmol/L and a high increase in lactate deshydrogenase (LDH) at 5239 U/L. An abdominopelvic angio-scanner was performed urgently to eliminate the hypothesis of thrombosis of the artery or vein of the graft. A kidney biopsy was performed the day after the transplant and revealed massive lesions of acute tubular necrosis including apoptosis, autophagy-associated cell death, and necrosis. Microvascular dysfunction with increased vascular permeability and endothelial cell inflammation were also present. Activation of coagulation is represented by thrombi in the lumens of the glomerular capillaries. DIAGNOSIS: The diagnosis was ischemia reperfusion injury responsible for delayed graft function (DGF). INTERVENTIONS: Immunosuppressive regimen was delayed use of calcineurin inhibitors, mycophenolate mofetil, and corticosteroids. OUTCOMES: At 1 year post transplant, the patient has a renal autonomy with a graft function stable and physiological proteinuria. LESSONS: The main clinical consequences of IRI in kidney transplant are DGF, acute and chronic graft rejection, and chronic graft dysfunction. Reducing IRI is one of the most relevant challenge in kidney transplantation.