Philipponnet Carole, Aniort Julien, Garrouste Cyril, Kemeny Jean-Louis, Heng Anne-Elisabeth
Department of Nephrology, Dialysis and Transplantation.
Department of Nephrology, Dialysis and Transplantation, UFR Medecine.
Medicine (Baltimore). 2018 Dec;97(52):e13650. doi: 10.1097/MD.0000000000013650.
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.
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.
The diagnosis was ischemia reperfusion injury responsible for delayed graft function (DGF).
Immunosuppressive regimen was delayed use of calcineurin inhibitors, mycophenolate mofetil, and corticosteroids.
At 1 year post transplant, the patient has a renal autonomy with a graft function stable and physiological proteinuria.
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.
肾移植被认为是终末期肾病患者的最佳治疗方法。缺血再灌注损伤(IRI)是尸体供肾移植后不可避免的事件,会影响移植肾的短期和长期预后。尽管IRI在肾移植中很常见且严重,但文献中关于其组织学的数据却很少。
一名64岁患者因首次肾移植入院。患者此前未进行过免疫接种。手术过程顺利,无并发症;冷缺血时间估计为37小时50分钟,热缺血时间为44分钟。免疫抑制方案如下:用抗胸腺细胞球蛋白诱导,联合霉酚酸酯和皮质类固醇。移植后数小时,患者仍无尿,生物学评估显示除肾衰竭外,乳酸水平升高至5mmol/L,乳酸脱氢酶(LDH)大幅升高至5239U/L。紧急进行了腹部盆腔血管扫描以排除移植肾动静脉血栓形成的可能性。移植后第二天进行了肾活检,并发现了急性肾小管坏死的大量病变,包括凋亡、自噬相关细胞死亡和坏死。还存在微血管功能障碍,伴有血管通透性增加和内皮细胞炎症。凝血激活表现为肾小球毛细血管腔内血栓形成。
诊断为缺血再灌注损伤导致移植肾功能延迟恢复(DGF)。
免疫抑制方案为延迟使用钙调神经磷酸酶抑制剂、霉酚酸酯和皮质类固醇。
移植后1年,患者肾功能自主,移植肾功能稳定,蛋白尿正常。
肾移植中IRI的主要临床后果是DGF、急慢性移植肾排斥反应和慢性移植肾功能障碍。减少IRI是肾移植中最相关的挑战之一。