Chatauret N, Badet L, Barrou B, Hauet T
INSERM, U1087, Ischémie-reperfusion en transplantation d'organe : mécanismes et innovations thérapeutiques, Poitiers ; université de Poitiers, faculté de Médecine et de Pharmacie, 86021 Poitiers, France; CHU de Poitiers, Laboratoire de biochimie, 86021 Poitiers, France.
INSERM, U1087, Ischémie-reperfusion en transplantation d'organe : mécanismes et innovations thérapeutiques, Poitiers ; université de Poitiers, faculté de Médecine et de Pharmacie, 86021 Poitiers, France.
Prog Urol. 2014 Jun;24 Suppl 1:S4-12. doi: 10.1016/S1166-7087(14)70057-0.
Ischemia reperfusion injury occurs in the kidney when blood supply is interrupted in clinical settings such as kidney transplantation or nephron sparing surgery for renal tumors. These lesions lead to acute kidney injury (AKI) a detrimental situation associated with impaired short-term allograft function (delayed graft function or primary non function) but also long-term transplant survival through the onset of chronic allograft nephropathy. The present review details the cellular and molecular consequences of ischemia reperfusion in a native kidney as well as in a kidney graft after cold ischemia time, giving a comprehensive description of biological pathways involved during the phase of ischemia and during the reperfusion period where the rapid return to normoxia leads to a large burst of reactive oxygen species along with a dramatic reduction in antioxidant defenses. This work also focuses on the distinct susceptibilities of kidney cells to ischemia (endothelial vs epithelial) and the outcome of acute kidney injury.
在肾移植或肾肿瘤保留肾单位手术等临床情况下，当肾脏血液供应中断时，就会发生缺血再灌注损伤。这些损伤会导致急性肾损伤（AKI），这是一种有害情况，不仅与短期移植肾功能受损（移植肾功能延迟恢复或原发性无功能）有关，还与慢性移植肾肾病的发生导致的长期移植肾存活有关。本综述详细阐述了在冷缺血时间后，天然肾脏以及肾移植中缺血再灌注的细胞和分子后果，全面描述了缺血期和再灌注期所涉及的生物学途径，在再灌注期，迅速恢复到正常氧合会导致大量活性氧的爆发以及抗氧化防御的显著降低。这项工作还关注肾细胞对缺血的不同易感性（内皮细胞与上皮细胞）以及急性肾损伤的结果。
