肾小管细胞损伤机制的研究进展

急性肾衰（ａｃｕｔｅ ｒｅｎａｌ ｆａｉｌｕｒｅ， ＡＲＦ）是一种常见的肾脏疾病［１］，急性肾衰病人的主要功能变化是肾小球滤过率（ＧＲＦ）减少，从而影响含氮代谢废物由尿排出、水、电解质和酸碱平衡。从病理学角度，多数急性肾小管损伤病人急性肾小管坏死的原因被解释为肾小管细胞死亡并不合适［２］。从形态学来看，人肾小管细胞损伤的本质常表现为亚致死和包括细胞肿胀、空泡的形成、表面变化（刷状缘丧失，形成尖疱等）以及细胞损伤［３］。在缺血性急性肾衰竭中，肾小管细胞损伤（包括坏死或凋亡）和引起功能紊乱的亚致死损伤…

Advances of the mechanisms of renal tubular cell injury

The nature of renal tubular cell injury in ischemic acute renal failure includes not only cell death (necrosis or apoptosis) but also sublethal injury causing cell dysfunction. The role of intracellu- lar calcium, calcium - dependent enzymes calpain, nitric oxide, phospholipase A2, loss of tubule cell polarity and tubular obstruction in the pathophysiology of the renal tubular cell injury during hypoxia/ischemia is described. The effects of vascular factors, infiltrating activited leukocytes, apoptosis and growth factors on renal tubular cell injury are discussed. Potential mechanisms that tubular injury leads to a profound fall in glomerular filtration rate are proposed.