Edelstein C L, Ling H, Wangsiripaisan A, Schrier R W
Department of Medicine, University of Colorado School of Medicine, Denver 80262, USA.
Am J Kidney Dis. 1997 Nov;30(5 Suppl 4):S89-95. doi: 10.1016/s0272-6386(97)90548-5.
Ischemia is the most common cause of acute renal failure (ARF). In the last decade, several new and important pathophysiological mechanisms that underlie the renal dysfunction have been discovered. These pathophysiological mechanisms include the role of both calcium and calcium-dependent enzymes, oxidant stress, loss of polarity of the tubular cell, tubular obstruction and arginine-glycine-aspartic acid (RGD) peptides, neutrophils, intracellular adhesion molecules (ICAM), and growth factors. A better understanding of tubular and vascular mechanisms has led to therapeutic studies in animals and clinical trials in humans. In this review, the pathophysiology of ischemic ARF will be correlated with the rationale for both current and future therapies.
缺血是急性肾衰竭(ARF)最常见的病因。在过去十年中,已经发现了几种导致肾功能障碍的新的重要病理生理机制。这些病理生理机制包括钙和钙依赖性酶的作用、氧化应激、肾小管细胞极性丧失、肾小管阻塞以及精氨酸-甘氨酸-天冬氨酸(RGD)肽、中性粒细胞、细胞间黏附分子(ICAM)和生长因子。对肾小管和血管机制的更好理解已促成了动物治疗研究和人体临床试验。在本综述中,缺血性ARF的病理生理学将与当前及未来治疗的理论依据相关联。