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, cal...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.展开更多
文摘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.
