Cell survival or death in renal tubular epithelium after ischemia-reperfusion injury

• Published in: Kidney international Vol. 56; no. 4; pp. 1299 - 1304
• Main Authors: Gobé, Glenda, Willgoss, Desley, Hogg, Nicole, Schoch, Estelle, Endre, Zoltan
• Format: Journal Article Conference Proceeding
• Language: English
• Published: New York, NY Elsevier Inc 01.10.1999; Nature Publishing
• Subjects: Acute Kidney Injury - pathology; Animals; apoptosis; Apoptosis - physiology; Bcl-2 gene; bcl-X Protein; Biological and medical sciences; Body Weight; Cell Division - physiology; Cell Survival - physiology; Epidermal Growth Factor - analysis; Epithelial Cells - cytology; Insulin-Like Growth Factor I - analysis; ischemic renal injury; Loop of Henle - blood supply; Loop of Henle - chemistry; Loop of Henle - cytology; Male; Medical sciences; Necrosis; Nephrology. Urinary tract diseases; Nephropathies. Renovascular diseases. Renal failure; Proliferating Cell Nuclear Antigen - analysis; Proto-Oncogene Proteins c-bcl-2 - analysis; Proto-Oncogene Proteins c-bcl-2 - physiology; Rats; Rats, Sprague-Dawley; Regeneration - physiology; Renovascular diseases; Reperfusion Injury - pathology; Transforming Growth Factor beta - analysis; Tropical medicine; apoptosis; ischemic renal injury; necrosis; Bcl-2 gene; Kidney disease; Urinary system disease; Rat; Acute; Rodentia; Cardiovascular disease; Kidney; Vascular disease; Vertebrata; Experimental disease; Renal tubule; Mammalia; Reperfusion; Ischemia; Cell death; Dysfunction; Animal; Renal failure; Epithelial cell; Apoptosis
• ISSN: 0085-2538; 1523-1755
• DOI: 10.1046/j.1523-1755.1999.00701.x

Cell survival or death in renal tubular epithelium after ischemia-reperfusion injury. A major contributor to the development and progression of ischemia-reperfusion (IR)–induced acute renal failure (ARF) is the loss of functioning tubular epithelial cells by means of various cell deletion or death processes. Although the term “acute tubular necrosis” is still used to describe the pathology of ARF, this is a misnomer because apoptotic cell death, as well as necrosis, occurs[1],[2] along with desquamation and loss of viable epithelial cells[3]. Apoptosis was first described in renal disease in 1987 in an animal model of hydronephrosis[4]. In ARF, with reference to only the death processes, the relative contribution of necrosis or apoptosis possibly depends on the extent of the initiating events. For example, after prolonged total renal ischemia, necrosis or “accidental cell death” occurs from the resultant negation of the cell's energy and protein levels. In apoptosis, the cells use their own energy processes and proteins to die, and often the initiating ischemia is more mild[5]. Finally, despite prolonged ischemia, within the heterogeneous renal cell populations there are those that are more sensitive to ischemia, such as the proximal straight tubule and to some extent the thick ascending limb (TAL) of the loop of Henle. It may be hypothesized that these cells tend to undergo necrosis in comparison with the less sensitive segments that undergo apoptosis. Because apoptosis is gene driven, its identification is important because of the possibility of its modulation via molecular controls. However, despite these new concepts of ARF, patient death remains high, at approximately 30 to 50% of ARF cases. Recovery from ARF depends not only on the replacement or regeneration of cells deleted by death, the theme of many recent studies, but also on protection of cells from death. Both processes are dependent on many of the cellular and molecular controls that have evolved in multicellular organisms to manage normal development, differentiation and growth processes, but that then become involved in the pathogenesis and progression of many renal diseases, including ARF.