Abstract
It is becoming increasingly clear that the final common pathogenetic pathway for the development of ischemic acute renal failure is renal tubular cell injury.1,2 Acute renal failure developing from an ischemic insult occurs from tubular cell injury that produces segmental necrosis in renal tubules, so that a patchy distribution of frankly necrotic lesions appears to be the rule rather than the exception in the pathology of acute renal failure.3 The segmental, patchy renal tubular cell necrosis initiates a variety of factors responsible at the nephronal level for excretory failure of the kidney. These factors include intratubular obstruction, backleak of glomerular filtrate, and glomerular hemodynamic alterations. Ultimately, the understanding of the pathogenesis of acute tubular necrosis resides in the understanding of the biochemical alterations responsible for renal tubular cell injury. In this regard, declines in levels of high energy phosphates within the cell, alterations in cellular calcium metabolism, and degradation of membrane phospholipids appear to be metabolic derangements induced by ischemia critical in the evolution of cell injury.
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© 1986 Plenum Press, New York
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Humes, H.D., Nguyen, V.D., Hunt, D.A. (1986). High Energy Phosphates, Phospholipids, and Calcium in Ischemic Renal Tubular Cell Injury. In: Massry, S.G., Olmer, M., Ritz, E. (eds) Phosphate and Mineral Homeostasis. Advances in Experimental Medicine and Biology, vol 208. Springer, Boston, MA. https://doi.org/10.1007/978-1-4684-5206-8_1
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DOI: https://doi.org/10.1007/978-1-4684-5206-8_1
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