Figure 171

Schematic representation of some of the events pursuant to a renal insult and epithelial cell repair. Subcellular; Initial events include a decrease in cellular ATP and an increase in intracellular free calcium. There is blebbing of the endoplasmic reticulum with mitochondrial swelling and dysfunction. The brush border of the proximal tubules is sloughed into the tubule lumen, and there is redistribution of membrane proteins with the loss of cellular polarity. Cellular; At a cellular level this results in three populations of tubule cells, depending on the severity of the insult. Some cells are intact and are poised to participate in the proliferative process (Pathway 1). Growth factors participate by stimulating cells to undergo mitosis. Nonlethally injured cells have the potential to follow one of two pathways. In the appropriate setting, perhaps stimulated by growth factors, these cells may recover with restoration of cellular integrity and function (Pathway 2); however, if the injury is significant the cell may still die, but through a process of programmed cell death or apopto-sis. The third population of cells are those with severe injury that undergo necrotic cell death. Nephron/Kidney; With the reepithelialization of damaged nephron segments and cellular recovery of structural and functional integrity, renal function is restored. (Modified from Toback [1]; with permission.)

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