Figure 612

Expression of human leukocyte antigen class II and adhesion molecules released by injured tubular epithelial cells, as well as by infiltrating cells, modulate and magnify the process to repair the injury (Figure 6-10). When the process becomes unresponsive to controlling feedback mechanisms, fibroblasts proliferate and increase fibrotic matrix deposition. The precise mechanism of TIN remains to be identified. A number of pathogenetic pathways have been proposed to operate at different stages of the disease process. Each of these individual pathways usually is part of a recuperative process that works in concert in response to injury. However, it is the loss of their controlling feedback in chronic TIN that seems to account for the altered balance and results in persistent cellular infiltrates, progressive fibrosis, and tubular degeneration.

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