Figure 69

Schematic presentation of the potential pathways incriminated in the pathogenesis of chronic TIN caused by primary tubular injury (dark boxes) or secondary to glomerular disease (light boxes). The mechanism by which TIN is mediated remains to be elucidated. Chronic tubular epithelial cell injury appears to be pivotal in the process. The injury may be direct through cytotoxicity or indirect by the induction of an inflammatory or immunologic reaction. Studies in experimental models and humans provide compelling evidence for a role of immune mechanisms. The infiltrating lymphocytes have been shown to be activated immunologically. It is the inappropriate release of cytokines by the infiltrating cells and loss of regulatory balance of normal cellular regeneration that results in increased fibrous tissue deposition and tubular atrophy. Another potential mechanism of injury is that of increased tubular ammonia-genesis by the residual functioning but hypertrophic tubules. Increased tubular ammoniagenesis contributes to the immunologic injury by activating the alternate complement pathway.

Altered glomerular permeability with consequent proteinuria appears to be important in the development of TIN in primary glomerular diseases. By the same token, the proteinuria that develops late in the course of primary TIN may contribute to the tubular cell injury and aggravate the course of the disease.

In primary vascular diseases TIN has been attributed to ischemic injury. In fact, hypertension is probably the most common cause of TIN. The vascular lesions that develop late in the course of primary TIN, in turn, can contribute to the progression of TIN. (From Eknoyan [3]; with permission.)

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