FIGURE 6-25 (s

Chronic TIN secondary to vesicoureteral reflux (VUR). Clearly demonstrated is an area that is fairly intact (lower left corner) adjacent to one that shows marked damage. Urinary tract obstruction, whether congenital or acquired, is a common cause of chronic TIN. Clinically, superimposed infection plays a secondary, adjunctive, and definitely aggravating role in the progressive changes of TIN. However, the entire process can occur in the absence of infection.

As clearly demonstrated in experimental models of obstruction, mononuclear inflammatory cell infiltration is one of the earliest responses of the kidney to ureteral obstruction. The infiltrating cells consist of macrophages and suppressor-cytotoxic lymphocytes. The release of various cytokines by the infiltrating cells of the hydronephrotic kidney appears to exert a significant modulating role in the transport processes and hemodynamic changes seen early in the course of obstruction. With persistent obstruction, changes of chronic TIN set in within weeks. Fibrosis gradually becomes prominent.

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