Figure

Secondary chronic TIN. The arrow indicates a glomerulus with a cellular crescent. The diagnosis of TIN can be established only by morphologic examination of kidney tissue. The extent of the lesions of TIN, whether focal or diffuse, correlates with the degree of impairment in renal function.

Tubular atrophy and dilation comprise a principal feature of TIN. The changes are patchy in distribution, with areas of atrophic chronically damaged tubules adjacent to dilated tubules displaying compensatory hypertrophy. In atrophic tubules the epithelial cells show simplification, decreased cell height, loss of brush border, and varying degrees of thickened basement membrane. In dilated tubules the epithelial cells are hypertrophic and the lumen may contain hyalinized casts, giving them the appearance of thyroid follicles. Hence the term thyroidization is used.

The interstitium is expanded by fibrous tissue, in which are interspersed proliferating fibroblasts and inflammatory cells comprised mostly of activated T lymphocytes and macrophages. Rarely, B lymphocytes, plasma cells, neutrophils, and even eosinophils may be present.

The glomeruli, which may appear crowded in some areas owing to tubulointerstitial loss, usually are normal in the early stages of the disease. Ultimately, the glomeruli become sclerosed and develop periglomerular fibrosis.

The large blood vessels are unremarkable in the early phases of the disease. Ultimately, these vessels develop intimal fibrosis, medial hypertrophy, and arteriolosclerosis. These vascular changes, which also are associated with hypertension, can be present even in the absence of elevated blood pressure in cases of chronic TIN.

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