Lead nephropathy. Arrows indicate the characteristic intranuclear inclusions. Exposure to a variety of heavy metals results in development of chronic TIN. Of these metals, the more common and clinically important implicated agent is lead. Major sources of exposure to lead are lead-based paints; lead leaked into food during storage or processing, particularly in illegal alcoholic beverages (moonshine); and increasingly, through environmental exposure (gasoline and industrial fumes). This insidious accumulation of lead in the body has been implicated in the causation of hyperuricemia, hypertension, and progressive renal failure. Gout occurs in over half of cases. Blood levels of lead usually are normal. The diagnosis is established by demonstrating increased levels of urinary lead after infusion of 1 g of the chelating agent erthylenediamine tetraacetic acid (EDTA).
The renal lesions of lead nephropathy are those of chronic TIN. Cases examined early, before the onset of end-stage renal disease, show primarily focal lesions of TIN with relatively little interstitial cellular infiltrates. In more advanced cases the kidneys are fibrotic and shrunken. On microscopy, the kidneys show diffuse lesions of TIN. As expected from the clinical features, hypertensive vascular changes are prominent.
Other heavy metals associated with TIN are cadmium, silicon, copper, bismuth, and barium. Sufficient experimental evidence and some weak epidemiologic evidence suggest a possible role of organic solvents in the development of chronic TIN.
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