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Geoffrey M. Calvert, MD, MPH; Kyle Steenland, PhD
National Institute for Occupational Safety and Health Centers for Disease Control and Prevention Cincinnati, Ohio

JAMA. 1997;278(7):547.

	Since this article does not have an abstract, we have provided the first 150 words of the full text PDF and any section headings.

We agree with Dr Wilke that the pathogenesis for the increased risk of ESRD caused by glomerulonephritis among silica-exposed gold miners is unclear. In our article, we described the competing theories of pathogenesis, ie, immunologic injury vs direct toxic effect of silica. Our intent was to give equal attention to these 2 theories. As is the case with silicosis, evidence of immunologic injury has been observed in some, but not all, silica-exposed patients with renal injury.¹

Therefore, different mechanisms of toxicity may be operating in different patients. In patients with evidence of immunologic abnormality, it is not clear if these abnormalities are directly responsible for renal injury or if they are a response to the direct toxic effect of silica. It is worth noting that there is evidence linking silica exposure to a broad range of autoimmune diseases.²

One factor responsible for the variability in the mechanism of . . . [Full Text PDF of this Article]

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