Renal disease rapidly progressive glomerulonephritis

During the past decade a number of case reports have described the occurrence of different forms of renal disease in patients exposed to silica [58-66]. However, only a few reports concerned subjects exposed to sihca but without silicosis. Most of the cases demonstrated renal lesions compatible with rapidly progressive glomerulonephritis with a necrotizing component present in most cases. Crescent formation was described in a patient with proliferative glomerulonephritis [59] and three individuals with IgA nephropathy [60]. 

Chronic renal failure as a result of toxic or environmental exposures usually involve progressive chronic interstitial nephropathy, which, in addition to prolonged analgesic abuse, may result from chronic lithium ingestion, heavy metal exposure or treatment with cyclosporine [2]. Exposure to hydrocarbons may accentuate the renal insufficiency in patients with preexisting renal disease or result in the appearance of the nephrotic syndrome or a form a rapidly progressive glomerulonephritis. 

By summarizing various studies and case reports, Gregorini (working in Brescia) showed that extrapul-monary silicotic lesions and/or autoimmune processes may play a role in kidney diseases after silica exposure, more specifically MPO-ANCA-positive microscopic polyangiitis and its renal-limited form of idiopathic , rapidly progressive glomerulonephritis (Conrad et al. 

Kidney disease is observed in 16% to 49% of CSS patients, usually presenting as rapidly progressive glomerulonephritis with necrosis, crescents, or both (2,3,37,38). Interstitial eosinophil and neutrophil infiltration with edema is also possible. Although mostly associated with anti-MPO Ab (2,3), it is a pauci-immune glomerulonephritis. Other renal manifestations include proteinuria, hypertension, renal insufficiency, and/or renal infarction with or without microaneurysms (1,4,16,22-24,36,38). 

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