Occupational exposure to
heavy metals, organic
solvents and
silica is associated with a variety of renal manifestations. Improved understanding of occupational renal disease provides insight into environmental renal disease, improving knowledge of disease pathogenesis.
Silica (SiO2) is an abundant
mineral found in
sand, rock, and soil. Workers exposed to
silica include sandblasters, miners, quarry workers, masons, ceramic workers and glass manufacturers. New cases of
silicosis per year have been estimated in the US to be 3600-7300. Exposure to
silica has been associated with tubulointerstitial
disease, immune-mediated multisystem
disease, chronic kidney disease and
end-stage renal disease. A rare syndrome of painful, nodular skin lesions has been described in dialysis patients with excessive levels of
silicon.
Balkan endemic nephropathy is postulated to be due to chronic intoxication with
drinking water polluted by
silicates released during soil erosion. The mechanism of
silica nephrotoxicity is thought to be through direct nephrotoxicity, as well as
silica-induced
autoimmune diseases such as scleroderma and
systemic lupus erythematosus. The renal histopathology varies from focal to crescentic and necrotizing
glomerulonephritis with
aneurysm formation suggestive of
polyarteritis nodosa. The treatment for
silica nephrotoxicity is non-specific and depends on the mechanism and stage of the disease. It is quite clear that further research is needed, particularly to elucidate the pathogenesis of
silica nephropathy. Considering the importance of diagnosing exposure-related renal disease at early stages, it is imperative to obtain a thorough occupational history in all patients with renal disease, with particular emphasis on exposure to
silica,
heavy metals, and
solvents.