When Silica Causes The Immune System To Attack The Kidneys
Why does glomerulonephritis happen?
Glomerulonephritis is usually the result of a problem with the immune system, which causes it to attack healthy tissue in the kidneys. However, there are many cases where the exact cause is unknown.
It can occur by itself or be part of a more general condition, such as
vasculitis or
lupus.
Glomerulonephritis is sometimes short-lived (acute), but often lasts for a long time (chronic).
Silica and glomerulonephritis: case report and review of the literature.
Abstract
A 54-year-old foundry worker with extensive silica exposure, but no pulmonary disease, developed the nephrotic syndrome and renal failure over a 3-month period. Renal biopsy demonstrated a proliferative glomerulonephritis; energy dispersive x-ray analysis detected silicon within the renal tubules. Measurements of respirable silica at the foundry revealed levels up to 2.5 times the current occupational standard. Similar glomerular disease has been reported in silica-exposed animals and workers with silicosis. This case suggests that clinicians should include silica exposure in the differential diagnosis of unexplained diffuse proliferative glomerulonephritis, renal disease may occur without clinically evident pulmonary disease in silica exposure, and silica-induced glomerulonephritis warrants further clinical and epidemiologic research.
Silica and renal diseases: no longer a problem in the 21st century?
Abstract
Silicosis and other occupational diseases are still important even in the most developed countries. In fact, at present, silica exposure may be a risk factor for human health not only for workers but also for consumers. Furthermore, this exposure is associated with many other different disorders besides pulmonary silicosis, such as progressive systemic sclerosis, systemic lupus erythematosus, rheumatoid arthritis, dermatomyositis, glomerulonephritis and vasculitis. The relationships between these silica-related diseases need to be clarified, but pathogenic responses to silica are likely to be mediated by interaction of silica particles with the immune system, mainly by activation of macrophages. As regards renal pathology, there is no single specific clinical or laboratory finding of silica-induced nephropathy: renal involvement may occur as a toxic effect or in a context of autoimmune disease, and silica damage may act as an additive factor on an existing, well-established renal disease. An occupational history must be obtained for all renal patients, checking particularly for exposure to silica, heavy metals, and solvents.
[Pulmonary silicosis and glomerular nephropathy. Apropos of 1 case].
[Article in French]
Abstract
A 43-year-old stone cutter with 13 years of exposure to silica developed a pulmonary silicosis and a glomerulonephritis with moderate renal failure. Renal biopsy demonstrated in light microscopy a segmental and focal mesangial proliferation and in electron microscopy distinct alterations of the proximal tubular cells. Renal histology suggest silica may play a part in the pathogenesis of renal damage. Clinicians should therefore include silica exposure in the differential diagnosis of unexplained glomerulonephritis.
Association between silica exposure and necrotizing crescentic glomerulonephritis with p-ANCA and anti-MPO antibodies: a hospital-based case-control study.
- 1Department of Nephrology, University of Brescia, Italy.
Abstract
A hospital-based case-control study was carried out to investigate the association between ANCA positive rapidly progressive glomerulonephritis (RPGN) and occupational exposure to silica dust. All ANCA positive male patients admitted to the Department of Nephrology of the University of Brescia between 1987 and 1992 were enrolled in the study as cases. The controls were pts of the same age, admitted at the Department immediately before or after the cases, affected by other renal diseases. Seven of the 16 cases and one of the 32 controls, had a positive history for jobs exposing to silica dust (relative risk 14; 95% C.I.: 1.7-113.8, p < 0.001). ANCA pattern was p-ANCA with anti-MPO antibodies in 6/7 of exposed pts. The review of renal histology showed a distinctive glomerular lesion consisting in peripheral nodular areas of glomerular sclerosis, in addition to the crescentic necrotizing glomerulonephritis, in 3/6 silica exposed pts, but in none of the unexposed pts.
