Silicon nephropathy

Saldanha, Leopoldo F.; Rosen, Victor J.; Gonick, Harvey C.

doi:10.1016/0002-9343(75)90326-5

Cited by 50 publications

(25 citation statements)

References 15 publications

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“…Numerous case reports of severe glomerulonephritis with renal failure occurring in persons with acute silicosis have been described as "silicon nephropathy" (27,28). Immunologic abnormalities are often reported as common in these cases and a potential exists for immune-mediated renal injury.…”

Section: Glomerulonepliritismentioning

confidence: 99%

Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

310

176

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Exposure to coal mine dust and/or crystalline silica results in pneumoconiosis with initiation and progression of pulmonary fibrosis. This review presents characteristics of simple and complicated coal workers' pneumoconiosis (CWP) as well as pathologic indices of acute and chronic silicosis by summarizing results of in vitro, animal, and human investigations. These results support four basic mechanisms in the etiology of CWP and silicosis: a) direct cytotoxicity of coal dust or silica, resulting in lung cell damage, release of lipases and proteases, and eventual lung scarring; b) activation of oxidant production by pulmonary phagocytes, which overwhelms the antioxidant defenses and leads to lipid peroxidation, protein nitrosation, cell injury, and lung scarring; c) activation of mediator release from alveolar macrophages and epithelial cells, which leads to recruitment of polymorphonuclear leukocytes and macrophages, resulting in the production of proinflammatory cytokines and reactive species and in further lung injury and scarring; o) secretion of growth factors from alveolar macrophages and epithelial cells, stimulating fibroblast proliferation and eventual scarring. Results of in vitro and animal studies provide a basis for proposing these mechanisms for the initiation and progression of pneumoconiosis. Data obtained from exposed workers lend support to these mechanisms.

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Section: Glomerulonepliritismentioning

confidence: 99%

Silicosis and coal workers' pneumoconiosis.

Castranova

Vallyathan

2000

Environ Health Perspect

310

176

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“…Anecdotal reports and uncontrolled studies of clinical and pathological case series suggest that severe pulmonary silicosis, especially acute silicosis, is associated with glomerulotubular disease. [1][2][3][4][5][6][7][8] We have also reported preliminary findings from a recent cross 907 sectional study of an increased urinary excretion of albumin, a-l-microglobulin (AMG), and [-Nacetyl-glucosaminidase (NAG) in granite workers with high exposure to silica compared with healthy unexposed subjects.9 Some of these alterations in renal function, particularly for albumin and NAG, were apparently greater and persistent in silicotic subjects who were assumed to have had greater exposure to dust and who had not been exposed to silica for many years. We have replicated the study in another larger group of granite workers, with the further aim of elucidating the exposure-effect relation between the urinary alterations on the one hand and the intensity and duration of exposure to silica on the other.…”

Section: Introductionmentioning

confidence: 99%

Further evidence of human silica nephrotoxicity in occupationally exposed workers.

Lee²,

Phoon³

1993

Occupational and Environmental Medicine

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It has previously been shown that granite workers with heavy exposure to silica had glomerular and proximal tubular dysfunction evidenced by increased urinary excretions of albumin, a-l-microglobulin (AMG), and -Nacetyl-glucosaminidase (NAG). The investigation was replicated in another group of granite workers to further elucidate the exposure effect relation. The urinary excretion of albumin, a-l-microglobulin (AMG), /-2-microglobulin (BMG), and /-N-acetylglucosaminidase (NAG) was determined in two groups of granite workers with low and high exposure to silica. Low molecular weight proteinuria and enzymuria were significantly correlated with duration of exposure in the high but not the low exposure group. These increases were most pronounced in those with 10 or more years of heavy exposure, and in those with radiological evidence of pulmonary fibrosis, particularly those with rounded small opacities denoting classical silicosis. These results provide further evidence that prolonged and heavy exposure to silica is associated with nephrotoxic effects in granite workers. (British J7ournal ofIndustrial Medicine 1993;50:907-912).The evidence that silica is nephrotoxic in occupationally exposed persons is limited. Anecdotal reports and uncontrolled studies of clinical and pathological case series suggest that severe pulmonary silicosis, especially acute silicosis, is associated with glomerulotubular disease. [1][2][3][4][5][6][7][8] We have also reported preliminary findings from a recent cross 907 sectional study of an increased urinary excretion of albumin, a-l-microglobulin (AMG), and [-Nacetyl-glucosaminidase (NAG) in granite workers with high exposure to silica compared with healthy unexposed subjects.9 Some of these alterations in renal function, particularly for albumin and NAG, were apparently greater and persistent in silicotic subjects who were assumed to have had greater exposure to dust and who had not been exposed to silica for many years. We have replicated the study in another larger group of granite workers, with the further aim of elucidating the exposure-effect relation between the urinary alterations on the one hand and the intensity and duration of exposure to silica on the other. Materials and methodsThe study subjects were selected from among a total of 159 workers in three granite quarries (not covered in the previous study), who held jobs with differing intensities of exposure to dust. A high dust exposure group of workers included those who were employed regularly in rock drilling and rock crushing jobs for at least a year; whereas a low exposure group included the rest of the workers who were mostly employed in equipment and vehicle maintenance and servicing work in the workshops, as loader operators and dumper truck drivers, and other administrative workers (clerks, office assistants, storemen etc). The exclusion criteria were a known history of glomerulonephritis, urinary calculi, or other renal diseases or diabetes, hypertension, or regular recent ingestion of analgesics. A total ...

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“…Saldanha et al [4] were the first to write about a case with albuminuria and high blood pressure along with industrial silicone exposure, describing silicone in renal tissue and modification of the proximal tubules. An epidemiological study was performed by Calvert et al [5] investigating gold miners' silicosis and end-stage renal diseases.…”

Section: Discussionmentioning

confidence: 99%

Silicosis and urinary analysis

Altinoz¹

2018

South Clin Ist Euras

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Silicon nephropathy

Cited by 50 publications

References 15 publications

Silicosis and coal workers' pneumoconiosis.

Silicosis and coal workers' pneumoconiosis.

Further evidence of human silica nephrotoxicity in occupationally exposed workers.

Silicosis and urinary analysis

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