Table 3.

Cases describing silicosis combined with renal pathological changes in literatures.

Year	Author	Case descriptions	Renal pathologic features	References
1975	Saldanha LF et al.	A 44-year-old man with history of significant industrial silica exposure who presented with hypertension and proteinuria.	Focal glomerulonephritis, intraluminal sloughing of the proximal convoluted tubule, cytoplasmic vacuolization and granularity.	[25]
1977	Suratt PM et al.	Four men developed silicosis after sandblasting tombstones for an average of 35 months and two of them developed lupus erythematosus and focal glomerulonephritis respectively.	Mild proliferative glomerulonephritis.	[30]
1978	Giles RD et al.	A 23-year-old sandblaster who developed acute onset massive proteinuria and fatal renal failure.	Mild proliferative glomerulonephritis with loss of colloidal iron staining for sialoprotein, and electron microscopy disclosed an increased density of epithelial cytoplasm, altered lysosomes and endothelial cell microtubular structures.	[26]
1980	Hauglustaine D et al.	A 37-year-old white male, working in a tile factory, presented proteinuria with no obvious tubular dysfunctional.	Mild focal segmental proliferative glomerulonephritis. Distinct alterations were found by electron microscopy, especially in the proximal tubular cells.	[31]
1981	Bolton WK et al.	Rapidly progressive renal failure developed in 4 patients with silica exposure. 3 presented with manifestations of a connective tissue disorders. All had abnormal proteinuria, hypoalbuminemia and active urinary sediments.	Glomerular hypercellularity and sclerosis, crescents, interstitial cellular infiltrates and tubular necrosis with red cell casts as seen on light microscopy. On electron microscopy there was foot process obliteration, characteristic cytoplasmic dense lysosomes, microtubules and dense deposits.	[32]
1983	Cledes J et al.	A 59-year old sand-blaster, histologically proven silicosis was complicated by systemic lupus erythematosus (SLE) and nephritis.	Focal glomerulonephritis with IgG, IgA and C1q deposits.	[33]
1983	Banks DE et al.	A coal miner presented with pulmonary changes consistent with acute silico lipoproteinosis who developed proteinuria and hematuria.	Diffusely thickened glomerular basement membrane, foot process effacement, and dense lamellar inclusions in swollen glomerular epithelial cells, similar to those seen in Fabry’s disease.	[34]
1987	Osorio AM et al.	A 54-year-old foundry worker with extensive silica exposure, developed the nephrotic syndrome and renal failure over a 3-month period.	Proliferative glomerulonephritis.	[27]
1987	Bonnin A et al.	Three men, (50, 67 and 69 years old) with the history of pulmonary silicosis, and two of them presented with microscopic hematuria, mild renal failure, and high blood pressure, and all had glomerular type proteinuria.	Crescentic IgA mesangial nephropathy.	[28]
1989	Arnalich F et al.	A 55-year-old white male, with silicosis diagnosed 10 years earlier, presented massive proteinuria with microscopic hematuria, moderate renal failure and distal polyneuropathy.	Focal segmental necrotizing glomerulonephritis and arteriolitis.	[35]
1989	Sherson D et al.	A 56-year-old man worked as a sandblaster for 30 years, and had rapidly progressive crescentic glomerulonephritis.	Severe crescentic glomerulonephritis with significant edema and cellular infiltration in the interstitium.	[36]
1990	Dracon M et al.	A series of 11 coal miners demonstrating a progressive renal failure with a syndrome of rapidly progressive glomerulonephritis and 3 of them had IgA deposition.	Crescentic glomerulonephritis.	[37]
1991	Pouthier D et al.	A 43-year-old stone cutter with 13 years of exposure to silica developed a pulmonary silicosis and a glomerulonephritis with moderate renal failure.	Segmental and focal mesangial proliferation and on electron microscopy, distinct alterations of the proximal tubular cells.	[38]
1994	Neyer U et al.	A 55-year-old male had Wegener’s granulomatosis after silica exposure.	Severe active glomerulonephritis with intra- and extra-capillary proliferation and crescents in more than 50% of the glomerulus.	[39]
1996	Wilke RA et al.	A 58-year-old coal miner as an employee of the chemical industry suffered from end-stage renal disease.	Glomerulosclerosis and chronic interstitial nephritis	[40]
2001	Nakajima H et al.	A 63-year-old man had the history of silicosisand had been diagnosed as glomerulonephritis.	Pauci-immune necrotizing crescentic glomerulonephritis	[41]
2001	Fujii Y et al.	A 51-year-old male who had been working as a building wrecker for 20 years suffered from IgA nephropathy.	Mild mesangial matrix expansion and mesangial cell proliferation with IgA deposition.	[42]
2003	Mulloy KB et al.	A 63-year-old male who worked in Department of Energy facilities and was diagnosed as microscopic polyangiitis, systemic necrotizing vasculitis, vasculitis, and glomerulonephritis.	Proliferative (crescentic) and necrotizing glomerulonephritis.	[43]
2010	Dahlgren J et al.	A 38-year-old male was diagnosed as Goodpasture’s syndrome after high level of exposure to crystalline silica	Global glomerulonephritis	[44]
2016	Riccò M et al.	A 68-year-old male (smoker) was diagnosed as IgA nephropathy after exposure to magnanimous silica dusts.	Glomerular sclerosis with IgA deposition, signs of diffuse vasculitis and tubular atrophy	[45]
2016	Lee JW et al.	A 56-year-old male presented with silicosis and had an occupational history of precious metal processing for 30 years and a 30 pack-year smoking history, and diagnostic analysis revealed perinuclear ANCA-associated microscopic polyangiitis	Chronic sclerosing glomerulonephritis suggesting ANCA-associated crescentic glomerulonephritis	[46]